NASDAQ: LTRN

We
have active clinical programs for our three lead small
molecule drug candidates: LP-300, LP-184, and LP-284. These programs are focused on multiple important
cancer indications, including both solid tumors and blood cancers. We have established a wholly-owned subsidiary, Starlight Therapeutics,
to focus exclusively on the clinical development of our promising opportunities for central nervous system (“CNS”)
and brain cancers, many of which have no effective treatment options. We are also advancing an antibody-drug conjugate (“ADC”)
program focused on developing highly specific ADCs with highly potent drug-payloads.

In January 2026, we introduced withZeta.ai — a generative AI platform purpose-built to empower researchers
and clinicians to accelerate rare cancer research and drug development, dramatically improve research quality, and reduce R&D costs.
withZeta’s multi-agentic architecture combines intelligent orchestration using a combination of proprietary knowledge bases and publicly
available data with autonomous task completion to deliver a true “co-scientist” experience — one that brings the collective
insight of thousands of domain experts, millions of publications, and billions of data points to address some of oncology’s most difficult
challenges and disease subtypes.

In
2025, the FDA cleared two new Phase 1b/2 investigational new drug (IND) applications for LP-184, further expanding our clinical pipeline
opportunities. The first planned LP-184 Phase 1b/2 trial is positioned to evaluate LP-184 in recurrent triple negative breast cancer
(TNBC) patients as both a monotherapy and in combination with the PARP inhibitor olaparib. The second planned LP-184 Phase 1b/2 trial
is positioned to evaluate LP-184 in a biomarker-defined population of non-small cell lung cancer (NSCLC) patients harboring KEAP1 and/or
STK11 mutations with low PD-L1 expression, in combination with the immune checkpoint inhibitors nivolumab and ipilimumab — a population
with high unmet clinical need and a market opportunity estimated to exceed $2 billion annually. Additionally, LP-184 has received FDA
Fast Track Designations for GBM and TNBC, as well as multiple Orphan Drug and Rare Pediatric Disease Designations across various solid
tumor indications.

Our
strategy is to both develop new drug candidates using our RADR® platform and other machine learning driven methodologies,
and to pursue the development of drug candidates that have undergone previous clinical trial testing or that may have been halted in
development or deprioritized because of insufficient clinical trial efficacy or for strategic reasons by the owner or development team
responsible for the compound. Importantly, these historical drug candidates appear to have been well-tolerated in many instances, and
often have considerable data from previous toxicity, tolerability and ADME studies that have been completed. Our dual approach to both
develop de-novo, biomarker-guided drug candidates and “rescue” historical drug candidates by leveraging A.I., recent advances
in genomics, computational biology and cloud computing is emblematic of a new era in drug development that is being driven by data-intensive
approaches meant to de-risk development and accelerate the clinical trial process. In this context, we are working to create a diverse
portfolio of oncology drug candidates for further development towards regulatory and marketing approval with the objective of establishing
a leading A.I. driven, methodology for treating the right patient with the right oncology therapy.

1

A
key component of our strategy is to target specific cancer patient populations and treatment indications identified by leveraging our
RADR® platform, a proprietary A.I. enabled engine created and owned by us. Our RADR® platform has grown
to encompass more than 200 billion oncology-focused data points across proprietary, collaborative, and public sources, and employs a
library of 200+ advanced machine learning algorithms. During 2025, we have continued to expand the RADR® platform with
several significant new modules, including: (i) an AI-powered ADC development module that identifies targets, payloads, and tumor selectivity
using a multiomic approach; (ii) a combination regimen module trained on 221 clinical trials to predict the activity and efficacy of
DNA-damaging agent and DNA repair inhibitor combinations; and (iii) a blood-brain barrier (BBB) permeability prediction model that can
process up to 100,000 molecules per hour, for which a PCT patent application has been published with a favorable search report indicating
no significant prior art. Lantern’s BBB prediction algorithms currently hold five of the top ten positions on the Therapeutic Data
Commons (TDC) Leaderboard. We plan to commercially release select RADR® AI modules to the broader research and drug development
community to foster collaborative, open-source innovation in oncology.

Scientific
literature offers a definition for “drug rescue” as research involving abandoned small molecules and biologics that have
not been approved by the U.S. Food and Drug Administration (“FDA”). These rescued molecular compounds are often abandoned
by pharmaceutical companies in the drug discovery or preclinical testing phase, typically because they do not prove effective for the
specific use for which they were developed. Some of these compounds may be useful in treating other diseases for which they have not
been tested. See, Hemphill, Thomas A., “The NIH Promotes Drug Repurposing and Rescue,” Research Technology Management,
v. 5, no. 5, pp. 6-8 (2012). Our use of the term “rescue”, “drug rescue”, or “drug rescuing” refers
to, “…a system of developing new uses for chemical and biological entities that previously were investigated in clinical
studies but not further developed or submitted for regulatory approval, or had to be removed from the market for safety reasons.”,
which is a definition we believe is recognized in the drug discovery, drug development and pharmaceutical and biotechnology industries.
See, Naylor, S. and Schonfeld J., “Therapeutic Drug Repurposing, Repositioning and Rescue,” DDW (Drug Discovery World)
Winter 2014, and Mucke, HAM, A New Journal for the Drug Repurposing Community. Drug Repurposing, Rescue & Repositioning 1, 3-4 (2014).
The use of the term “drug rescue,” “rescuing,” or words of similar meaning in this report should not be construed
to mean that our RADR® platform has resolved all issues of safety and/or efficacy for any of our drug candidates. Issues
of safety and efficacy for any drug candidate may only be determined by the U.S. FDA or other applicable regulatory authorities in jurisdictions
outside the United States.

Our
current portfolio consists of three lead drug candidates that are in clinical phases (known as LP-300, LP-184 and LP-284) and an Antibody
Drug Conjugate (ADC) program that is in preclinical research optimization. In January 2023, we formed a wholly owned subsidiary, Starlight
Therapeutics Inc. (“Starlight”), to develop drug candidate LP-184’s central nervous system (CNS) and brain cancer indications
– including glioblastoma (GBM), brain metastases (brain mets.), and several rare pediatric CNS cancers. Following the formation
of Starlight, we may also refer to the molecule LP-184, as it is developed in CNS indications, as “STAR-001”. All of these
drug candidates and our ADC program are leveraging precision oncology, A.I. and genomic driven approaches to accelerate and direct development
efforts.

We
are conducting a targeted phase 2 trial (the Harmonic™ trial) for LP-300 in never smoking
patients with advanced non-small cell lung cancer (“NSCLC”) in combination with chemotherapy, under an existing investigational
new drug application. Our candidate LP-184 has shown promising in-vitro and in
vivo anticancer activity in multiple solid tumor indications (including pancreatic, lung, bladder,
glioblastoma and triple negative breast cancer), and enrollment has now been completed in a Phase 1a clinical trial for LP-184. Based
on the results and insights from the LP-184 Phase 1a clinical trial, we are advancing and optimizing development plans for multiple future
LP-184 clinical studies. Our candidate LP-284 has shown promising in-vitro and
in vivo anticancer activity in multiple hematological cancers, which are distinct
from the indications targeted by LP-184. LP-284 is advancing in a Phase 1A clinical trial.

2

Our
ADC program has also continued to advance. During 2024 and in 2025, we continued to apply our RADR® A.I. platform to advance
and refine an A.I. powered module focused on improving the precision, cost and timelines of ADC development for cancer. In
2023, we entered into a research collaboration with Bielefeld University in Germany focused on development of ADCs utilizing cryptophycin
as the ADC drug-payload. Cryptophycins are promising antitumor molecules that have demonstrated potency at ultra-low, picomolar, concentrations.
In a broad range of preclinical studies, the cryptophycin-ADC synthesized as part of the Bielefeld
collaboration demonstrated promising picomolar level potency and anti-tumor activity in multiple solid tumor cell lines, including breast,
bladder, colorectal, gastric, pancreatic and ovarian.

In
addition to our lead drug candidates and ADC program, we also have an additional drug candidate, LP-100, that we believe has potential
for future development in combination with the class of anticancer agents known as PARP inhibitors (PARPi). For LP-100, as well as our
lead drug candidate LP-300, we have leveraged data from prior preclinical studies and clinical trials, along with insights generated
from our A.I. platform, to target the types of tumors and patient groups we believe will be most responsive to the drug. Both LP-100
and LP-300 showed promise in important patient subgroups, but failed pivotal Phase 3 trials when the overall results did not meet the
predefined clinical endpoints. We believe that this was due to a lack of biomarker-driven patient stratification.

LP-300
has been studied in multiple randomized, controlled, multi-center non-small cell lung cancer, or NSCLC, trials that included administration
of either paclitaxel and cisplatin and/or docetaxel and cisplatin. LP-100 has previously been in a genomic signature guided phase 2 clinical
trial in Denmark for patients with metastatic castration resistant prostate cancer (mCRPC). 9 patients (out of a targeted enrollment
of 27) were treated in the trial. The median overall survival (OS) for the initial group of 9 patients was approximately 12.5 months,
which is an improvement over other similar fourth-line treatment regimens for mCRPC. Based on our evaluation of the synergies of LP-100
with PARP inhibitors, the decision was made in the first quarter of 2023 to close the phase 2 clinical trial in Denmark, to allow the
focus of LP-100-directed resources on positioning the molecule for development in earlier lines of therapy with potentially larger market
opportunities. LP-100 was previously out-licensed by us to Allarity Therapeutics A/S. In July 2021, we entered into an Asset Purchase
Agreement to reacquire global development and commercialization rights for LP-100 from Allarity.

Our
development strategy is to pursue an increasing number of oncology focused, molecularly targeted therapies where artificial intelligence
and genomic data can help us provide biological insights, reduce the risk associated with development efforts and help clarify potential
patient response. We plan on strategically evaluating these on a program-by-program basis as they advance into clinical development,
either to be done entirely by us or with out-licensing partners to maximize the commercial opportunity and reduce the time it takes to
bring the right drug to the right patient.

As
part of our overall growth strategy, we plan to grow our pipeline by identifying new drug candidates and pursuing potential indications
for LP-300, LP-184, LP-284, our ADC program and other drug candidates while leveraging our RADR® platform. We are also
pursuing the identification and design of potential combination therapies in cancer for our compounds by leveraging our RADR®
platform to analyze synergistic genomic networks and biological pathways with other currently approved drugs.

In addition, in 2026 we plan to introduce our proprietary artificial intelligence (AI) platforms and related technologies
as a potential source of revenue. This initiative is intended to leverage our existing AI infrastructure, technologies and drug development
expertise to create new opportunities in precision oncology and translational research support. We expect to evaluate multiple partnership
and commercialization models as our platforms advance and approach market readiness through both subscriptions, access and services for
biopharma companies, researchers, drug developers, and other users.

We
have an extensive multi-national portfolio of intellectual property directed to our drug candidates, and to protect the targeted use
and development of our portfolio of compounds in specific patient populations and in specific therapeutic indications. In addition, as
our RADR® platform and other machine learning driven methodologies progress and mature, we will continue to evaluate additional
ways to further protect these assets.

As
of March 1, 2026, we own or control over 200 active patents and patent applications across 20 patent families whose claims are directed
to our drug candidates and what we plan to do with our drug candidates. We have in-licensed or acquired patents and patent applications
from AF Chemicals and BioNumerik Pharmaceuticals that are directed to the compounds LP-184, LP-284, LP-100 and LP-300, and methods of
using the compounds. Additionally, we have also filed patent applications to further enhance and extend the use of these compounds. Our
patent families are directed to our drug candidates, their usage, manufacturing and other matters. These matters are essential to precision
oncology and relate to: (a) data-driven, biologically relevant biomarker signatures, (b) patient selection and stratification approaches
that rely on prediction of response derived from these signatures and, (c) the ability to develop novel, combination therapy approaches
with existing therapeutics.

3

Our
Drug Candidate Pipeline

One
of the ways we built our drug candidate pipeline is by in-licensing clinical stage drug candidates that may have been discontinued for
development. We use our RADR® platform to assist in analyzing prior clinical research conducted by others to identify
small-molecule oncology drug candidates that have (i) a well-tolerated profile evidenced by completion of phase 1 clinical trials, and
(ii) demonstrated at least limited antitumor or anticancer activity in clinical trials. We intend to advance the drug candidates in our
pipeline as potential precision medicine treatments for cancer. Our targeted development workflow includes preclinical studies where
drug activity and associated gene signatures are identified, in part through strategic collaborations with some of the top academic institutions
and clinical translational centers in the world. Using this collaborative approach, together with innovative observations from our RADR®
platform, we intend to develop and add drug candidates for our pipeline with the objective of treating the right patient populations
with the right oncology therapies.

Our
current pipeline of development programs includes our three lead small molecule drug candidates: LP-300, LP-184, and LP-284, and our
Antibody Drug Conjugate (ADC) program.

●
LP-300
(Sodium 2,2’-disulfanediyldiethanesulfonate) (Tavocept®): We are currently advancing LP-300 in a Phase 2
clinical trial, the HARMONIC™ trial, in combination with chemotherapy (carboplatin + pemetrexed) in never-smokers with NSCLC
adenocarcinoma who have progressed after tyrosine kinase inhibitor (TKI) therapy. The trial is designed to enroll approximately 90
patients across the U.S., Japan, and Taiwan. The Phase 2 U.S. safety lead-in cohort demonstrated an 86% clinical benefit rate and
a 43% objective response rate. A durable complete response has been observed in one patient who had previously failed three lines
of therapy, with survival continuing for nearly two years and no clinically significant adverse drug reactions over 21 cycles of
treatment.

●
LP-184.
( (-) hydroxyureamethylacylfulvene): LP-184 is a synthetically lethal small molecule (next-generation acylfulvene) with nanomolar
potency that has potential for treatment of solid tumors including breast, pancreatic, bladder, and lung cancers, glioblastoma and
other CNS cancers, and rare pediatric brain tumors. LP-184 preferentially damages DNA in cancer cells overexpressing PTGR1, the enzyme
that bioactivates LP-184 into its cytotoxic form. We recently completed a Phase 1a clinical
trial for LP-184. Based on the results and insights from the LP-184 Phase 1a clinical trial, we are advancing and optimizing
development plans for multiple future LP-184 clinical studies. We have FDA-cleared Phase 1b/2 trials planned in TNBC and biomarker-defined
NSCLC. LP-184 has received Fast Track Designation for GBM and TNBC, multiple Orphan Drug Designations, and four Rare Pediatric Disease
Designations. Independent preclinical data from Johns Hopkins presented at the SNO Pediatric Conference confirmed LP-184’s
strong activity in atypical teratoid rhabdoid tumors (ATRT), with a 345% improvement in median survival in one mouse model (p<0.0001).
For CNS indications, LP-184 is referred to as STAR-001 and is being developed through our wholly-owned subsidiary, Starlight Therapeutics.

4

●
LP-284.
( (+) hydroxyureamethylacylfulvene): LP-284, the stereoisomer (enantiomer) of LP-184, has shown promising in vitro and in
vivo anticancer activity in multiple hematological cancers, including relapsed or refractory non-Hodgkin’s lymphoma (NHL),
mantle cell lymphoma (MCL), and high-grade B-cell lymphomas (HGBL). LP-284 is advancing in a Phase 1 clinical trial (NCT06132503).
In 2025, LP-284 achieved a first complete metabolic response in a heavily pre-treated patient with aggressive DLBCL who had failed
three prior regimens including CAR-T cell therapy, after just two cycles of LP-284 treatment. LP-284 has received multiple Orphan
Drug Designations from the FDA for MCL, HGBL, and soft tissue sarcoma, and composition of matter patents relating to LP-284 have
been granted in the U.S., EU, Japan, China, India, Mexico, Australia, and South Korea

●
ADC
Program: Our ADC program continues to advance. We have applied our RADR® A.I. platform to advance an A.I. powered
module focused on improving the precision, cost and timelines of ADC development for cancer. In 2023 we entered into a research collaboration
with Bielefeld University in Germany focused on development of ADCs utilizing cryptophycin as the ADC drug-payload. Cryptophycins
are promising antitumor molecules that have demonstrated potency at ultra-low, picomolar, concentrations.

We
currently have INDs in the U.S. for LP-300, LP-184 and LP-284.

Our
Precision Cancer Therapy Development Using Our Innovative RADR® Platform

We
believe RADR® is one of the world’s largest A.I and machine learning (M.L.) oncology drug discovery and development
platforms, consisting of over 200 billion oncology-focused data points. These data points consist of large-scale multi-omic data, derived
from over 130,000 patient records, over 150 drug-tumor interactions, thousands of drug classes, and covering over 135 cancer subtypes.
RADR® leverages this data and over 200 advanced ML algorithms to power its drug discovery and development modules. RADR®’s
data, capabilities, and insights have powered the development of new Lantern drug candidates, advancement of new indications for existing
drugs, and identification of potential new drug combinations.

Historically,
cancer treatment protocols include surgery, chemotherapy and radiation therapy. Treatments have been selected based on histologic type
and disease spread, irrespective of genetic differences among patients. With the advent of precision therapies, cancer treatments increasingly
target specific genes or mechanisms of action for a more personalized approach to patient care. This trend represents a substantial advance
in cancer treatment because tumor growth is highly dependent on genetic changes and the genetic profile of the individual and the progression
of the disease is highly variable amongst patients.

Our
RADR® platform is core to our drug development approach for identifying the desired candidates to in-license and develop.
Oncology drug development is exceedingly challenging, with an overall estimated Phase 1-to-approval probability of success of just 3.3
percent (according to reports from DIA Global Forum: What Are the Chances of Getting a Cancer Drug Approved?, May 2019)
and an estimated mean cost to deliver a new oncology medicine of $4.4 billion (Study published in Targeted Oncology, 2023; Analysis
of the Cost of Developing Oncology Drugs Approved by the FDA Between 1997 and 2020). There is a critical need to rescue clinical
research on drugs that have failed clinical trials in order to provide additional possible therapies for patients while reducing the
overall cost of therapeutic development. Many drug failures within oncology may be attributed to the heterogeneity of the tested patient
population, even though there may be a strongly positive therapeutic impact on certain patient subgroups within that population.

5

As
data-centric and machine learning approaches are beginning to change the pace and scale of drug discovery and development, research and
development (“R&D”) we believe efforts in large biopharma companies are beginning to shift away from traditional approaches
towards new data and A.I.-centric approaches. According to Deloitte Consulting, in Ten Years On | Measuring the return from pharmaceutical
innovation 2019, “decades of advances in science and technology have driven improvements in health care outcomes and influenced
stakeholder expectations of the role of the biopharmaceutical industry (biopharma)”. The Deloitte Consulting report further describes
that R&D costs will, “shift from traditional discovery and trial execution to a process driven by large datasets, advanced
computing power and cloud storage”. Continuing the trend of scientific advancement impacting biopharma, as noted in Deloitte’s
2019 report, the findings in Deloitte’s 2023 report show R&D returns rebounding, with regulatory challenges and the need for
AI integration remaining as key future hurdles for the industry.

Analysts
estimate that this shift from traditional screening, and trial-based studies to leveraging in silico, data and A.I. methodologies has
driven a significant increase in the spending on A.I. by the biopharma and drug discovery community. According to GlobalData, the drive
to reduce drug development time and costs through AI-enhanced computer-aided drug design, coupled with a surge of AI-focused startups,
is projected to result in biopharma AI spending reaching $3 billion by 2025. As a result of these trends and changes in the R&D model
in biopharma, we believe that we, and companies that are using data-centric and A.I. centric approaches to drug discovery and development,
are in an ideal position to benefit from this industry shift that has the potential to help deliver drugs to the right patients faster,
with a higher degree of personalization and a potentially lower amount of average costs in the development cycle.

Our
drug rescue approach leverages substantial prior research and development investments in candidates that were withdrawn from development
prior to submission for FDA approval. The large volume of failed compounds, recent developments that permit increased access to validated
genomic and biomarker data, and the rapid evolution of A.I. technology creates an opportunity to efficiently capitalize on these investments.

Our
RADR® platform is rapidly emerging as a robust and scalable platform for targeted cancer therapy development. Through
the use of A.I., machine learning, and multi-agentic research systems, RADR® is designed to quickly identify and guide
the development of compounds that we can develop as potential oncology agents through either a process of drug rescue, drug repositioning
or de-novo development. RADR® is being developed through an accumulation and curation of genomic data, biomarker data,
chemical structural data, and detailed ontologically indexed documents that are directly relevant to the measurement and classification
of drug-tumor interaction, clinical datapoints related to patient response and patient stratification, and de-novo drug design.

Predicting
optimal drug responses in cancer patients requires the identification and validation of predictive biomarkers. Our RADR® platform
seeks to identify biomarkers to assist in selecting patients who have the highest likelihood to respond to our drug candidates. For example,
the targeted indications for our drug candidate LP-184 were selected in part because they are known to highly express the protein coding
gene PTGR1. Our clinical development plans for LP-184 are intended to provide additional information regarding biomarkers related to
LP-184’s molecular and cellular targets. This method of using and validating targeted biomarkers during development and then using
these biomarkers during future clinical trials can lead to shortening of the development timeline and compression of costs associated
with oncology drug development.

Similarly,
we believe LP-300 targets molecular pathways that are more common in never smokers than in other groups and also targets kinases involved
in key signaling pathways involving enzymes critical for DNA synthesis and repair, such as Excision Repair Cross-Complementation Group
1 (ERCC1), Ribonucleotide Reductase 1 (RNR1), Ribonucleotide Reductase 2 (RNR2), as well as enzymes and proteins important in regulating
cell redox status, such as Thioredoxin (TRX), Peroxiredoxin (PRX), Glutaredoxin (GRX), and Protein Disulfide Isomerase (PDI).

6

Our
RADR® Platform

The
human genome consists of 19,000 to 20,000 protein coding genes. One input record derived from available data bases and analyzed by our
RADR® platform consists of datapoints (expression values) from approximately 20,000 genes, another input record type is
drug sensitivity data (IC20, IC50), and other sets include key clinical parameters from HIPAA compliant patient data and clinical histories.
Our RADR® platform uses a data-driven gene feature selection methodology that is a combination of biology, informatics,
and statistics – computational biology. The architecture, tools and software of our platform are depicted in the figures below.

We
developed our platform using primarily open-source supervised algorithms such as Neural Networks, Support Vector Machine, Random Forest,
K-Nearest Neighbors, Logistic Regression and Penalized Multivariate Regression. Each algorithm is trained with labeled input data to
predict characteristics such as drug sensitivity (regressor models), stratify patient response as responder or non-responder (classifier
models), or drug behaviors such as ability to cross the blood-brain barrier (ensemble classification). Model tuning and optimization
is then performed using a hyperparameter search algorithm in order to produce the predicted lowest cross validation error. The models
are then evaluated using traditional performance metrics such as accuracy, area under the curve, sensitivity, specificity, precision,
root mean square error and mean absolute error calculations.

7

A
feature reduction algorithm is used to reduce the number of genes under analysis to a biomarker gene panel of less than approximately
50 genes. This set of genes is intended to carry the highest coefficient to predict drug sensitivity and the highest variable importance
in classifying a responder from a non-responder. Genes that do not help in predicting the output variable are eliminated to allow for
better prediction generalization and understand mechanisms based on key genes only.

Our
RADR® Platform Workflow

Our
RADR® platform’s proprietary workflow involves preliminary statistical analysis on approximately 18,000 features
typically from whole transcriptomic datasets and then reducing the set to approximately 2,000 features. This is followed by gene filtering
via biological and statistical methodologies yielding approximately 200 significant genes. The platform currently contains multiple feature
selection methods and multiple machine learning methods to analyze the drug and omics data, in order to fine tune the model and get better
and improved prediction accuracy. Feature selection ensures that genes that do not contribute to response prediction are excluded from
the output dataset. The prediction component subsequently applies an A.I.-driven reduction algorithm to the previously filtered genes
generating a targeted set of typically less than 50 candidate biomarkers predictive of response to a particular molecule. The figure
below illustrates RADR®’s workflow.

A
distinct and unique benefit of the RADR® platform is its ability to integrate biological knowledge and data-driven feature
selection to generate hypothesis-free biomarker signatures. This can then aid in identifying novel targets for predictive screening and
drug development.

8

Our
RADR® platform is enabled through access to, and analysis of, a number of key datasets: (i) publicly available databases,
(ii) data from commercial clinical studies and trials and (iii) our proprietary data generated from ex vivo 3D tumor models specific
to drug-tumor interactions. We incorporate automated supervised machine learning strategies along with big data analytics, statistics
and systems biology to facilitate identification of new correlations of genetic biomarkers with drug activity.

The
value of the platform architecture is derived from its validation through the analysis of over 200 billion oncology-specific clinical
and preclinical data points, more than 154 drug-cancer interactions, thousands of drug classes, data covering more than 135 cancer subtypes,
and over 130,000 patient records from 16 databases, one of which is our internal database. RADR® leverages this data and
over 200+ advanced ML algorithms to power its drug discovery and development modules. Our target objectives for additional data growth
efforts of the RADR® platform include a focus on drug sensitivity data, combination treatment outcome data, biomarker
data in rare cancers, and on emerging synthetic lethal targets that are aimed at accelerating the development of new therapies. Additionally,
the RADR® platform’s generative A.I. capabilities, focusing on molecular optimization and automated feature extraction
to improve understanding and prediction of molecular dynamics, safety, and drug-drug interactions are planned to increase in functionality
and scope for both small molecule development and for ADC development, analytics and characterization.

We
use cancer cell line gene expression profiles and drug sensitivity data (IC50) as one of the RADR® platform’s input
types. In a population of 10 case studies our platform was able to distinguish responders from non-responders with an average historical
accuracy of over 80%. We have also used our platform to generate genetic signatures that we believe to have applicability for the majority
of FDA approved drug-tumor indications. External validation, through retrospective data analysis, of patient datasets from 10 independent
clinical studies achieved an average response prediction accuracy greater than 80%, and internal analysis of 120 drug-tumor interactions
in cell lines achieved an accuracy of greater than 85%. The figure below illustrates examples of RADR®’s algorithms
and how they can be used.

We
have developed our platform in a cloud environment that efficiently uses parallel processing to analyze patient stratification and biomarker
selection. Best software engineering practices are followed while designing and developing our platform’s architecture. In order
to track modifications in the software, a version control system is in place. We use a software release process, including a rigorous
regression testing process, to ensure functions and programs are working as designed.

Our
platform uses a simple user input and GUI based AI architecture that can be used in many pharmaceutical research areas such as biomarker
identification, patient stratification, drug rescue and reposition by bioinformaticians, clinicians and trained wet-lab scientists.

In
late 2021, the Code Ocean Platform, a secure cloud-based computing environment manager, was integrated into RADR®. The
Code Ocean environment has upgraded RADR®’s data organization, synchronization, scalability and accessibility. These
architecture changes have enhanced the reproducibility of RADR® aided insights and analysis and created an environment
that improves the ability to collaborate and share insights within Lantern and with Lantern’s collaborators.

In
2025 and early 2026, RADR introduced two AI services intended to serve the needs of clinical researchers and biomedical scientists by
predicting which drugs can cross the blood brain barrier, and a rapid research “co-scientist” collaborator for research in
rare cancers and drug development. Both of these services provide an initial free introductory experience, with an opportunity for further
use through collaborations.

In 2026 we also plan to introduce our proprietary artificial intelligence (AI) platforms and related technologies
as a potential source of revenue. This initiative is intended to leverage our existing AI infrastructure, technologies and drug development
expertise to create new opportunities in precision oncology and translational research support. We expect to evaluate multiple partnership
and commercialization models as our platforms advance and approach market readiness through both subscriptions, access and services for
biopharma companies, researchers, drug developers, and other users.

9

PredictBBB
web application

PredictBBB
allows the prediction of which small molecules will cross the blood-brain barrier. It is one of many drug development modules that
we have created through the use of RADR®. With
94% accuracy in predicting which small molecules will cross the blood-brain barrier, users only need to provide a SMILES string
which represents the chemical’s structure in order to obtain a prediction. A drug name search bar provides users an easy
method to look up SMILES strings from PubChem and click to use it as the input for predictions, or users can provide their own
SMILES string for proprietary compounds. The model is based on over 4,000 molecular characteristics derived from the chemical
structure which the web application automatically generates and validates for the user input compounds, then returns a prediction
and report in less than approximately 1 minute.

withZeta.AI Rare Cancer Research Platform

withZeta
is a novel generative AI platform built to empower researchers and clinicians to dramatically improve the quality and reduce the time
of rare cancer research, therapeutic development, drug repurposing, biomarker targeting, and clinical trial design.

Built
securely in the AWS Cloud with a serverless, Lambda-based architecture and state-of-the-art large language model (LLM) inference, withZeta integrates an indexed
ontology of 438 rare cancer types, over 559,000 clinical trial records, over 204,000 published papers pertaining to rare cancers, and
532 FDA-approved oncology drug records. In conjunction with these curated databases, Zeta also utilizes a suite of tools including open-weight
specialized language models for de-novo chemical design, integration of predictBBB, molecular feature descriptions, and a collection
of targeted external resources which seamlessly integrate into a unified chat interface through task-aligned system prompts.

Actuate
Therapeutics Collaboration Utilizing RADR Platform

In
May 2021, we entered into a Collaboration Agreement with Actuate Therapeutics, Inc. (“Actuate”), a clinical stage private
biopharmaceutical company focused on the development of compounds for use in the treatment of cancer, and inflammatory diseases leading
to fibrosis. Pursuant to the agreement, we collaborated on utilization of our RADR® platform to develop novel biomarker
derived signatures for use with one of Actuate’s product candidates. As part of the collaboration, we received shares of Actuate
stock subject to meeting certain conditions of the collaboration, as well as the potential to receive additional Actuate stock if results
from the collaboration are utilized in future development efforts.

10

TTC
Oncology Collaboration to Expand the Clinical Development of Drug Candidate TTC-352

In
February 2023, we entered into a Collaboration Agreement with TTC Oncology (“TTC”). The collaboration focused on using RADR®
to accelerate and sharpen the drug development of TTC’s Phase 2 ready drug candidate TTC-352. TTC-352, is a novel, first-
and best-in-class selective human estrogen receptor (ER) partial agonist (ShERPA) for the treatment of patients with metastatic ER+ breast
cancer. TTC-352 was evaluated in a Phase 1 accelerated dose escalation study for hormone receptor positive metastatic breast cancer,
and it showed early anti-tumor activity signals in heavily pretreated hormone refractory patients. The aims of the collaboration were
to 1) identify biomarker or gene signatures to power potential patient selection for a planned TTC-352 Phase 2 clinical trial, 2) further
characterize TTC-352’s mechanism of action, and 3) discover additional treatment indications for TTC-352.

Oregon
Therapeutics Collaboration to Optimize Precision Development of Drug Candidate XCE853

In
mid-2024, we entered into a strategic A.I.-driven collaboration with French biotechnology company, Oregon Therapeutics, to optimize the
development of its first-in-class protein disulfide isomerase (PDI) inhibitor drug candidate XCE853 in novel and targeted cancer indications.
As part of the collaboration, we leveraged our proprietary RADR® A.I. platform to uncover biomarkers and anticancer-associated
signatures of XCE853 across solid tumors aimed at assisting in precision development. Oregon Therapeutics has focused on developing XCE853
in various cancer indications, including drug-resistant ovarian and pancreatic cancer, certain hematological cancers and several pediatric
cancers including CNS cancers. The objectives of the collaboration included a focus on 1) uncovering biomarkers and efficacy-associated
gene signatures to guide in the eventual stratification and selection of patients for future clinical trials, 2) efforts to identify
tumor-based response and resistance mechanisms to XCE853 and strategies to overcome treatment resistance, and 3) identification of opportunities
to expand the use of XCE853 in additional therapeutic cancer indications for XCE853.

Our
Strategy

Our
mission is to bring the right cancer drugs to the right patients by transforming the drug development process through the use of artificial
intelligence and data-driven development approaches. Our proprietary A.I.-enabled, and precision oncology approach, which focuses on
developing our own pipeline of compounds by rescuing drug candidates that have previously failed and developing new compounds that are
targeted to specific biological activity and genomic pathways, has the potential, we believe, to bring drugs to market faster, with lower
costs, and with reduced risk, thereby enabling a change in the cost and availability of precision cancer therapy. The strength of this
approach is demonstrated by our track record of advancing newly developed drug programs from initial AI insights to first-in-human clinical
trials in 2–3 years and at approximately $1.0 – $2.5 million per program. We work with leading research laboratories, translational
medicine and cancer centers to develop our studies and clinical trials for our portfolio, and actively update and improve our RADR®
platform to incorporate additional biomarker data, patient outcome data, cancer drug efficacy studies and computational models that relate
to oncology drug development and prediction of patient response. Our RADR® platform has grown to over 200 billion oncology-focused
data points and a library of 200+ advanced machine learning algorithms, and we are actively expanding its capabilities through new modules
focused on ADC development, combination regimen prediction, and blood-brain barrier permeability assessment.

As
part of our strategy, we plan to:

●
Pursue
existing indications for LP-300, LP-184, LP-284, our ADC program and our other product candidates, leveraging our RADR®
platform to refine and optimize our trial design and biomarker signatures that correlate to potential patient response.

●
Expand
our pipeline by identifying new drug candidates that have either been abandoned or have failed in late stage clinical trials, and
have the potential to benefit from a precision medicine approach that leverages our expertise and A.I. platform.

11

●
Identify
and design potential combination therapy approaches to use our compounds in conjunction with currently approved drugs by leveraging
our RADR® platform to analyze and uncover synergistic mechanisms and biological pathways using genomics and machine
learning.

●
Advance
the algorithms, methodologies and models that underlie our computational and machine learning platform to improve the predictive
power, and to develop additional capabilities that are focused on accelerating or de-risking oncology drug development.

●
Pursue
collaborations and partnerships with other biotech and pharma companies where our A.I. and precision oncology expertise can be used
to de-risk or accelerate development programs and where our stockholders can receive a significant economic benefit.

●
Continue
to develop and patent intellectual property and advance our intellectual property portfolio associated with both fundamental patents
and patents associated with precision, patient stratified, targeted therapies and genomic or biomarker signatures.

●
Continue
to evaluate, select and launch additional clinical development programs.

LP-300

General
Overview

We
are currently advancing LP-300 in a Phase 2 clinical trial (the “HARMONIC™ Study”) of LP-300 in combination with carboplatin
and pemetrexed in never smoker patients with relapsed advanced primary adenocarcinoma of the lung after treatment with tyrosine kinase
inhibitors (TKIs).

LP-300
is a cysteine-modifying molecular entity that works to modulate multiple cellular pathways simultaneously and is a potential combination
agent for targeted indications in NSCLC. LP-300 is a small molecule (molecular weight 326.4 Da) that was in-licensed from BioNumerik
Pharmaceuticals, Inc. in May 2016, and subsequently acquired by us in 2018. We are focused on repositioning LP-300 as a potential combination
therapy for never smoker NSCLC patients with histologically defined adenocarcinoma. Prior clinical trials conducted by BioNumerik for
LP-300 did not meet their primary clinical endpoints, and at least one or more future clinical trials that meet their pre-specified primary
endpoints with statistical significance will be required before we can obtain a regulatory marketing approval, if any, to commercialize
LP-300. Safety and efficacy determinations are solely within the authority of the FDA in the U.S. or other regulatory agencies in other
jurisdictions. Currently there is no approved therapy specifically for the growing indication of never-smokers with NSCLC, and female
never smokers appear to be uniquely responsive to LP-300. With both chemosensitizing and chemoprotective activity, LP-300 has potential
as a combination agent or adjuvant in front line, second line or salvage therapy in newly diagnosed, relapsed, metastatic or advanced
NSCLC for overall survival enhancement and toxicity alleviation from primary chemotherapy or standard of care. We are currently in the
early stages of defining a specific biomarker signature that correlates with heightened sensitivity to LP-300. We believe that this signature
may help accelerate the clinical development of LP-300 and has the potential to guide patient selection for targeted clinical trials.

Prior
clinical trials conducted by BioNumerik for LP-300 did not meet their primary clinical endpoints and at least one or more future clinical
trials that meet their pre-specified primary endpoints with statistical significance will be required before we can obtain a regulatory
marketing approval, if any, to commercialize LP-300. Prior clinical trial observations are not necessarily predictive of the outcome
of any future clinical trials we may conduct.

12

LP-300
has been administered in multiple clinical trials to more than 1,000 subjects and has been generally well-tolerated. Retrospective analyses
of the results of a multi-country phase 3 lung cancer trial (study ID DMS32212R) in subgroups of adenocarcinoma patients receiving LP-300,
paclitaxel and cisplatin demonstrated substantial improvement in overall survival, particularly among female never smokers, where a 13.6
month improvement in overall survival (p-value 0.0167, hazard ratio 0.367) in favor of LP-300 was observed, as compared to placebo in
the subgroup of paclitaxel/cisplatin-treated patients. Similar retrospective findings of increased overall survival in the subgroup of
LP-300/paclitaxel/cisplatin treated female Asian patients with adenocarcinoma of the lung were observed in a randomized, double-blind,
placebo-controlled trial in Japan. Prior historical clinical trial observations are not necessarily predictive of the outcome of future
trials. No assurances can be given that we will be successful in obtaining marketing approval for LP-300. The chemical structure of LP-300
is depicted below.

LP-300
Chemical Structure

The
Ongoing HARMONIC™ Study

We
are conducting a Phase 2 clinical trial (the “HARMONIC™ Study”) of LP-300 in combination with carboplatin and pemetrexed
in never smoker patients with relapsed advanced primary adenocarcinoma of the lung after treatment with tyrosine kinase inhibitors. Our
purpose in conducting the study is to determine the potential clinical advantages and benefits for this drug combination in the study-defined
patient population. As of March 17, 2026, we have 4 clinical trial sites in the US, 5 clinical trial sites in Japan, and 5 clinical trial
sites in Taiwan. Enrollment of patients on the Harmonic™ Study in the U.S. has been challenging, and we have implemented a strategy
of increasing enrollment by expanding the study to East Asian countries where approximately 30-35+% of all lung cancer cases occur in
never-smokers with NSCLC.

The
Harmonic™ Study is designed as a multicenter, open label, Phase 2 trial with planned total enrollment of approximately 90 patients.
Patients who are never smokers with lung adenocarcinoma and have relapsed after prior treatment with tyrosine kinase inhibitors will
be eligible for enrollment. Patients who are former smokers but carry actionable genomic alteration(s) may also be eligible. Following
completion of a seven-patient safety lead-in phase in which patients received the triplet regimen of carboplatin, pemetrexed, and LP-300,
the trial advanced to the randomization stage, which consists of enrolling patients in a 2:1 allocation ratio to one of two arms: Arm
A (consisting of carboplatin, pemetrexed, and LP-300) or Arm B (consisting of carboplatin and pemetrexed). As of March 17, 2026, 24 and
10 patients have received treatment in Arm A and Arm B, respectively, of the randomization stage of the study.

The
primary objective of this study is to determine progression-free survival and overall survival in the study-defined patient population
when co-administered LP-300 with combination chemotherapy (carboplatin and pemetrexed) versus carboplatin and pemetrexed alone. The secondary
objectives of the study are to evaluate tumor response measured by objective response rate, duration of objective response, and clinical
benefit rate. We will also determine any associations between the efficacy endpoints and patient biomarkers (e.g., circulating tumor
DNA and tumor genome characteristics) as an exploratory objective. Other exploratory objectives for the study may include evaluating
quality of life in all patients and performance of patients based on the type, duration, and number of tyrosine kinase inhibitors received.

Summarized
below are some key findings from the ongoing Phase 2 clinical trial as of March 17, 2026:

● The
combination of carboplatin, pemetrexed, and LP-300 was well tolerated. Addition of LP-300
to the chemotherapy backbone showed no increased clinically significant toxicities.

● No
dose limiting toxicities were observed is the safety lead-in and Arm A of the study.

● No
treatment-related serious adverse events reported.

● No
suspected unexpected serious adverse reactions.

● Encouraging
clinical efficacy data (in safety lead-in) that outperformed chemotherapy alone data for
similar populations in other pivotal trials.

In
March 2026, we submitted a Type C meeting package to the U.S. Food and Drug Administration (FDA) regarding the ongoing Phase 2
HARMONIC study. The meeting, currently scheduled for mid May 2026, seeks FDA feedback and concurrence on proposed protocol
amendments to the HARMONIC study. The proposed amendments include: (i) focusing future enrollment to patients with EGFR exon 21
L858R mutation (a subtype of tyrosine kinase mutations); (ii) increasing the maximum number of LP-300 treatment cycles from six to
eight; and (iii) converting the current randomized study design to a Phase 2 single-arm Simon two-stage study by discontinuing
enrollment into the control arm. We feel that the proposed amendments are supported by a preliminary analysis of study data
suggesting that patients with the EGFR exon 21 L858R mutation may derive greater clinical benefit from the LP-300 triplet regimen;
the evolution of the treatment landscape for TKI-refractory NSCLC that has made continued randomization to the control arm
increasingly challenging; and historical safety data indicating that up to eight cycles of LP-300 at the current dose level did not
alter the established safety profile of the drug. There can be no assurance that the FDA will concur with the proposed amendments,
and any changes to the study protocol will be subject to FDA review and clearance, during and after the Type C meeting.

13

Key
Findings from Prior LP-300 Clinical Trials

Summarized
below are some key findings from LP-300’s prior clinical trials:

●
LP-300
showed that females had a survival increase from 13 months to 25 months, based on a retrospective subgroup analysis of a Phase 3
NSCLC adenocarcinoma trial. Results from a Phase 3 NSCLC adenocarcinoma trial exhibited an overall survival of 25.0 months, with
a 2-year survival of 51.4%, in the subgroup of females with advanced adenocarcinoma of the lung receiving paclitaxel/cisplatin and
LP-300. The observed results were statistically significant (p-value = 0.0477; HR=0.579) and were observed in a subgroup of 114 patients
in retrospective analyses. Consistent statistically significant retrospective subgroup analysis results were observed in female NSCLC
adenocarcinoma patients receiving paclitaxel/cisplatin and LP-300 in a prior LP-300 double-blind, placebo-controlled phase 3 trial
conducted in Japan.

●
LP-300
exhibits potential to reduce anemia and protect against chemotherapy-induced kidney toxicity, both of which are conditions that disproportionately
affect females. The LP-300 arm of the Phase 3 NSCLC adenocarcinoma trial also demonstrated the potential for LP-300 to protect
against chemotherapy-induced kidney toxicity and anemia. These findings complement earlier clinical observations regarding LP-300’s
potential to protect against neuropathy and other chemotherapy-induced toxicities.

Background-Scope
of Prior Phase 3 NSCLC Adenocarcinoma Trial (LP-300)

LP-300
was studied in a randomized, multi-center (trial locations in four US states and five European countries), double-blind and placebo-controlled
Phase 3 trial from 2010 to 2013 in patients with adenocarcinoma of the lung (the “Phase 3 NSCLC adenocarcinoma trial”). The
aim of the trial was to determine whether LP-300, combined with a standard combination of chemotherapy drugs, would increase survival
in patients with advanced NSCLC adenocarcinoma. The secondary aim of the trial was to determine if the chemoprotective properties of
LP-300 were effective in preventing or reducing common side-effects of cancer treatment, including kidney damage, anemia, nausea and
vomiting that can occur with these drug combinations. The trial enrolled NSCLC patients with newly diagnosed or recurrent advanced (stage
IIIB/IV) primary adenocarcinoma of the lung. Patients with confirmed histopathological diagnosis of inoperable and measurable advanced
primary adenocarcinoma (including bronchioalveolar cell carcinoma) of the lung, and no prior systemic treatment for NSCLC including chemotherapy,
immunotherapy, hormonal therapy, targeted therapies or investigational drugs, were included in the trial. Overall survival was the primary
outcome measure. Patients in the control arm received standard of care (cisplatin and either paclitaxel or docetaxel) plus placebo, whereas
patients in the treatment arm received standard of care (cisplatin and either paclitaxel or docetaxel) plus LP-300. The primary results
of the trial for patients receiving cisplatin and paclitaxel are outlined in the table below. While the overall results of the Phase
3 NSCLC adenocarcinoma trial did not meet the specified endpoint of the trial in increasing overall survival in all patients, when the
data were retrospectively separated by gender and smoking status, the trial data demonstrated that all never smokers, especially female
never smokers, saw increased survival with LP-300 combination treatment with paclitaxel and cisplatin. Furthermore, the LP-300 group
in the phase 3 NSCLC adenocarcinoma trial exhibited well-tolerated advantages relating to the potential to protect against chemotherapy-induced
nephrotoxicity, neuropathy and nausea along with reduced anemia.

14

The
figure below depicts the survival curves for cisplatin/paclitaxel subgroups for the Phase 3 NSCLC adenocarcinoma trial that ended in
2013, as summarized. The Kaplan Meier curves maintain consistent separation between treatment arms for the never smokers, females, and
female never smokers.

Rationale
Behind LP-300 Rescue and Repositioning Efforts

Based
on the results from the prior Phase 3 NSCL adenocarcinoma trial, we launched the HARMONIC™ LP-300 Phase 2 clinical trial to target
the subpopulation of never smokers with adenocarcinoma that saw strong benefit in the previous Phase 3 trial. Although the incidence
of never-smokers with NSCLC is rising currently there is no approved therapy specifically for the growing indication of never-smokers
with NSCLC. Preclinical observations support that LP-300 preferentially modulates ALK and EGFR, two commonly mutated genes in non-smokers
with adenocarcinoma. Based on the findings from the previous Phase 3 NSCL adenocarcinoma trial, it is possible that the benefits of combining
LP-300 with standard of care chemotherapy could be further improved by identifying additional molecular biomarkers in patients who respond
well to LP-300 combination treatment. We continue to seek additional opportunities for LP-300. Some of our considerations include a never
smoker population with a specific genetic signature that correlates to increased LP-300 sensitivity.

Disease
Background and Opportunity

Lung
cancer is the second most prevalent cancer globally, and it accounts for the highest level of cancer-related deaths worldwide. Lung cancer
accounts for approximately 12% of all new cancer diagnoses, but 21% of all cancer deaths in the US. Lung cancer kills more people annually
than cancers of the breast, prostate, colon, liver, kidney, pancreatic, and melanoma combined. The American Cancer Society’s estimates
for lung cancer in the US for 2026 are:

●
Approximately
229,410 new cases of lung cancer (110,910 in men and 118,500 in women)

●
Approximately
124,990 deaths from lung cancer (63,040 in men and 61,950 in women)

The
most common type of lung cancer is called non-small cell lung cancer (“NSCLC”), which represents about 80% to 85% of all
lung cancer.

Lung
adenocarcinoma, a histological subtype of NSCLC that originates within the glands that line the lung, is the most common subtype of lung
cancer in the world inflicting approximately 50% to 65% of non-Asians and approximately 70% to 85% of Asians diagnosed with lung cancer.
According to LUNGevity Foundation, the National Institutes of Health and other published literature, 60% to 65% of all new lung cancer
diagnoses are among people who are former smokers or have never smoked, while 10-15% of new lung cancer cases are among never-smokers.

15

Over
one-half of the patients diagnosed with NSCLC in any given year will present with inoperable advanced (stage IV) disease, for which there
is no cure. Patients with stage IV NSCLC exhibit a median overall survival time of 7 to 12 months; approximately one-third of patients
will survive for a year, and only 10% to 21% of those patients will survive for two years.

Lung
cancer is the most common cause of global cancer-related mortality, leading to over a million deaths each year and adenocarcinoma is
its most common histological subtype. Worldwide, lung cancer occurred in approximately 2.5 million patients in 2022 and caused an estimated
1.8 million deaths. NSCLC is described as any type of epithelial lung cancer other than small cell lung cancer (“SCLC”).
The 5-year survival rate for NSCLC is about 28%.

Rapid
advances in understanding the molecular pathogenesis of NSCLC have demonstrated that NSCLC is a heterogeneous group of diseases. Although
the initial treatment of localized disease is the same, the molecular characterization of tumor tissue in patients with NSCLC serves
as a guide to treatment both in those who present with metastatic disease and in those who relapse after primary therapy. Molecularly
targeted therapies have dramatically improved treatment for patients whose tumors harbor somatically activated oncogenes such as mutant
EGFR1 or translocated ALK, RET, or ROS1. Smoking is the major cause of lung adenocarcinoma but, as smoking rates decrease, proportionally
more cases occur in never-smokers (defined as less than 100 cigarettes in a lifetime). KRAS mutations in lung cancer cases are nearly
exclusive to smokers. KRAS, “Kristen rat sarcoma viral oncogene homolog,” is a protein involved in regulating cell division.
KRAS mutation is a gain-of-function mutation (i.e. somatic mutation turns RAS, a benign gene “proto-oncogene” into KRAS,
an oncogenic driver of many tumors). KRAS-mutated non-small cell lung cancer represents 20% to 25% of all NSCLC. In 2022, FDA granted
accelerated approval to Antibody Drug Conjugate trastuzumab deruxtecan (Enhertu) for HER2 mutated advanced stages of non-small cell lung
cancer (NSCLC). In 2022, the combination of CTLA-4 inhibitor tremelimumab and the anti-PDL1 antibody durvalumab was approved by FDA for
treating metastatic NSCLC patients lacking EGFR mutation or ALK translocation. In 2023, FDA approvals included pralsetinib (Gavreto)
for RET fusion-positive NSCLC and repotrectinib (Augtyro) for ROS1-positive NSCLC, offering the first approval for both TKI-naïve
and previously treated patients.

In
2024, the FDA approved Osimertinib (Tagrisso) in combination with platinum-based chemotherapy for EGFR-mutated NSCLC.
Amivantamab-vmjw (Rybrevant) was also approved, in combination with carboplatin and pemetrexed, as a first-line treatment for NSCLC
with EGFR exon 20 insertion mutations. Amivantamab has also been approved (1) in combination with lazertinib for the first-line
treatment of adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor
receptor (EGFR) exon 19 deletions or exon 21 L858R substitution mutations, as detected by an FDA-approved test, (2) in combination
with carboplatin and pemetrexed for the treatment of adult patients with locally advanced or metastatic NSCLC with EGFR exon 19
deletions or exon 21 L858R substitution mutations, whose disease has progressed on or after treatment with an EGFR tyrosine kinase
inhibitor, and (3) as a single agent for the treatment of adult patients with locally advanced or metastatic NSCLC with EGFR exon 20
insertion mutations, as detected by an FDA-approved test, whose disease has progressed on or after platinum-based chemotherapy.
Additionally, ensartinib was approved for first-line treatment in ALK-positive, advanced or metastatic NSCLC patients who had not
previously received an ALK inhibitor. Tepotinib (Tepmetko) was approved for patients with MET exon 14 skipping alterations, and
alectinib (Alecensa) was approved for adjuvant treatment after tumor resection in ALK-positive NSCLC patients, as detected by an
FDA-approved test. Tumor suppressor gene abnormalities, such as those in TP53, CDKN2A8, KEAP1, and SMARCA4 are also common but are
not currently clinically actionable.

In
reviewing lung cancer incidence and mortality rates among never-smokers in the Journal of Clinical Oncology, Wakelee, H.A. et al. have
reported that the age-adjusted incidence rates of lung cancer among never-smokers aged 40 to 79 years from large population-based cohorts
ranged from 14.4 to 20.8 per 100,000 person-years in women and 4.8 to 13.7 per 100,000 person-years in men, supporting earlier observations
that women are more likely than men to have never smoking-associated lung cancer. The biology of lung cancer in never-smokers is apparent
in differential responses to epidermal growth factor receptor inhibitors and an increased prevalence of adenocarcinoma histology in never-smokers.
Lung cancer in never-smokers is an important public health issue needing further exploration of its incidence patterns, etiology, and
biology. Due to the fact that there is currently no approved therapy specifically for this group, we believe that aggressive development
of therapy options is needed and is a high unmet clinical need.

In
the US in 2025, there were be an estimated 11,444 diagnosed cases of NSCLC in female non-smokers, accounting for approximately 5% of
all lung cancer cases. Globally in 2022, there were an estimated 125,231 adenocarcinoma cases of NSCLC in female non-smokers. Due to
the specificity of this indication, it may be possible to classify it as a rare disease. When attempting to explain some gender susceptibility
differences, research has demonstrated that women with NSCLC tend to be:

●
Younger;

●
Asian;

●
2-3
times more likely to be non-smokers;

●
more
likely to develop adenocarcinoma and;

●
more
likely to have metastatic disease.

16

The
high rate of adenocarcinomas in non-smoking women suggests the possible existence of other etiological factors in addition to smoking.
Some factors that have been considered include gender-specific genetic alterations and predispositions, passive smoke effects, different
nicotine metabolism in women, occupational exposure, diet, and chronic obstructive pulmonary disease. Based upon estimates published
by Global Cancer Statistics in 2022 and 2026 estimates published by the American Cancer Society, below is an overview of relevant potential
patient population and market sizes that we believe LP-300 could address, if approved:

Lung cancer

Global

(2022)

US

(2026)

Total lung cancer estimated incidence (new cases)
2,480,301
229,410

NSCLC incidence (~85% of all lung cancer cases)
2,108,256
194,999

NSCLC adenocarcinoma incidence (~60% of all NSCLC)
1,264,954
116,999

Never-smokers estimate (~15% of adenocarcinoma)
189,744
17,550

Female never-smoker estimate (~66% of never-smokers with lung cancer are female)
125,231
11,583

Total Potential Patient Segment in New Lung Cancer
5.0%-7.6 %
5.0%-7.6 %

Limitations
on Current Treatment

Treatment
of patients with advanced NSCLC in the first-line setting usually includes chemotherapy (including taxanes, vinorelbine, or gemcitabine)
in combination with a platinum doublet (cisplatin or carboplatin). According to the clinical practice guidelines published by the National
Comprehensive Cancer Network, many of these combinations have reached a plateau in terms of overall response (≥ 25% to 35%), time
to progression (four to six months), median survival time (eight to ten months), one-year survival rate (30% to 40%), and two-year survival
rate (10% to 15%) in patients with good performance status. Treatment remains palliative and is limited due to inherent toxicities that
may affect the quality of life resulting from treatment. Toxicities can be life-threatening or cause treatment delays, thereby limiting
the intensity of treatment delivered and affecting its efficacy. Common and serious chemotherapy-induced toxicities, such as anemia,
emesis, and peripheral neurotoxicity resulting from treatment with platinum and taxanes, and nephrotoxicity due to cisplatin can result
in treatment delays, dose modifications, and in severe cases, discontinuation of treatment.

The
identification of gene mutations in lung cancer has led to the development of molecularly targeted therapy to improve the survival of
subsets of patients with metastatic disease. In particular, genetic abnormalities in EGFR, MAPK, and PI3K signaling
pathways in subsets of NSCLC may define mechanisms of drug sensitivity and primary or acquired resistance to tyrosine kinase inhibitors
(TKIs). To date, approximately 21 TKIs have been approved for use in treating NSCLC with identified tyrosine kinase (TK) mutations; the
TKs targeted by these inhibitors include EGFR, ALK, ROS1, BRAF/MEK, RET, and MET. If patients are found to have specific TK mutations
to which inhibitors are known to respond, treatment with such TKIs is currently standard-of-care for this population of advanced NSCLC.
Most tumors will respond to initial treatment with TKIs, exhibiting tumor shrinking or delayed progression. Unfortunately, most patients
will eventually develop resistance to the inhibitory effects of initial used inhibitors. Therefore, second- or third-line therapy often
involves treatment with alternate inhibitors targeting the same kinase but with differing mutations. Such treatment again is often initially
successful, but further kinase mutations, or mutations arising in different kinases, often leads to relapse and the need to switch to
alternative treatment schemes. This next therapy usually involves chemotherapy (often carboplatin plus pemetrexed), sometimes used in
combination with immunotherapy, or enrollment in clinical trials testing new treatment approaches.

We
believe it is important to pursue the development of novel therapies and combinations thereof that can substantially improve patient
survival and quality of life by potentiating the antitumor activity of chemotherapy treatment while protecting against chemotherapy-induced
toxicity.

17

Market
Opportunity

Most
never-smoker patients with lung cancer are women, and adenocarcinoma is the most common type. Non-smoker patients with non-small-cell
lung cancer (“NSCLC”) generally have a better response to inhibitors of epidermal-growth-factor receptor (EGFR) tyrosine
kinase, including without limitation gefitinib and erlotinib, than do those with a history of tobacco smoking. Studies have identified
differences in chromosomal aberrations, genetic polymorphisms, gene mutations, and methylation status between lung cancer in non-smokers
and tobacco-associated lung cancer. These clinical and biological differences suggest that the two cancers have overlapping but unique
pathways of carcinogenesis. The EGFR mutation is one of the most important genetic change in lung cancer in people who have never smoked
because it is more common in lung cancer in never-smokers than in tobacco associated lung cancer and is associated with greater therapeutic
benefit from inhibitors of EGFR. Other alterations associated with never-smokers include mutations, fusions or amplifications in ALK,
ROS1, RET and MET genes. Based on published articles in JCI Insight, 2024: The genomic landscape of lung cancer in never-smokers
from the Women’s Health Initiative, lung cancer in never-smokers accounts for 10-15% of US cases and up to 20% globally,
with recent trends showing an increase to 17% in men and 24% in women in never-smokers. As detailed in the study “Characteristics
of never-smoker lung cancer patients in Korea” published in Lung Cancer, 2004, in Asia, over 30% of patients with lung cancer
are never-smokers, with at least 50% of lung cancers occurring in women who have never smoked.

We
are focused on advancing LP-300 as a potential combination therapy for never smoking NSCLC patients with adenocarcinoma by leveraging
our A.I. platform to help uncover the genomic and biomarker networks that are associated with response in the never-smoker and non-smoker
groups. Additionally, through our early, preclinical work to define a gene signature that correlates with heightened sensitivity to LP-300,
we believe there is potential to further expand the indication to include all NSCLC patients that have this identified genetic profile
in their cancer. Currently there is no approved therapy specifically for the growing indication of never-smokers with NSCLC, and female
never smokers appear to be uniquely responsive to LP-300. If successful, LP-300 could provide improved patient benefit in terms of improved
survival, and secondarily through the concurrent prevention and mitigation of common and serious chemotherapy-induced toxicities.

Prior
Completed Trials of LP-300

Phase
1. LP-300 has been evaluated in five Phase 1 studies (DMS10001, BioNumerik, 09/1997 through 04/2004; DMS10002, BioNumerik, 12/1997
through 08/2001; DMS12209, ASKA Pharmaceutical, 04/2000 through 12/2001; DMS10011, BioNumerik, 02/2006 through 07/2006; and DMS12307,
Baxter, 07/2002 through 07/2005) to determine the maximum tolerated dose (“MTD”), and to evaluate the safety, tolerability,
pharmacokinetics, and potential efficacy of LP-300 (alone or in combination with cisplatin, cisplatin/paclitaxel, or carboplatin/paclitaxel).
An MTD for LP-300 was not reached in any of the Phase 1 studies at dose levels of up to 41 g/m2.

Phase
2. In a U.S. multi-center, randomized, open-label trial (n=160 patients) with advanced (Stage IIIB and IV) NSCLC treated with LP-300
or no LP-300 (DMS22210/CALGB 30303, Cancer and Leukemia Group B, 08/2004 through 03/2007), although the overall population did not meet
the pre-specified primary endpoint, an analysis of a subgroup of patients with adenocarcinoma revealed that the difference in the median
overall survival period between the 2 treatment groups was statistically significant (LP-300 = 15.6 months, no LP-300 = 8.9 months; Log-rank
p=0.0326), and the median overall survival for patients who received LP-300 was 6.7 months longer than that of those who did not receive
LP-300.

Phase
3. LP-300 has been evaluated in five Phase 3 studies: two in patients with metastatic breast cancer, with a primary endpoint examining
the ability to reduce platinum/taxane induced peripheral neuropathy, and three in patients with NSCLC or advanced primary lung adenocarcinoma.
(DMS32205R, ASKA Pharmaceutical, 08/2005 through 02/2008; DMS30203R, BioNumerik, 09/2001 through 10/2006; DMS30204R, ASKA Pharmaceutical,
04/2003 through 03/2006; DMS32206R, Baxter, 10/2002 through 04/2006; and DMS32212R, BioNumerik, 04/2010 through 06/2013) Although the
overall population did not meet the pre-specified primary endpoints in any of the trials, analysis of subgroups of patients in one multi-country
lung adenocarcinoma trial and one Japanese NSCLC trial revealed differences in the median overall survival between the two treatment
arms (with or without LP-300 treatment). The results from the two key lung cancer trials obtained from retrospective analyses are described
below:

●
Multi-country,
double-blind, randomized, multi-center & placebo-controlled trial (n=540 patients) with advanced primary lung adenocarcinoma
treated with LP-300 or Placebo & paclitaxel or docetaxel with cisplatin (DMS32212R). (the Phase 3 NSCLC adenocarcinoma trial)

Ø
Treatment
with LP-300 nearly doubled the Overall Survival in women receiving paclitaxel/cisplatin (25.0-month median OS in LP-300 arm vs. 13.2-month
OS in control arm) and the results in this subgroup were statistically significant (P-value = 0.0477; HR = 0.579)

Ø
For
never smoking women with adenocarcinoma of the lung receiving paclitaxel/cisplatin, the Overall Survival in the LP-300 arm was more
than double the control arm (27.0 months vs. 13.4 months, respectively) also being statistically significant in favor of LP-300 (P-value
= 0.0167; HR = 0.367) and the 2-year survival was 72.4% in the LP-300 arm vs. 32.3% in the control arm.

18

●
Statistically
significant subgroup analyses and trends from this LP-300 Phase 3 NSCLC adenocarcinoma trial support repositioning LP-300 for non-
or never smokers with adenocarcinoma of the lung.

●
Randomized,
double-blind, placebo-controlled and multi-center trial in patients with advanced NSCLC receiving paclitaxel & cisplatin (Japan
Trial) (DMS32205R). The Japan Trial observations support and complement observations in the multi-country Phase 3 NSCLC adenocarcinoma
trial. The observations for the female adenocarcinoma patient population in the LP-300 multi-country Phase 3 NSCLC adenocarcinoma
trial are consistent with observations made for the subgroup of females with adenocarcinoma of the lung receiving paclitaxel/cisplatin
and LP-300 or placebo in the Japan Trial. Although the overall population in the Japanese trial did not meet the pre-specified primary
endpoint, a retrospective analysis of the subgroup consisting of female patients with adenocarcinoma revealed that the difference
in the median overall survival period between the two treatment arms in this subgroup was significant (P-value = 0.0456, HR = 0.376).

The
LP-300 arm of the multi-country Phase 3 NSCLC adenocarcinoma trial also demonstrated safety profile advantages in terms of the potential
to protect against chemotherapy-induced kidney toxicity and chemotherapy-induced anemia. These observations complemented earlier clinical
observations regarding LP-300’s potential to protect against neuropathy and other chemotherapy-induced toxicities. Results from
these trials indicate that treatment with LP-300 may, in further clinical testing, lead to improved survival in female and non- or never
smoking patients with primary adenocarcinoma of the lung receiving cisplatin/paclitaxel combination chemotherapy.

Phase
2 and 3 LP-300 Adverse Events Summary

The
following summarizes adverse events reported from a total of 1,712 patients enrolled in five randomized multi-center phase 2 and phase
3 studies with chemotherapy, with or without LP-300. A total of 1,712 patients were enrolled in these studies, of which 856 patients
received LP-300 with chemotherapy.

●
All
Adverse Events (AEs). The most frequently-occurring adverse events in patients receiving LP-300 with chemotherapy were generally
similar to patients receiving placebo or chemotherapy alone. These events included blood and lymphatic system disorders (myelosuppression
manifested as anemia, leukopenia, lymphopenia, neutropenia, and thrombocytopenia; also including decreased hematocrit, hemoglobin,
lymphocyte count, neutrophil count, red blood cell count, platelet count, and white blood cell count), with an incidence ranging
from 12% to 83%; gastrointestinal disorders including constipation, abdominal pain, diarrhea, nausea, stomatitis, and vomiting, with
an incidence ranging from 22% to 83%; general disorders and administrative site conditions including fatigue (ranging from 17% to
85%); infusion/injection site pain/reactions (ranging from 12% to 18%); malaise (ranging from 16% to 28%); peripheral edema (ranging
from 13% to 22%); pyrexia (ranging from 10% to 17%); infections and infestations disorders including nasopharyngitis (ranging from
11% to 16%); investigations including increased liver function tests including ALT, AST, and alkaline phosphatase (ranging from approximately
10% to 55%); increased blood lactate dehydrogenase (ranging from approximately 17% to 26%); increased blood urea or blood uric acid
(ranging from approximately 11% to 32%); increased gamma-glutamyltransferase (ranging from approximately 23% to 33%); decreased total
protein (ranging from approximately 12% to 21%); metabolic and nutritional disorders including weight decreased (ranging from 15%
to 22%), anorexia (ranging from 14% to 82%), and hypomagnesemia (ranging from 22% to 30%); musculoskeletal and connective tissue
disorders including arthralgia, back pain, and myalgia (ranging from 7% to 80%); nervous system disorders including dysgeusia (ranging
from 12% to 22%), headache (ranging from 14% to 17%), and peripheral neuropathy (motor and sensory – ranging from 22% to 86%);
psychiatric disorders including insomnia (ranging from 12% to 17%); respiratory, thoracic, and mediastinal disorders including dyspnea
(ranging from 12% to 40%); skin and subcutaneous disorders including alopecia (ranging from 33% to 92%); rash (ranging from 22% to
29%); nail disorder/discoloration (10%); and vascular disorders including angiopathy (ranging from 64% to 69%) and flushing (ranging
from 15% to 39%).

●
Treatment-Related
Adverse Events. Frequently occurring treatment-related AEs experienced by patients receiving LP-300 with chemotherapy included
gastrointestinal disorders manifesting as nausea and vomiting (ranging from 12% to 67%, and 12% to 32%, respectively); fatigue (ranging
from 22% to 82%); infusion/injection site pain/reactions (ranging from 11% to 18%); increased ALT (alanine aminotransferase) and
gamma-glutamyltransferase (ranging from approximately 13% to 18%, and approximately 11% to 12%, respectively); peripheral neuropathy
(motor and sensory – ranging from 14% to 54%); and vascular disorders including angiopathy (ranging from 60% to 69%), and flushing
(ranging from 8% to 11%).

19

●
Serious
Adverse Events (SAEs). 11% to 49% of patients receiving LP-300 with chemotherapy, and 7% to 42% of patients in control groups
receiving chemotherapy alone experienced SAEs during randomized multicenter studies. Frequently-occurring SAEs in patients receiving
LP-300 with chemotherapy included pneumonia, hypersensitivity or drug hypersensitivity, dyspnea, pyrexia and dehydration, diarrhea,
anaphylactic shock or anaphylactic reactions, vomiting, disease progression, infection, bronchospasm, pleural effusion, pulmonary
embolism, thrombosis, hemolysis, nausea, chills, fatigue, sudden death, neutropenic infection, sepsis, anorexia, neutropenia, febrile
neutropenia, pneumonitis, rash, and hypotension. Multiple allergic reactions have been reported in clinical trials of LP-300, and
some of these reactions have been severe. It is possible that patients could experience an allergic reaction that is life-threatening.
Five reports of grade 3 or 4 hemolysis events with three fatal outcomes were reported in patients receiving LP-300 with chemotherapy
in a study involving the weekly drug administration schedule. Two events of hemolysis were reported in a study involving drug administration
every two weeks. No events of hemolysis were reported in studies using the three weeks schedule of administration, which is the administration
schedule used for the multi-country Phase 3 NSCLC adenocarcinoma trial.

●
Treatment-Related
Serious Adverse Events. Approximately 7% of patients receiving LP-300 with chemotherapy experienced treatment-related SAEs during
randomized multicenter studies. The most frequently-occurring treatment-related SAEs experienced by patients receiving LP-300 with
chemotherapy were hypersensitivity or drug hypersensitivity (five and two patients, respectively) and neutropenia (six patients).
Other treatment-related SAEs experienced by patients receiving LP-300 with chemotherapy included hemolysis, bronchospasm, febrile
neutropenia, anemia, nausea, and pulmonary edema (three patients, each); chills, diarrhea, pyrexia, neutropenic infection, hyperglycemia,
acute respiratory distress syndrome, pulmonary embolism, sudden death, infection, and rash (two patients, each); and angina pectoris,
cardiac arrest, tachycardia, sudden hearing loss, abdominal pain, vomiting, adverse drug reaction, anaphylactic shock, C. difficile
colitis, pneumonia, sepsis, chemical cystitis, thrombosis in device, dehydration, leukopenia, anorexia, atrial fibrillation,
fatigue, weight decrease, muscle disorder, pain in extremity, dizziness, peripheral sensory neuropathy, dyspnea, hypotension, and
thrombosis (one patient, each).

Clinical
Evidence of Toxicity Protection by LP-300

The
data from randomized multicenter studies of LP-300 and chemotherapy demonstrates objective evidence of several instances where treatment
with LP-300 appears to provide potential benefit in terms of preventing and mitigating chemotherapy-induced toxicities, particularly
in studies of LP-300 and chemotherapy in patients with advanced NSCLC. These data support that LP-300 has the potential to protect against
chemotherapy-induced toxicities, including gastrointestinal, renal, electrolyte disturbances, and anemia; and there is data supporting
the potential for LP-300 to protect against severe forms of these toxicities. In addition, treatment with LP-300 may protect against
severe platinum-induced hearing loss and dehydration.

LP-300
Mechanism of Action

LP-300
is a water-soluble disulfide compound that lacks a free thiol or sulfate moiety. We postulate this unique structure of LP-300 may allow
it to potentiate antitumor activity of certain types of cytotoxic chemotherapy, and exert chemoprotective effects, through distinct and
interrelated mechanisms. In plasma, the lack of a free thiol prevents untoward reactivity and drug-drug interactions, and thereby may
allow chemotherapeutic agents to retain their efficacy. Once inside the tumor cell, LP-300 is metabolized and may then potentiate antitumor
activity of cytotoxic certain types of chemotherapy. A significant fraction of LP-300 is taken up by the kidneys, where LP-300’s
metabolites can interact with chemotherapy drugs, such as cisplatin, and potentially diminish the chemotherapy drug’s ability to
cause organ damage. We believe the postulated mechanisms that can enhance tumor directed chemosensitivity include restoration of apoptotic
sensitivity thereby countering drug resistance; oxidative stress enhancement; anti-angiogenesis; decreased DNA synthesis and gene expression;
and decreased glutathione and precursors (limiting glutathione tumor-mediated drug resistance). When LP-300 accumulates in the kidneys
it appears to reduce the toxicity of certain drugs, such as cisplatin, that are excreted through the renal system.

20

As
depicted in the model below, we believe LP-300 and its metabolites can modulate key components of the thioredoxin and glutaredoxin systems,
which are believed to be involved as major mechanisms of the potentially enhanced antitumor effects of LP-300 with chemotherapy. The
thioredoxin pathway is commonly upregulated in adenocarcinomas, and examination of primary lung tumors from non-smokers have shown significantly
increased gene expression of thioredoxin. Overexpression of thioredoxin in cancer cells has been postulated to lead to resistance to
apoptosis, increased cellular proliferation, increased gene expression, increased angiogenesis, increased conversion of DNA into RNA,
and resistance to oxidative stress induction. We believe the modulation of thioredoxin expression is important for the observed increases
in patient survival identified in retrospective analyses of certain subgroups of patients with primary adenocarcinoma of the lung receiving
LP-300 in conjunction with cisplatin and paclitaxel chemotherapy. Different glutaredoxin transcript variants have been found to be elevated
in transformed cells, and glutaredoxin isoforms (e.g., variants of glutaredoxin 2) have been found to be elevated in NSCLC cell lines,
lending evidence for potential roles of glutaredoxin in tumor progression.

We
believe LP-300 and its metabolites may potentiate the antitumor activity of chemotherapy by:

(1)
shifting the redox balance and concentrations of reduced forms of thioredoxin and glutaredoxin to inactive oxidized forms of thioredoxin
and glutaredoxin, thereby restoring apoptotic sensitivity, increasing sensitivity to oxidative stress, inhibiting cell growth and angiogenesis,
RNA to DNA synthesis, and growth signaling, and

(2)
forming thioredoxin or glutaredoxin adducts, which as inactive forms lead to thioredoxin- and glutaredoxin-mediated reduction of downstream
targets in the cell that are important for tumor resistance to chemotherapy, angiogenesis and cell growth.

Working
Model for LP-300 Mechanism of Action

We
believe that LP-300 may potentiate antitumor activity of certain types of cytotoxic chemotherapy, and exert chemoprotective effects through
several distinct and interrelated mechanisms of action. LP-300 is a cysteine-modifying agent that appears to modulate multiple cellular
pathways simultaneously. Experimental data indicate that LP-300 modifies and/or modulates the following key pathways:

●
Kinases
involved in key signaling pathways (EGFR, ALK, ROS, MET)

21

●
Enzymes
critical for DNA synthesis and repair (ERCC1, RNR1, RNR2)

●
Enzymes
and proteins important in regulating cell redox status (TRX, PRX, GRX, PDI)

The
following key mechanisms have been observed to support our belief that LP-300 has potential to play an important role in the treatment
of females and never smokers with NSCLC adenocarcinoma. We believe these mechanisms help to explain the retrospective subgroup observations
for females and never smokers receiving LP-300 together with cisplatin and paclitaxel in the Phase 3 NSCLC adenocarcinoma trial:

●
LP-300
targets cysteine residues. Computational and experimental data indicate that LP-300 demonstrates specificity towards cysteines.
LP-300-mediated xenobiotic modulation of protein targets on cysteine results in distinct, (multi)target-specific effects correlated
to the role of the cysteine residue(s) in the target.

●
LP-300
alone inhibits human ALK and stimulates the inhibitory effect of crizotinib on human ALK. Alterations in ALK, along with MET,
ROS1 & PDGFRA are thought to underlie nearly 10% of NSCLC adenocarcinoma cancers. Liquid Chromatography (LC), Mass Spectrometry
(MS) and X-ray structural data demonstrate that LP-300 covalently modifies human ALK on Cys1156 and Cys1235. Enzyme assay data demonstrates
that LP-300 inhibits human ALK’s kinase activity and stimulates the inhibitory effect of crizotinib on human ALK’s kinase
activity.

●
LP-300
inhibits human MET kinase activity and stimulates Staurosporine inhibition of human MET kinase activity. Mesenchymal Epithelial
Transition Factor Kinase (MET) kinase mutations and amplification are an important, specific subset of NSCLC adenocarcinoma. Enzyme
assays demonstrate that LP-300 inhibits human MET kinase activity and stimulates the inhibitory activity of staurosporine on human
MET kinase.

●
LP-300
inhibits EGFR kinase activity. EGFR mutations are an important, specific subset of NSCLC adenocarcinoma, particularly in non-smoker
females. Enzyme assays demonstrate that LP-300 inhibits EGFR kinase activity and potentiates the inhibitory effect of eErlotinib
on wild type as well as mutant EGFR kinase activity.

●
LP-300
modestly inhibits retinal rod outer segment kinase (ROS1) activity. ROS1 chromosomal rearrangements are a recently identified
class of mutations in NSCLC. Estimates of frequency of ROS1 rearrangements range from 1% to 2%. Experimental data are as follows:

Ø
Enzyme
activity data demonstrates that LP-300 has an effect on Human ROS1 activity when ROS1 is preincubated with LP-300. We hypothesize
that pre-incubation allows slower reacting cysteine residues to be modulated by LP-300.

Ø
Based
on modeling studies, the cysteines on ROS1 appeared to be in less optimal orientations compared to cysteines in ALK.

Ø
LP-300
appears not to impact ROS1 activity unless ROS1 and LP-300 are pre-incubated prior to kinase assays. Therefore, to see an effect
in vivo, it may be necessary to administer LP-300 prior to LP-300’s effects on ROS1 through preincubation of ROS1 and
LP-300, suggesting slower xenobiotic modulation reactions. However, there are several possible explanations for the LP-300 effect
on ROS1 and in the absence of an X-ray structure this remains a hypothesis.

●
LP-300
modifies Ribonucleotide Reductase 1 and 2 (RNR1 and RNR2). Selective, elevated expression of the RNR1 subunit is associated with
gemcitabine resistance in NSCLC. RNR1/RNR2 are essential for DNA synthesis, DNA repair & cell proliferation. RNR1/2 catalyzes
the formation of deoxyribonucleotides needed for DNA synthesis, from ribonucleotides.

22

●
LP-300
targets proteins that may result in protection against chemotherapy-induced nephrotoxicity and neuropathy. The LP-300 derivative-cisplatin/paclitaxel
conjugate is inactive and this conjugate is not a substrate for aminopeptidase/γ-Glutamyl-transpeptidase (APN/GGT). These LP-300
heteroconjugates appear to cause potent inhibition of APN/GGT leading to suppression/bypass of renal APN/GGT xenobiotic metabolism
pathways promoting protection against chemotherapy-induced nephrotoxicity. In addition, binding of the LP-300 derivative with reactive
cisplatin/paclitaxel species, appears to inactivate the platinum-catalyzed microtubule hyper-polymerization. This action may serve
to protect against chemotherapy-induced peripheral neuropathy.

●
LP-300
modulates protein function in a way that may promote chemosensitization. LP-300 appears to promote covalent oxidation of redox
proteins Thioredoxin (TRX), Peroxiredoxin1 (PRX1) and Glutaredoxin (GRX). This action may keep these redox proteins in an inactive
non-signaling state, which could enhance sensitivity to oxidative stress and apoptosis induced by concomitant chemotherapy.

Using
various in vitro experimental approaches, LP-300 has been observed to form adducts on cysteines of various protein targets such
as those listed below. For several of these targets, studies evaluating enzyme activity associated with the targets have demonstrated
inhibition, modulation or impairment of such activity. In addition, X-ray crystallographic studies support LP-300 derived adducts at
specific cysteines on these proteins.

Targeted
Proteins Modified by LP-300

Cellular
Target of LP-300

Cellular
consequence of LP-300-modification and/or modulation

Cellular
thiol/disulfide balance

LP-300
and LP-300-derived mesna disulfide heteroconjugates are pharmacological surrogate/modulators of physiological thiols and disulfides
(e.g., glutathione, cysteine, and homocysteine).

Gamma-Glutamyltranspeptidase
Aminopeptidase N

LP-300
and LP-300-derived mesna disulfide heteroconjugates can inhibit gamma-glutamyltranspeptidase and aminopeptidase N enzyme activity.

Tubulin

LP-300
exerts direct and indirect protective interactions with tubulin.

Anaplastic
Lymphoma Kinase (ALK)

LP-300
disrupts/blocks ATP binding site resulting in inhibition of ALK kinase activity (vide infra).

Mesenchymal
Epithelial Transition (MET) Factor Kinase

Modification
of non-active site cysteine(s) resulting in enzyme inhibition (MET).

ROS1
kinase

LP-300
xenobiotically modifies ROS1 kinase in a time dependent manner.

Redox
Balance

LP-300
and LP-300-derived mesna disulfide heteroconjugates assist in the maintenance of cellular redox balance and support cellular defenses
against oxidative insult.

Thioredoxin
(Trx) Glutaredoxin (Grx)

LP-300
modifies non-catalytic cysteines important in redox protein function/structure (Grx and Trx).

Thioredoxin
(Trx) Glutaredoxin (Grx)

LP-300
and/or LP-300-derived mesna disulfide heteroconjugates function as alternative substrates/inhibitors (Trx, Grx) resulting in impaired
enzyme activity.

Peroxiredoxin
(Prx)

LP-300
disrupts active site structure (Prx) resulting in impaired enzyme activity.

Mechanistic
evaluation of LP-300 revealed that it has cysteine-modifying activity on select Receptor Tyrosine Kinases (RTKs) initiating proliferative
signaling such as ALK, EGFR, MET and ROS1. LP-300 may also serve as a potential chemosensitizer for certain combination chemotherapies
by inactivating proteins such as Thioredoxin (TRX), Glutaredoxin (GRX) and Peroxiredoxin (PRX) that are important in modulating cellular
redox status and in turn drug resistance. Higher levels of PRX gene expression have been shown to correlate significantly with the absence
of smoking history and with the female gender.

We
believe well-tolerated profile advantages of LP-300 are imparted through its chemoprotective action via production of inactive LP-300-chemotherapeutic
conjugates and preventing toxic taxane/platinum metabolites in the kidney, and targeting toxicity-inducing molecules and pathways (e.g.
APN, GGT, and Tubulin).

23

Our
RADR® Platform’s Approach to LP-300 Repositioning

Our
RADR® platform has been implemented with the objective of uncovering insights from LP-300 rescued preclinical data as
well as from lung cancer clinical trial data regarding actionable bioinformatics, biomarkers, target population demographics and smoking
history. Differential expression analyses of RNAseq data on LP-300 pre- and post-exposure in selected NSCLC cell lines has revealed gene
sets that could be upregulated and downregulated in response to LP-300 treatments involving the mapping of genes performing cellular
redox functions, kinases involved in proliferating signaling, and apoptotic markers. We are currently in the early stages of defining
a specific biomarker signature that correlates with heightened sensitivity to LP-300. We believe that this signature may help accelerate
the clinical development of LP-300 and has the potential to guide patient selection for targeted clinical trials. We are also developing
a list of approved cancer drugs that, when used in combination with LP-300, may have potential to improve the overall benefit to patients
through either potentially greater anticancer properties or improved tolerability. We believe identifying such combinations would be
attractive to established pharmaceutical and biotech companies.

Acquisition
of Tavocept® (LP-300) Rights from BioNumerik

In
January 2018, we entered into an Assignment Agreement (the “Assignment Agreement”) with BioNumerik Pharmaceuticals, Inc.
(“BioNumerik”), pursuant to which we acquired rights to domestic and international patents, trademarks and related technology
and data relating to LP-300 for human therapeutic treatment indications. Mr. Margrave, our Chief Financial Officer and Secretary, formerly
served as the President, Chief Administrative Officer, General Counsel and Secretary of BioNumerik and has a minority ownership interest
in BioNumerik. The Assignment Agreement replaced a License Agreement that was entered into between us and BioNumerik in May 2016. We
made upfront payments totaling $25,000 in connection with entry into the Assignment Agreement.

If
we commercialize LP-300 internally, we will be required to pay to the BioNumerik-related payment recipients designated in the Assignment
Agreement a percentage royalty in the low double digits of cumulative net revenue up to $100 million, with incremental increases in the
percentage royalty for net cumulative revenue between $100 million and $250 million, $250 million and $500 million, and $500 million
and $1 billion, with a percentage royalty payment that could exceed $200 million for net cumulative revenue in excess of $1 billion.
In addition, we have the right to first recover certain designated portions of patent costs and development and regulatory costs before
the payment of royalties described above. We are obligated to make royalty payments under the Assignment Agreement during the “Agreement
Term” that started on January 5, 2018 and continues (on a country-by-country and product-by-product basis) until the later
to occur of (i) five (5) years after the expiration of the last to expire Patent Rights, as defined in the Assignment Agreement, in an
applicable country in the Territory, as defined in the Assignment Agreement, and (ii) if no Patent Rights exist in such country, fifteen
(15) years after May 31, 2016.

If
we enter into a third party transaction for LP-300, we are required to pay the BioNumerik-related payment recipients a specified percentage
of any upfront, milestone, and royalty amounts received by us from the transaction, after first recovering specified direct costs incurred
by us for the development of LP-300 that are not otherwise reimbursed from such third party transaction. In addition, the Assignment
Agreement provides that we will use commercially diligent efforts to develop LP-300 and make specified regulatory filings and pay specified
development and regulatory costs related to LP-300. The Assignment Agreement also provides that we will provide TriviumVet DAC (“TriviumVet”)
with (i) specified data and information generated by us with respect to LP-300, and (ii) an exclusive license to use specified LP-300-related
patent rights, trademark rights and related intellectual property to support LP-300 development in non-human (animal) treatment indications.
Under the Assignment Agreement, we are required to pay all patent costs on covered patents related to LP-300. These patent costs are
fully recoverable at the time of any net revenue from LP-300, with up to 50% of net revenue amounts to be applied towards repayment of
patent costs until such costs are fully recovered. In addition to the recovery of patent costs, we have the right to recover the $25,000
upfront payments made in connection with entry into the Assignment Agreement, which payments are recoverable prior to making any royalty
or third-party transaction sharing payments. We also have the right to recover all previously incurred LP-300 development and regulatory
costs, with up to a mid-single digit percentage of net revenue amounts to be applied towards repayment of development and regulatory
costs until such costs are fully recovered.

24

LP-184

General
Overview

LP-184
(hydroxyureamethylacylfulvene) is a small molecule that preferentially damages DNA in cancer cells that overexpress certain biomarkers
or that harbor mutations in DNA repair pathways. LP-184 is converted into an active alkylating agent by the enzyme prostaglandin reductase
1 (PTGR1), which is overexpressed in many tumor types that are resistant to current standard of care treatments. The FDA has granted
LP-184 Orphan Drug Designation for the treatment of pancreatic cancer, Malignant Glioma and ATRT (Atypical Teratoid Rhabdoid
Tumors). We believe cancer cells are less likely to develop resistance to LP-184 because of its mode of action that is independent
of efflux pumps and oncogene/tumor suppressor mutations. We also believe that LP-184 has the potential to address a significant unmet
need in the current treatment landscape for multiple important cancer types.

LP-184
has nanomolar potency and it is a member of a new generation of acylfulvenes, a family of naturally-derived anticancer drug candidates.
Earlier generations of acylfulvenes showed great promise in preclinical studies, but were hampered in human clinical studies because
of the inability to deliver effective therapeutic doses due to unacceptable toxicities to normal cells. In preclinical studies, LP-184
has shown significantly enhanced antitumor activity as compared to earlier generation acylfulvenes. In addition, we have used our RADR®
platform, together with work of collaborators, to develop a patient-specific biomarker test we believe will be predictive of LP-184’s
anticancer activity in targeted patient populations. The chemical structure of LP-184 is depicted below.

LP-184
Chemical Structure

Starlight
Therapeutics Inc. and STAR-001

In
January 2023, we formed a wholly owned subsidiary, Starlight Therapeutics Inc. (“Starlight”), to develop drug candidate LP-184’s
central nervous system (CNS) and brain cancer indications – including glioblastoma (GBM), brain metastases (brain mets.), and several
rare pediatric CNS cancers. Following the formation of Starlight, we now refer to the molecule LP-184, as it is developed in CNS indications,
as “STAR-001”.

Phase
1 Clinical Trial for LP-184

The
LP-184 Phase 1a clinical trial focused on patients with advanced solid tumors and glioblastoma, which includes potential patients with
breast, lung, pancreatic, bladder, prostate, and ovarian cancers and other solid tumors. In addition to the primary objective of determining
the MTD (maximum tolerated dose) and RP2D (recommended Phase 2 dose), other objectives include pharmacokinetics and preliminary clinical
activities of LP-184, correlations of clinical activity with tumor expression of the gene PTGR1 (Prostaglandin Reductase 1) and/or genomic
alterations in DNA damage repair pathway genes.

For
the Phase 1a trial, LP-184 was administered on Days 1 and 8 of each 21-day cycle. The trial followed a modified Fibonacci schedule until
the maximum tolerated dose (MTD) and/or recommended Phase 2 dose (RP2D) was determined.

25

The
enrollment of the dose escalation portion of the study has been completed. Between September 2023 and July 2025, a total of 63 patients
were treated with LP-184. Overall, LP-184 was well tolerated with primarily Grade 1 and Grade 2 adverse events (AEs) that were consistent
with expected side effects of alkylating agents and were generally clinically manageable and/or reversible. The projected therapeutic
concentration (282 nM) derived from preclinical studies was achieved at dose level (DL) 7. For the overall study, 11 of 51 (22%) evaluable
patients with post-treatment measurable target lesions achieved tumor shrinkage, with several individuals experiencing reduction approaching
the threshold of partial response. Notably, durable disease control (≥12 months) were reported in 3 patients and were substantially
longer than expected with the current existing later line therapies for their disease. Taken together, the study demonstrates that LP-184
has a manageable safety profile with encouraging antitumor signals.

Potential
Future LP-184 Clinical Studies

The
following is a summary of potential future clinical studies of LP-184. The conduct of these studies will be subject to evaluation of
the totality of the data from the LP-184 Phase 1a trial and obtaining additional funding.

Phase
1b/2 dose expansion study in adult patients with advanced triple negative breast cancer (TNBC), pancreatic cancer (PDAC), non small cell
lung cancer (NSCLC), and other solid tumors.

We
plan to conduct a Phase 1b/2 dose expansion study of LP-184 in adult patients with advanced triple negative breast cancer (TNBC), pancreatic
cancer (PDAC), non-small cell lung cancer (NSCLC), and other solid tumors. Our objective for the planned conduct of this study will be
to provide safety and potential preliminary efficacy data, and to inform the optimal dose of LP-184 monotherapy that can be administered
in the treatment of a subset of advanced solid tumors with known DNA Damage Repair (DDR) pathways. The Phase 1b portion of the study
is expected to be a multi-center study with the primary objective of determining the recommended Phase 2 dose (RP2D) of LP-184 in TNBC
and other indications, including NSCLC, PDAC, and other solid tumors.

●
It
is estimated that approximately 30% of solid tumors (including ovarian, breast, pancreatic, colon, and prostate cancers, as well
as melanoma and leiomyosarcoma) harbor alterations in DDR pathways. DNA repair targeting therapies exploit DDR alterations in cancer
cells to achieve synthetic lethality, a therapeutic rationale that has led to the development of a variety of DDR inhibitors, such
as PARP inhibitors. Although DDR inhibitors that are approved or under development have shown promising clinical activity, approximately
40%-70% of patients develop resistance over time and necessitate additional therapies.

●
LP-184
is a synthetically lethal small molecule that in preclinical studies has been observed to induce DNA double strand breaks upon bioactivation
by the enzyme prostaglandin reductase 1 (PTGR1) in cancer cells. In preclinical studies, LP-184 showed a high degree of anti-tumor
activity in triple-negative breast cancer (TNBC), pancreatic ductal adenocarcinoma (PDAC), non-small cell lung cancer (NSCLC) and
other solid tumors. Preclinical studies and artificial intelligence-driven in silico modeling suggest that cancers with DNA
Damage Response (DDR) gene alterations may preferentially respond to LP-184.

Phase
1b/2 Study of LP-184 in combination with olaparib in adult patients with Advanced HR-Negative and HER2-Negative Breast Cancer (Triple-Negative
Breast Cancer; TNBC).

We
plan to conduct a Phase 1b/2 Study of LP-184 in combination with olaparib in adult patients with Advanced HR-Negative and HER2-Negative
Breast Cancer (Triple-Negative Breast Cancer; TNBC). Our objective for the planned conduct of this study will be to provide safety and
potential preliminary efficacy data, to inform the optimal dose(s) of LP-184 that can be administered in a specified dosing regimen,
in combination with olaparib, in future pivotal clinical studies. This is expected to be a multicenter study with the primary objective
of evaluating the safety, tolerability, and preliminary estimates of clinical activity of LP-184 in combination with olaparib in patients
with HR-negative and HER2-negative breast cancer patients (TNBC).

26

●
TNBC
accounts for approximately 15% of breast cancers and presents with the worst prognosis. It does not benefit from targeted treatment
and hormonal treatment options for breast cancer. TNBC is a heterogeneous disease with a high frequency of homologous recombination
deficiency (HRD). Despite advances made in the development of therapies for TNBC, overall survival remains poor and strategies to
overcome resistance to approved therapies, including approved PARP inhibitors like olaparib, are needed.

●
In
vitro, LP-184 has demonstrated inhibitory activity (with sub micromolar IC50 values) in multiple TNBC breast cancer cell lines. In
vivo, in TNBC PDX models, LP-184 showed 107% – 132% tumor growth inhibition with complete tumor regression observed, especially
in models harboring HRD and irrespective of their sensitivity to PARP inhibitors. In addition, the combination of LP-184 with olaparib
resulted in synergistic tumor growth inhibition in TNBC PDX models when compared to monotherapy with either LP-184 or olaparib.

Phase
1b/2 Study of LP-184 in combination with nivolumab and ipilimumab in KEAP1 and/or STK11-mutated and PD-L1-low non-small cell lung cancer
(NSCLC).

We
plan to conduct a Phase 1b/2 Study of LP-184 in combination with nivolumab and ipilimumab in KEAP1 and/or STK11-mutated
and PD-L1-low non-small cell lung cancer (NSCLC). Our objective for the planned conduct of this study will be to provide safety and potential
preliminary efficacy data, and to inform the optimal dose(s) and regimen of LP-184 that can be administered in combination with the standard
of care nivolumab and ipilimumab immunotherapy regimen. This is expected to be a multicenter study with the primary objective of evaluating
the safety tolerability, and preliminary estimates of clinical activity of LP-184 in combination with standard of care immunotherapy
treatment in patients with KEAP1 and/or STK11-mutated and PD-L1-low non-small cell lung cancer (NSCLC).

●
Lung
cancer is the most frequent cause of cancer-related death worldwide with NSCLC being the most common type, and accounting for approximately
85% of lung cancers. Despite the progress made in the last decade with immunotherapy, targeted therapy, and other treatments, there
is still a significant unmet need for effective therapies for NSCLC patients. Specifically, alterations in the KEAP1 and STK11
genes are common in NSCLC patients and often associated with worse prognosis. Most KEAP1 and/or STK11 mutated NSCLC
patients have no or low PD-L1 expression, further limiting the benefits from PD-(L)1 blockage therapies. There is a high unmet need
for effective therapies for NSCLC patients harboring the above alterations, which have often been considered undruggable and/or associated
with mechanisms of resistance to approved therapies.

●
We
believe LP-184 has the potential to improve outcomes in the KEAP1 and/or STK11 mutated NSCLC subset of patients. In
the H460 (KEAP1 and STK11 double mutant) human NSCLC cell line derived xenograft tumor model, LP-184 single agent demonstrated
102% tumor growth inhibition (TGI). We also believe that LP-184 holds potential promise for boosting the efficacy of immune checkpoint
inhibitors (ICIs), likely via reprogramming the tumor microenvironment. In preclinical studies, we have observed that, when combined
with ICIs, LP-184 has the capacity to produce a synergistic anti-tumor response by amplifying DNA damage, reducing immunosuppression
and targeting vulnerabilities underlying KEAP1 and/or STK11 mutations thereby also helping to reverse ICI resistance.
In a proof-of-concept study in mouse triple-negative breast cancer tumor models that were non-hypermutated and ICI resistant, LP-184
combined with an anti-PD-1 agent synergized and elicited a greater anti-tumor response than monotherapies. The LP-184 and anti-PD-1
combination also enhanced antigen presentation and interferon signaling in these models.

27

Phase
1b/2 Trial of LP-184 Monotherapy in Advanced Urothelial Carcinoma with PTGR1 Positive and TC-NER/HR Deficiency

An
investigator-sponsored Phase 1b/2 trial of LP-184 as a monotherapy in advanced urothelial carcinoma patients with positive PTGR1 and
deficient TC-NER/HR is being planned. Dr. Helle Pappot from Rigshospitalet University, Denmark is the leading investigator. The primary
objective of the Phase 1b portion is to evaluate the safety and tolerability of LP-184 in the study population. The primary objective
of the Phase 2 portion is to evaluate the preliminary objective response rate.

● Despite
recent advances, metastatic urothelial carcinoma (mUC) continues to carry a poor prognosis.
Platinum-based chemotherapy as the first-line standard has been supplanted by enfortumab
vedotin plus pembrolizumab, which has shown strong efficacy. Yet options remain limited for
patients ineligible for these therapies or who develop resistance, underscoring the need
for alternative approaches and increasingly biomarker-guided, individualized treatment strategies.

● The
study’s patient selection will be based on specific tumor characteristics, including
genotyping for NER and HR deficiencies and PTGR1 positivity. NER and HR deficiencies are
identified using ctDNA analysis, while PTGR1 positivity is determined through immunohistochemical
screening of archival tissue. This population was selected based on preclinical data suggesting
potential efficacy of LP-184 in tumors with these characteristics. The results of this study
are expected to be particularly relevant for this specific subgroup of UC patients, who represent
a population with significant unmet medical need.

Additional
LP-184 (STAR-001) Development Opportunities – Starlight Therapeutics Inc.

STAR-001
in Glioblastoma and other CNS Cancers

Glioblastoma
is an aggressive type of cancer that begins in the brain and accounts for more than half of all gliomas. Glioblastoma has an
overall five-year survival rate of 5%, meaning that only approximately 5 in 100 people survive GBM for five years and beyond. We
believe that STAR-001’s molecular features and distinct mechanism of action, preclinical anti-tumor activity and strong
correlation of activity with specific biomarkers have the potential to provide a unique approach aimed at addressing
high unmet needs in GBM and other aggressive CNS tumors.

Data
and observations supporting the development of STAR-001 for GBM and other brain cancers include the following:

●
We
have obtained favorable preclinical in vivo and in vitro data supporting the ability of STAR-001 to cross the blood brain barrier.

●
STAR-001
treatment induced tumor regression evidenced by greater than 106% tumor growth inhibition in two subcutaneous xenograft models of
GBM (U87 and M1123). STAR-001 also prolonged survival in mice bearing an intracranially implanted tumor model of GBM (U87), as compared
with those that did not receive any drug substance.

●
Intravenous
administration of STAR-001 over two cycles reduced subcutaneous xenograft tumor volume in mice by greater than 85% within the treatment
group.

●
In
an orthotopic GBM xenograft tumor model in mice, a single cycle of STAR-001 resulted in a statistically significant (p < 0.0001)
extension of median overall survival in the STAR-001-treated group (42 days) versus the control group (33 days).

●
Analyses
driven by RADR® have identified, in clinical databases, GBMs with elevated PTGR1 expression and harboring defects
in DNA damage repair components as a targeted subset of genetically defined patients who could potentially benefit from STAR-001-based
therapy.

●
Preclinical
data supports the observation that STAR-001 has potential to be an effective treatment in GBM regardless of MGMT (a DNA repair enzyme)
status of the cancer. This has significant potential to provide a much-needed alternative to the standard-of-care drug, temozolomide
(TMZ), especially in GBMs that over-express MGMT — which can be up to 50% of GBM cancers.

●
In
August 2021, the FDA granted STAR-001 Orphan Drug Designation for the treatment of GBM and other malignant gliomas.

28

The
standard treatment for glioblastoma includes radiation and chemotherapy with temozolomide. Based on an article in the journal Genes and
Diseases (Temozolomide resistance in glioblastoma multiforme, Genes Dis., 2016 May 11;3(3):198-210) and other publications, at
least fifty percent of temozolomide treated patients do not respond to this treatment, and others often form resistance to temozolomide
based regimens. We have obtained preclinical data supporting the observation that STAR-001 has potential to be an effective treatment
in GBM regardless of the MGMT (a DNA repair enzyme) status of the cancer. This has significant potential to provide a much-needed alternative
to the standard-of-care drug, temozolomide (TMZ), especially in GBMs that over-express MGMT — which can be up to 50% of GBM cancers.
Patients that have GBMs that over-express MGMT are generally unresponsive to TMZ and need new therapy options that can exploit other
molecular pathways and mechanisms.

We
believe STAR-001’s ability to cross the blood-brain barrier, together with its preclinical anti-tumor activity and sensitivity
correlations with relevant biomarkers, highlight STAR-001’s potential for use as both monotherapy as well as a synergistic agent
in combination with other drugs to address the unmet needs in GBM and other aggressive central nervous system tumors.

Potential
Future STAR-001 Clinical Studies

The
following is a summary of potential future clinical studies of STAR-001. The conduct of these studies will be subject to the evaluation
of the totality of the data from the LP-184 Phase 1a study and obtaining additional funding.

A
Phase 1b/2a Study to Evaluate the Safety, Pharmacokinetics, and Objective Response of STAR-001 (LP-184) in combination with Spironolactone
in Supratentorial Glioblastoma at First Progression

In
preclinical tumor models, co-treatment with Spironolactone (SP), a transcription-coupled nucleotide excision repair (TC-NER) inhibitor,
sensitized GBM cells and xenografts to STAR-001. SP is an FDA approved blood-brain barrier (BBB) permeable aldosterone antagonist that
inhibits TC-NER by inducing ubiquitin-mediated proteolytic degradation of ERCC3. SP and its active metabolites are specific pharmacologic
antagonists of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange
site in the distal convoluted renal tubule. SP acts both as a diuretic and as an antihypertensive drug by this mechanism. SP is commonly
used for the treatment of heart failure, hypertension, and complications of cirrhosis by antagonizing the mineralocorticoid receptor.

The
objective for the planned conduct of this study will be to evaluate the safety and tolerability of STAR-001 when administered with spironolactone
in subjects with recurrent glioblastoma. The trial will also evaluate the pharmacokinetics of STAR-001 with spironolactone in subjects
and the preliminary anti-tumor activity in combination with spironolactone. Additional measures of anti-cancer activity, including duration
of response (DOR), disease control rate (DCR), progression-free survival (PFS), and overall survival are also expected to be evaluated.

A Phase 1a Single Center Investigator-Initiated Study of STAR-001
(LP-184) Plus Spironolactone in Adult Patients with IDH wild type MGMT Unmethylated Newly Diagnosed Supratentorial Glioblastoma

We are also pursuing a Phase 1a single center
dose escalation investigator-initiated study of STAR-001 plus spironolactone in adult patients with IDH wild type MGMT unmethylated newly
diagnosed supratentorial glioblastoma. Subjects are planned to be treated following tumor resection with 6-weeks of involved-field radiotherapy
and concurrent STAR-001 plus spironolactone followed by 6 cycles of STAR-001 and spironolactone. The primary objective will be to determine
safety and tolerability and a dose for expansion. Further objectives will be to evaluate the pharmacokinetics (PK), pharmacodynamics (PD),
and progression free and overall survival of STAR-001 in newly diagnosed adult patients.

STAR-001
in ATRT and Pediatric Rare Disease Designation

ATRTs
(Atypical Teratoid Rhabdoid Tumors) are rare neurological tumors that primarily affect children under the
age of three. These clinically aggressive tumors are associated with a very poor prognosis, including a median survival of 6-12 months
and a 5 year survival rate of 30%. The National Cancer Institute (NCI) estimates that in the U.S. there are 600 living ATRT patients
with 60 new patients diagnosed annually. These tumors are typically pathogenetically driven by loss of function of the SMARCB1 or SMARCA4
genes. We believe that STAR-001’s molecular features and distinct mechanism of action, observed preclinical anti-tumor activity
and correlation with specific biomarkers have the potential to provide a unique and powerful approach aimed at addressing unmet needs
for this ultrarare pediatric cancer. We plan to pursue further preclinical studies of STAR-001 in this indication.

Data
and Observations supporting the development of STAR-001 for ATRT include the following:

●
We
have obtained favorable preclinical in vivo and in vitro data supporting the ability of STAR-001 to cross the blood brain barrier.

29

●
STAR-001
was observed to have a potent activity in ATRT cell lines CHLA-02, CHLA-05, and CHLA-06 with IC50s (nM) of 1776, 162, and 37.4, respectively.

●
In
ATRT xenograft tumor models in mice, i.v. injections of STAR-001 at either 2 mg/kg or 4 mg/kg had high in vivo activity. At both
concentrations xenografts showed complete tumor regression compared to the vehicle control group.

●
Preclinical
in vivo and in vitro data supports the in-silico observation that STAR-001 can be an effective treatment for ATRT. Currently, there
is no standard of care for treatment of children with ATRT.

●
STAR-001
has been granted Orphan Drug Designation and Rare Pediatric Disease Designation to treat ATRT.

The
FDA grants rare pediatric disease designation for serious and life-threatening diseases that primarily affect children ages 18 years
or younger and fewer than 200,000 people in the United States. The Rare Pediatric Disease Priority Review Voucher Program is intended
to address the challenges that drug companies face when developing treatments for these unique patient populations. Under this program,
companies are eligible to receive a priority review voucher following approval of a product with rare pediatric disease designation if
the marketing application submitted for the product satisfies certain conditions. If issued, a sponsor may redeem a priority review voucher for priority review of a subsequent marketing application
for a different product candidate, or the priority review voucher could be sold or transferred to another sponsor.

Potential
Future STAR-001 Pediatric Clinical Studies

The
following is a summary of potential future pediatric clinical studies of STAR-001. The conduct of these studies will be subject to the
evaluation of data from the LP-184 Phase 1a study and obtaining additional funding.

A
Phase 1, Multicenter, Open-Label, Dose Escalation Study of STAR-001 as a Single Agent and in Combination with Spironolactone in Pediatric
Patients with Relapsed or Refractory Central Nervous System Malignancies

Pediatric
central nervous system (CNS) tumors are the second most common cancer in childhood and the leading cause of childhood death from cancer.
Children and young adults with relapsed or refractory malignant CNS tumors have a dismal prognosis, and outcomes remain very poor. While
many children with CNS malignancies can be cured from multimodal treatment including surgery, radiation, and chemotherapy those with
relapsed or refractory disease post radiation typically do not have curative therapy. Additionally, those children who survive their
brain cancer diagnosis often have significant morbidity from their tumor, hydrocephalus, surgery, or treatment. Thus, novel treatments
are needed in this patient population to improve outcomes in survival and quality of life after treatment.

The
objective for Part 1 of the planned conduct of this study will be to evaluate the safety, tolerability, MTD and the RP2D of STAR-001
in pediatric patients with relapsed/refractory CNS malignancies who have failed standard therapy or for whom no standard therapy is available.
Part 2 of this planned study is expected to evaluate the safety and tolerability of STAR-001 in combination with spironolactone at the
MTD established in Part 1, in pediatric patients with relapsed/refractory CNS malignancies who have failed standard therapy or for whom
no standard therapy is available.

LP-184
in Triple Negative Breast Cancer:

Triple
negative breast cancers (TNBCs) represent approximately 24% of newly diagnosed breast cancers. The median overall survival (mOS) for
TNBC is: 11.6 months after the first line of treatment; 6.5 months after the second line of treatment; and 6.5 months after the third
line of treatment. The mOS for de novo metastatic TNBC is 8.3 months, while the mOS for those with a relapse within 18 months of primary
diagnosis is 10.0 months.

30

LP-184
in Pancreatic Cancer

Pancreatic
cancer is the 3rd leading cause of cancer death in the U.S. Despite rigorous highly cytotoxic therapies and a few approved targeted therapies,
the 5 year overall survival for advanced pancreatic cancer is approximately 3%, leaving a large number of patients with no additional
treatment options. LP-184 has demonstrated significant potency in multiple preclinical studies focused on pancreatic cancer, and we are
positioning LP-184 for areas of high unmet need in genetically targeted pancreatic cancers.

Data
and observations supporting the development of LP-184 for pancreatic cancer include the following:

●
We
believe LP-184 acts by selectively damaging DNA in tumors that express high levels of the enzyme PTGR1 – which occurs in several
solid tumors. Analysis with our data platform, RADR®, indicates that 35-40% of pancreatic tumors overexpress PTGR1.

●
Preclinical
studies have shown significant and targeted anti-tumor effects of LP-184, even in pancreatic cancers that are resistant to standard-of-care
drugs.

●
Pancreatic
tumors with DNA-damage repair deficiencies were significantly more sensitive (by two times) to LP-184 in preclinical studies. This
and other observations support LP-184’s potential as a synthetic lethal agent in many HRD (homologous recombination deficient)
and NERD (nucleotide excision repair deficient) cancers.

●
LP-184,
demonstrated significant and rapid pancreatic tumor shrinkage, by over 90%, in in-vivo mouse models in 8 weeks. In comparison,
the tumors in the untreated mice grew by over eleven-fold in volume during the same 8 week period.

●
Additional
positive preclinical data on the anti-cancer activity and potency of LP-184 was gathered from 6 pancreatic cancer cell lines, and
an additional 5 patient-derived xenograft (PDX) ex-vivo tumor models. Significant reduction of cancer cells and cancer cell
growth was observed across all pancreatic cancer cell lines and PDX models that were tested in the study with IC50 values in the
nanomolar range (45-270 nM).

●
Our
A.I. based identification of the key gene in the drug mechanism-of-action for LP-184 was validated by leveraging gene-editing (CRISPR)
technology to validate PTGR1 as a fundamental driver of tumor sensitivity and cancer cell death.

●
LP-184
treatment of 2 PDX models for HR deficient pancreatic cancer in preclinical studies resulted in 110-140% tumor growth inhibition.

●
In
August 2021, the FDA granted LP-184 Orphan Drug Designation for the treatment of pancreatic cancer.

Additional
LP-184 Background

We
have evaluated LP-184 in a number of solid tumors that overexpress certain biomarkers that have been identified as correlating with potential
response to LP-184. Our analysis indicates that LP-184 is expected to be a pro-drug activated by the enzyme Prostaglandin Reductase 1
(“PTGR1”). We believe LP-184’s mechanism of action is to alkylate DNA and protein macromolecules, form adducts, and
arrest cells in the S-phase of the cell cycle.

Using
our RADR® platform, we have derived a 10-gene signature composed of candidate biomarkers determining sensitivity to LP-184.
Genes from this signature, such as PTGR1, were found to be implicated in the potential induction of bioactivation of LP-184. We believe
LP-184 may be well positioned as a new drug candidate for individual patient genetic profiles identified as having DNA repair complex
deficiencies or other commonly prevalent gene signatures. LP-184 displayed less bone marrow toxicity in preclinical studies (dog and
mouse), had an improved pharmacokinetic profile (increased bioavailability as reflected by increased AUC), was stable in plasma, and
had an increased shelf life or stability in pharmaceutical grade material (sterile glass containers) for its class of compounds. LP-184
retained selective cytotoxicity towards solid tumor derived cell lines in vitro.

31

We
believe LP-184 is a non-hormone, next generation alkylating agent with nanomolar potency that preferentially damages DNA in cancer cells
that overexpress certain biomarkers indicated primarily in solid tumors such as those in prostate, pancreatic and ovarian cancers. LP-184
was initially developed using combinatorial chemistry approaches. Based on screening against conventional therapies both in vitro
and in vivo, LP-184 cytotoxicity appears to be mediated through the Transcription Coupled Nucleotide Excision Repair (TC-NER)
pathway, via alkylation of DNA leading to cell cycle arrest in S phase. Additional cytotoxic effects on tumors may include the generation
of reactive oxygen species, chemical modification of various intracellular proteins, and induction of the Mitogen Activated Protein Kinase
(“MAPK”) pathway followed by apoptosis. A proposed model for the mechanism of action of LP-184 is illustrated below.

Working
Model for LP-148 Mechanism of Action

Our
RADR® platform has identified multiple solid tumor cancer indications that highly express PTGR1, including prostate, ovarian,
kidney, liver, lung, pancreatic and thyroid cancers. Our RADR® platform has and will be employed to correlate results
from ongoing preclinical studies with gene expression data with the aim of determining the likely anticancer activity of LP-184 in these
cancer indications. With the assistance of insights from RADR®, we have also conducted studies in patient derived xenografts
(PDX) models to further elucidate precise targets and potential patient groups for future LP-184 clinical trials.

Use
of RADR® in LP-184 Development

Using
our RADR® platform,
we matched LP-184 drug response data in cell lines and in ex vivo PDX models with gene expression from matched RNA-seq experiments
in over 100 samples to build models that predict LP-184 response using a small number of gene expression values. (See Figure A below)
The machine learning model was able to accurately predict LP-184 response. (See Figure B below) The final model required only 10 genes
- as opposed to the entire transcriptome - to make predictions, with PTGR1 making a dominant contribution. This suggests PTGR1
is required for activity or has a strong effect to enhance drug sensitivity. (See Figure C below)

To
test this hypothesis, PTGR1 was knocked down with a CRISPR-interference construct that ablated PTGR1 expression, and consequently,
LP-184 sensitivity was lost. (See Figure C below) Because the LP-184 model can predict drug response with any RNA data, we surveyed public
RNA-seq data to support targeted cancer indications of interest for LP-184. (See Figure D below)

32

We
observed that Atypical Teratoid Rhabdoid Tumor (ATRT) was predicted to be highly responsive to LP-184, and the presence of its characteristic
SWI/SNF-complex mutations in SMARCB1 or SMARCA4 were associated with lower predicted IC50 values. (See Figure E below)
We performed mouse xenografts with an ATRT line and validated extreme responsivity to LP-184 that was previously predicted by RADR. This
demonstrates RADR’s ability to make valid drug response model predictions based on gene expression, which can be used to optimize
drug positioning, uncover drug mechanism-of-action, and discover relevant biomarkers.

Disease
Background for Pancreatic Cancer, Glioblastoma, Triple Negative Breast Cancer, Atypical Teratoid Rhabdoid Tumors (ATRT), and Prostate
Cancer

Initial
target patient populations for LP-184 include pancreatic cancer, glioblastoma, triple negative breast cancer, atypical teratoid rhabdoid
tumors (ATRT) and prostate cancer.

Pancreatic
Cancer

Pancreatic
cancer is the third leading cause of cancer deaths in the United States with a five-year survival rate of 12.8%. This means that only
approximately 13 in 100 people will have survived for five years and beyond. Pancreatic cancer has among the lowest 5-year survival rate
of any of the 22 common cancers. Global Cancer Statistics 2022 estimates that for pancreatic cancer there are approximately 510,566 new
cases of pancreatic cancer globally.

The
American Cancer Society’s estimates for pancreatic cancer in the United States for 2026 are:

●
About
67,530 people (35,190 men and 32,340 women) will be diagnosed with pancreatic cancer; and

●
About
52,740 people (27,230 men and 25,510 women) will die of pancreatic cancer.

Targeting
a specific subset of pancreatic cancer patients that are genetically defined has the potential to increase beneficial therapeutic options
for patients and may ultimately improve survival for those with this cancer.

Glioblastoma

Glioblastoma
is a fast-growing, aggressive type of CNS (Central Nervous System) tumor that forms on the supportive tissue of the brain. Glioblastoma
is the most common high grade glioma (HGG). The American Cancer Society estimates that approximately 24,740 malignant tumors of the brain
or spinal cord (13,830 in males and 10,910 in females) will occur in the U.S. in 2026. It also estimates that in 2026, approximately
18,350 deaths will occur from brain and other nervous system cancers. Approximately 250,000 new glioblastoma cases are estimated to occur
each year worldwide, with approximately 11,000 to 13,000 new glioblastoma cases estimated to occur each year in the U.S. Glioblastomas
usually affect adults. Treating glioblastoma is very difficult due to the brain-blood barrier and treatment often focuses primarily on
relieving symptoms.

Triple-Negative
Breast Cancer

Triple-negative
breast cancer (TNBC) accounts for about 15% of all breast cancers. TNBCs lack three hormone receptors that usually exist in healthy breast
cells: estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). As such, hormone therapy
and medicines that target HER2 protein receptors are not effective against this type of cancer. Triple negative breast cancer is also
more aggressive and has a higher grade than other breast cancers. TNBC is the subtype of breast cancer with the highest rates of recurrence
and mortality.

33

The
5-year survival rate for TNBC is set forth below, categorized by the stage of the cancer:

●
Local
or Stage 0–Stage 1: 91%

●
Regional
or Stage II–Stage III: 66%

●
Distant
or Stage IV: 12%

ATRT

Atypical
Teratoid Rhabdoid Tumors (ATRT) are rare, rapidly progressing, and malignant pediatric tumors of the central nervous system and are primarily
found in children under the age of three. The National Cancer Institute estimates there are 73 cases of ATRT diagnosed per year and 470
patients currently living with ATRTs, of which only 10% are in adults 20 years or older. Patients with ATRTs have a very poor prognosis
including a median survival of approximately 12 months and a 5 year overall survival of approximately 30%. ATRTs are difficult to treat
due to the very rapid onset of these tumors as well as a requirement for therapies that can penetrate the blood-brain barrier. The U.S.
is expected to capture the majority share of the ATRT market with ~65%.

Prostate
Cancer

Prostate
cancer is the most commonly diagnosed cancer in men in the US and the second leading cause of cancer-related death in men in the US.
The American Cancer Society’s estimates for prostate cancer in the United States for 2026 are:

●
Approximately
333,830 new cases of prostate cancer

●
Approximately
36,320 deaths from prostate cancer

Approximately
50% of patients who die from prostate cancer have metastases at diagnosis. The survival gains over the last decade have been modest with
acceleration in life-extending drug development occurring in the last three years. Hormonal therapy works to reduce testosterone levels
in the body to a level equal to that seen if physical castration were to occur. However, hormonal therapy can become refractory after
one to three years and tumor growth may resume. This is referred to as Castration-Resistant Prostate Cancer (“CRPC”). About
10 - 20 % of prostate cancer patients develop CRPC within five years. Typically, standard hormonal therapy involving Androgen Deprivation
Therapy (ADT) was prescribed in the past for all comer patients. Current prescribed regimens involve intensified therapy for most patients
(docetaxel for high volume disease, and Zytiga for low and high volume disease) whereas upcoming molecularly selected agents in addition
to hormonal therapy are used in an individualized approach to metastasis-directed or local therapy. Standard of care agents for prostate
cancer include without limitation (i) Androgen production suppressors, such as Leuprolide (Lupron, Eligard), Goserelin (Zoladex), Triptorelin
(Trelstar), Histrelin (Vantas), Abiraterone (Zytiga), (ii) Androgen signaling blockers, such as Flutamide (Eulexin), Bicalutamide (Casodex),
Nilutamide (Nilandron), and Enzalutamide (Xtandi), and (iii) chemotherapeutics such as docetaxel and cabazitaxel. In 2022 Pluvicto (active
ingredient lutetium Lu 177 vipivotide tetraxetan) was approved by FDA for the treatment of prostate-specific membrane antigen (PSMA)
positive mCRPC. In 2023, FDA approved Akeega (fixed dose combination of niraparib and abiraterone acetate) with prednisone, targeting
adult patients with deleterious or suspected deleterious BRCA-mutated castration-resistant prostate cancer (mCRPC). Drug classes of new
small molecules in development include PARP inhibitors, PI3K inhibitors and DNA Damage Repair (DDR) inhibitors. The PARP inhibitors olaparib
(Lynparza) and rucaparib (Rubraca) and the PD1 inhibitor pembrolizumab (Keytruda) have been approved by the FDA for a subset of the patient
population. The identification and characterization of new molecular targets, agents exploiting new or non-parallel mechanisms of action,
and the discovery of predictive biomarkers for mCRPC, are three of the major unmet needs in the prostate cancer space in the era of precision
medicine that we believe LP-184 may address.

34

Market
Opportunity for LP-184

We
are targeting a set of indications for LP-184 based on combining the factors of predicted response, unmet clinical need and market opportunity.
These include triple negative breast cancer, pancreatic cancer, glioblastoma, prostate cancer, and ATRTs. Below is an overview of relevant
patient numbers and estimated market sizes of some of the indications that we believe LP-184 may potentially address, if approved, based
upon published estimates by the Global Cancer Observatory and other published sources:

Triple
Negative Breast Cancer:

TNBCs
represent approximately 24% of newly diagnosed breast cancers. The median overall survival (mOS) for TNBC is: 11.6 months after the first
line of treatment; 6.5 months after the second line of treatment; and 6.5 months after the third line of treatment. The mOS for de novo
metastatic TNBC is 8.3 months, while the mOS for those with a relapse within 18 months of primary diagnosis is 10.0 months.

Pancreatic cancer

Global

(2022)

US

(2026)

Pancreatic cancer cases
510,566
67,530

Advanced pancreatic cancer cases (80% of all pancreatic cancer)
408,453
54,024

85% of advanced pancreatic cases are treated in 1st line setting
347,185
45,921

60% of advanced pancreatic cases treated in 1st line are treated in 2nd line
208,311
27,553

30% of advanced pancreatic cases treated 2nd line are treated in 3rd line
62,494
8,266

Potential patient percentage in initial targeted segment
12.2 %
12.2 %

Glioblastoma
Global
US

Total glioblastoma (GBM) estimated incidence
250,000
13,000

Number of newly diagnosed GBM patients treated (treatment rate 76.6%)
191,500
9,958

Number of newly diagnosed MGMT unmethylated GBM patients
126,390
6,572

Potential patient percentage in initial targeted segment
50.5 %
50.5 %

Recurrent patients treated in 1st line (69% newly diagnosed patients received 1L)
132,135
6,872

Recurrent patients progressing to 2L treatment (70.3% recurred patients receive 2L)
92,890
4,831

Prostate cancer

Global

(2022)

US

(2026)

Total prostate cancer estimated incidence (new cases)
1,466,680
333,830

CRPC incidence, ~20% of all prostate cancer
293,336
66,766

Metastatic CRPC incidence, ~80% of newly diagnosed CRPC
234,669
53,413

Potential patient percentage in initial targeted segment
16 %
16 %

35

Strategic
Academic Collaborations for LP-184

We
are or have been involved in the following academic collaborations for LP-184:

●
The
Research Institute of Fox Chase Cancer Center (“FCCC”). Our collaboration with FCCC has yielded results that strongly
link LP-184 anti-tumor activity to the expression of PTGR1. PTGR1 was identified by our RADR® analysis as the lead
gene candidate, the expression of which is essential to LP-184 mediated cytotoxicity. Using CRISPR engineered cells, we demonstrated
a total lack of activity in tumor cell lines where PTGR1 expression is artificially knocked out. These data continue to support our
RADR based predictions and the strategies of using LP-184 for tumor indications based upon PTGR1 expression. Our RADR analysis has
identified a multitude of tumors with a higher than required threshold of PTGR1 expression. We have further validated the activity
of LP-184 in a panel of pancreatic cancer cell lines. We have also conducted studies to evaluate the anti-tumor activity of LP-184
in pancreatic cancer PDX models and in xenografts. Additional wet lab studies have been conducted with the aim of further validating
RADR defined combinations with standard of care drugs in order to identify optimal synergistic drugs that could be eventually used
in potential treatments with LP-184.

●
Kennedy
Krieger Institute and the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center. We have collaborated with Kennedy Krieger
Institute and investigators at the Johns Hopkins School of Medicine. We sought this collaboration following multiple unique findings
regarding LP-184, including: the preclinical anti-tumor activity of LP-184 in glioblastoma (GBM); a positive result suggesting the
ability of LP-184 to penetrate the Blood Brain Barrier, in amounts similar to the GBM standard of care agent Temozolomide (TMZ);
and LP-184’s special ability to kill GBM cells irrespective of the methylation status of MGMT promoter. We believe there is
an urgent unmet need for an effective therapy to treat GBM with unmethylated MGMT. Both wet lab data and RADR® based
gene correlations highlighted sensitivity of tumor cells that carry unmethylated MGMT to LP-184. We have obtained additional data
in an expanded panel of GBM tumor cell lines, neurospheres obtained from patient biopsies and evaluation of LP-184 in GBM xenografts.
Results from this collaboration support the promise of LP-184 (STAR-001) for GBM.

●
Georgetown
University. In the first phase of our collaboration with Georgetown University, we confirmed the preclinical anti-tumor activity
of LP-184 in a panel of prostate cancer organoid models. In the second phase, we focused on wet lab validation of the leads generated
by our A.I. models of the gene dependency of most sensitive prostate cancers. This project aimed at providing experimental data to
support use of LP-184 in a personalized medicine approach to treating prostate cancer. Our gene correlation data has highlighted
the deficiency of several pathways that hypothetically would allow LP-184 to be synthetically lethal in tumors with such disruptions.
Our RADR analysis also indicates that as many as 20% of prostate cancers carry markers that will make these tumors highly sensitive
to LP1-84. In Phase 2 of our collaboration with Georgetown, we focused on the development of gene specific isogenic engineered prostate
cancer cell lines to dissect the pathways as well as extend the 2D and 3D prostate cancer studies to in vivo genomically defined
prostate cancer PDXs. In addition, we designed studies to test LP-184 in combination with several other drugs that are known to inhibit
pathways needed to repair damage to DNA caused by LP-184. The potential advantage of combining our DNA damaging agent along with
a DNA damage repair inhibitor is that it is expected to substantially extend the tumor specific anti-tumor activity of LP-184, including
prostate cancers that might otherwise not carry deficiencies in the DNA repair pathway.

●
The
Danish Cancer Society-Research Center. In January of 2022 we entered a research collaboration with the Danish Cancer Society
Research Center (DCRC). The collaboration focused on examining the most common solid tumors in order to determine the patient populations
most likely to benefit from our drug candidates LP-100 (irofulven) and LP-184. LP-100 and LP-184 have both been shown to have a synthetically
lethal impact in tumors that are lacking nucleotide excision repair (NER) capabilities. An additional aim of this collaboration was
to help develop improved diagnostic tools to detect NER deficient patient profiles more accurately. The collaboration included a
focus on the role of NER deficiency in breast, ovarian, prostate, lung, kidney, bladder, stomach, pancreatic, and esophageal cancers.
The data, genomic signatures, and biological models generated from the collaboration have added to the oncology focused RADR®
data points.

●
The
Greehey Children’s Cancer Research Institute (GCCRI) at the University of Texas Health Science Center-San Antonio. In February
2022, we announced a research collaboration with the Greehey Children’s Cancer Research Institute (GCCRI) at the University
of Texas Health Science Center-San Antonio. The GCCRI research collaboration focused on the effectiveness of LP-184 and LP-284 in
genomically-defined pediatric cancers, including several without any effective therapeutic approach. The collaboration leveraged
GCCRI’s pediatric tumor research models and knowledge base to advance LP-184 for the potential treatment of rare pediatric
cancers including rhabdomyosarcoma, Ewing sarcoma, MRT (malignant rhabdoid tumor), Wilms tumor, and ATRT (atypical teratoid rhabdoid
tumor). Dr. Peter Houghton Ph.D. led the collaboration for the GCCRI and is widely regarded as leading expert on pediatric cancer
research and in the development of novel approaches to treating childhood cancers. An integral component of Dr. Houghton’s
research success has been the development and use of Patient-Derived Xenografts (PDX), which are clinically relevant cancer models
that allow researchers to test novel therapeutics - such as LP-184 - in-vivo, and to directly study how tumors respond to treatment.

36

LP-284

LP-284
Chemical Structure

General
Overview

LP-284
is a novel small molecule and DNA damaging agent being developed by Lantern for the treatment of several non-Hodgkin’s lymphomas
(NHL) including mantle cell lymphoma (MCL)
and double hit lymphoma (DHL). LP-284 belongs to the new generation of acylfulvenes, a family of naturally derived anti-cancer
drug candidates and is the stereoisomer (enantiomer) of our drug candidate LP-184. In comparison to LP-184, LP-284 has distinct anti-tumor
activities in a variety of hematological cancers including lymphoma, multiple myeloma, and leukemia. LP-284 has the potential to be developed
as a monotherapy or combination therapy with other drugs to treat a broad array of hematological cancers. The FDA has granted LP-284
three Orphan Drug Designation for: the treatment of mantle cell lymphoma; the treatment of high-grade
B-cell lymphoma with MYC and BCL2 rearrangements (HGBL-MYC/BCL2), previously known as DHL; the treatment of soft tissue sarcoma.

In
preclinical studies, LP-284 has shown nanomolar potency in several hematological cell lines. Of the hematological cell lines tested,
LP-284 had the highest potency against all 6 of the mantle cell lymphoma cell lines tested and 4 DHL cell lines tested. LP-284 is also
being explored for use as a combination therapy with rituximab. In the DHL cell line OCI-LY1 derived xenograft model, LP-284 in combination
with rituximab inhibited tumor growth by 93%, comparing to 57% tumor growth inhibition by rituximab alone. In addition, the absence of
ataxia telangiectasia mutated (ATM) function in these lymphomas and the need for new agents in the setting of relapsed refractory mantle
cell lymphomas support the development of LP-284 in this indication.

37

Additional
data from in vitro and in vivo studies supports LP-284’s development for MCL, an aggressive
form of B-cell non-Hodgkin’s lymphoma (NHL) with immediate patient needs. LP-284 treatment was demonstrated to have significantly
greater tumor growth inhibition (TGI) in mice implanted with MCL cell derived xenograft (CDX) tumors, when compared to treatment with
the standard-of-care (SOC) agents Ibrutinib or Bortezomib. The figure below describes results from LP-284 in-vitro and in-vivo
preclinical studies for MCL and other B-cell Non-Hodgkin’s lymphomas.

Phase
1 Clinical Trial for LP-284

We
are advancing LP-284 in a Phase 1 clinical trial open to enrollment of patients with relapsed refractory lymphomas and solid tumors.
In addition to determination of the recommended dose(s) for future Phase 1b and Phase 2 studies, we will also evaluate clinical activity
correlations with genomic alterations in DNA damage repair pathway genes. We expect to enroll up to 30 patients in the dose escalation
portion of the LP-284 Phase 1 trial, with the involvement of multiple clinical trial sites. LP-284 is administered via intravenous infusion
(IV) of each 28-day cycle. A dose escalation Phase 1a study has commenced and follows a modified Fibonacci schedule until the maximum
tolerated dose (MTD) and/or recommended Phase 2 dose (RP2D) are determined.

As
of March 17, 2026, a total of 13 patients have been exposed to LP-284 across 5 dose levels, with safety data collected and available
for reporting. Overall, LP-284 has been well tolerated with primarily Grade 1 and Grade 2 adverse events (AEs). As of March 17, 2026,
no dose limiting toxicities (DLT) or suspected unexpected serious adverse reactions (SUSAR) have
been observed. The most common treatment-related adverse events were consistent with expected side effects of alkylating agents
and were generally clinically manageable and/or reversible. Notably, a complete metabolic response was confirmed in a dose level (DL)
5 diffuse large B-cell lymphoma (DLBCL) patient with rapid progression after three prior therapies, including Pola-R-CHP, CAR T-cell
therapy, and glofitamab (a bispecific antibody).

Upon
completion of enrollment in the Phase 1a and analysis of safety, PK, and clinical activity data, we, together with the clinical investigators
participating in the study, will review the totality of the study data to determine the recommended dose(s) to be used in further clinical
testing of LP-284, including in Phase 1b.

The
following is a summary of potential future clinical testing of LP-284 in Phase 1b. The conduct of these studies will be subject to the
evaluation of data from the LP-284 Phase 1a study and obtaining additional funding.

38

For
Phase 1b, we currently plan to enroll up to 40 additional patients with Relapsed or Refractory Diffuse Large B-cell Lymphoma (DLBCL)
and Mantle Cell Lymphoma (MCL) at the recommended dose(s) determined in Phase 1a, for further clinical evaluation, to characterize the
preliminary clinical activity, and tolerability of the treatment regimen before confirming the RP2D.

Alteration
in DDR represents a vulnerability in lymphoma. Molecular profiling of lymphoma samples has shown that DDR is dysregulated in approximately
18% of the samples, with mantle cell lymphoma (MCL, 47%), and diffuse large cell lymphoma (DLBCL, 21%). Lymphoma cells are also characterized
by genomic instability in the form of chromosome translocation and fusion genes, leading to deregulated gene expression and uncontrolled
cell growth. Genetic aberrations in MCL include disrupted DDR response through Ataxia-Telangiectasia Mutated (ATM) gene mutation (which
occurs in approximately 43.5% of the MCL patients at baseline and 57.6% at disease progression) and TP53 gene mutation/deletion (occurring
in approximately 26.8% of MCL patients), deregulated B cell receptor (BCR) signaling pathway, and MYC rearrangement. DLBCL is genetically
heterogeneous. Some common dysregulated oncogenic pathways include PI3K, BCR, NF kappa B, and the apoptotic BCL2 family.

LP-284
exerts antitumor activity by acting as an alkylating agent, covalently binding to DNA, RNA, and proteins, which leads to DNA damage,
impaired DNA/RNA synthesis, cell cycle arrests, and apoptosis. LP-284’s antitumor activities were evaluated in 15 lymphoma cell
lines across various subtypes including MCL, DLBCL, and Burkitt’s lymphoma. TP53 mutation, which is typically associated with worse
lymphoma prognosis, did not affect lymphoma cells’ sensitivity to LP-284 in these studies. LP-284 appears to be particularly lethal
in cells with deficient DDR, a targetable vulnerability in lymphoma. LP-284 displays a unique profile of preclinical antitumor activities
compared to the FDA-approved alkylating agents for hematologic malignancy treatment. When LP-284’s in vivo anti-tumor activity
in JeKo-1 derived MCL xenograft models were benchmarked with bortezomib and ibrutinib, the percentage of tumor growth inhibition (TGI)
in the LP-284 arms of the study outperformed the TGI observed with bortezomib and ibrutinib and significantly prolonged MCL xenograft
mouse survival by at least two-fold compared to control vehicles. JeKo-1 MCL xenograft tumors refractory to bortezomib and ibrutinib,
showed near complete tumor regression after one cycle of LP-284 treatment in preclinical xenograft studies. In addition, LP-284 resulted
in approximately two times longer survival than vehicle treatment in the bortezomib or ibrutinib pre-treated and refractory xenograft
mice. We believe LP-284 treatment may be a viable salvage treatment plan for patients who are refractory to current approved therapies.

Disease
Background for Mantle Cell Lymphoma and DHL

Mantle
Cell Lymphoma (MCL) is a rare, heterogenous and aggressive subtype of B-cell Non-Hodgkin’s Lymphoma (NHL). MCL is a blood cancer
of the lymph nodes and tumor cells originating from the “mantle zone” of the lymph node and is characterized by constitutively
dysregulated cyclin D1 (CCND1) expression. MCL is usually diagnosed at an advanced stage when it is largely considered
incurable.

Nearly
all MCL patients relapse from the current MCL standard-of-care agents and there is an urgent and unmet need for novel improved therapeutic
options for these patients. According to Leukemia and Lymphoma society about 4,200 new cases of
MCL are diagnosed in the United States annually, representing approximately 6% of all NHL patients.

In
the most recent WHO classification of hematolymphoid malignancies, the entity diffuse large B-cell
lymphoma/high-grade B-cell lymphoma with MYC and BCL2 rearrangements (DLBCL/HGBL-MYC/BCL2) was named due to its distinct pathogenetic
and genomic features. DLBCL/HGBL-MYC/BCL2 is characterized by rearrangements in MYC and
BCL2 genes, previously known as double-hit or triple-hit lymphoma. This disease entity carries features intermediate between the DLBCL
and Burkitt lymphoma.

The
prognosis of DLBCL/HGBL-MYC/BCL2 is poor with no standard treatment approach. Combination chemo-immunotherapies such as R-CHOP consisting
of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone is the most commonly used therapy, followed by the more intensive
regimen DA-R-EPOCH (dose-adjusted, rituximab, etoposide, prednisone, vincristine, cyclophosphamide,
and doxorubicin). About 20%-30% of patients are refractory to these frontline chemo-immunotherapies and the 2-year survival is
about 66%. The survival patients with relapsed/refractory (R/R) disease have even poorer prognoses with a reported median survival of
8.6 to 16 months. According to the Leukemia Foundation, HGBL-MYB/BCL2 represents approximately 5% of all DLBCL.

39

Market
Opportunity for LP-284

LP-284
presents a potential future market opportunity for relapsed or refractory non-Hodgkin’s lymphoma (NHL). Approximately 40,000 to
80,000 patients annually have relapsed or refractory NHL, and many of these patients have limited therapeutic options. Potential LP-284
development opportunities include aggressive NHL subtypes, like mantle cell lymphoma (MCL) and high-grade B-cell lymphomas (HGBL), where
relapse rates are high and current treatments often fail. LP-284’s potential is further underscored by the FDA’s Orphan Drug
Designations for HGBL and MCL, together with granted composition of matter patents relating to LP-284 in the U.S., EU, Japan, China,
India, Mexico, Australia, and South Korea.

Manufacturing
Overview

We
do not currently own or operate any manufacturing facilities or have any manufacturing employees. We currently rely, and expect to continue
to rely, on third party contract manufacturing organizations (“CMOs”) for the manufacturing of our drug candidates for preclinical
uses, clinical trials as well as for commercial manufacturing if our drug candidates receive marketing approval. We require that our
CMOs produce bulk drug substances and finished drug products in accordance with current Good Manufacturing Practices (“cGMPs”)
and all other applicable laws and regulations. We maintain agreements with our manufacturers that include confidentiality and intellectual
property provisions to protect our proprietary rights related to our drug candidates. We obtain our supplies from these CMOs on a project
by project basis and do not have long-term supply arrangements in place. We do not currently have arrangements in place for redundant
supply. For all of our drug candidates, we intend to identify and qualify additional manufacturers to provide the active pharmaceutical
ingredient and fill-and-finish services prior to seeking regulatory approval.

LP-184
and LP-284 Manufacturing

We
have contracted with Shilpa Medicare Limited and affiliates (“Shilpa”) for the cGMP synthesis of LP-184 API material as well
as for drug product development and cGMP drug product manufacturing of LP-184. In addition, we have contracted with Shilpa for the cGMP
synthesis of LP-284 API material as well as for drug product development and cGMP drug product manufacturing of LP-284.

LP-300
Manufacturing

We
have contracted with Curia Global, Inc. (“Curia”) for the manufacture and supply of LP-300 cGMP API material. In 2025, the Curia site where the LP-300 API is manufactured changed its name to Siegfried Acceleration Hub (‘Siegfried”),
reflecting the acquisition of the manufacturing site by the Siegfried Group. We have contracted
with Berkshire Sterile Manufacturing (“Berkshire”) and Piramal Pharma Solutions (“Piramal”) for the provision
of services relating to cGMP drug product manufacturing of LP-300. Berkshire is now referred to as Sharp Sterile, reflecting the acquisition of Berkshire by Sharp, a global leader in commercial pharmaceutical
packaging and clinical trial supply services.

Commercialization

We
retain worldwide commercialization rights for our product candidates LP-300, LP-184, LP-284, and LP-100. We plan to continue considering
out-license and collaboration opportunities in order to maximize returns and pursue successful development of our key candidates. We
currently have no sales, marketing or product distribution capabilities. However, once we have key candidates closer to FDA approval,
we may build our own specialty sales force, partner with a larger pharmaceutical organization, or out-license our drug candidates.

We
are continually evaluating out-license opportunities for our candidates at later stages of development in order to focus on identifying
and licensing additional drug candidates for novel indications and/or patient subpopulations with an oncology focus for expansion of
our pipeline.

Our
commercial plans and strategy for each particular program may change as our programs advance, the markets change, we receive more clinical
data, and depending on availability of capital.

Intellectual
Property

We
have an extensive multi-national portfolio of intellectual property rights directed to our drug candidates, and their targeted use and
development in specific patient populations and in specific therapeutic indications.

40

As
of March 1, 2026, we own or control rights in over 200 active patents and patent applications across over 20 patent families whose claims
are directed to our drug candidates and what we plan to do with our drug candidates. We have in-licensed or acquired patents and patent
applications from AF Chemicals, and BioNumerik directed to the compounds, LP-100, LP-184, LP-284 and LP-300, our RADR® platform,
and methods of using the compounds. Additionally, we have also filed patent applications to further enhance and extend the use of these
compounds. Our patents are directed to our drug candidates, their usage, manufacturing, and other matters. These matters are essential
to precision oncology and relate to: (a) data-driven, biologically relevant biomarker signatures, (b) patient selection and stratification
approaches that rely on prediction of response deriving from these signatures and, (c) the ability to develop novel, combination therapy
approaches with existing approved therapeutics.

We
rely on a combination of patents, trade secrets, copyrights, trademarks, license agreements, nondisclosure and other contractual provisions
and technical measures to protect our intellectual property rights. Additionally, we also rely on the patent applications, trade secrets,
and other contractual provisions and technical measures to protect the development of our genomic and biomarker signatures that help
us in making predictions about the sensitivity to our drug candidates, our patient stratification approaches, and the development of
potential combination therapies with our drug candidates.

Intellectual
Property Portfolio by the Numbers

As
of March 1, 2026, our intellectual property portfolio consisted of over 20 patent families covered by:

●
Over
44 issued patents across our portfolio of compounds in key, commercially important geographies;

●
Over
170 pending patent applications, including eight pending Patent Cooperation Treaty (PCT) applications;

●
as
well as trademark registrations, and trademark applications in the U.S., Japan, Europe, Canada and Australia.

Our
policy is to protect the proprietary technologies, inventions, and improvements that are commercially important to our business in the
United States, Europe, Japan, Australia and other key jurisdictions important to our business. We fully expect that additional advances
will come out of our ongoing work in developing biomarker signatures and patient stratification approaches and that these advances will
form the basis of additional intellectual property protection through new patent filings, trademarks, trade secrets, and copyrights.
We will continue to file patent applications and use trade secret laws to protect the uses of our genomic and biomarker signatures, response
prediction and patient stratification discoveries. We plan to rely on these intellectual property advances to develop, strengthen, and
maintain our proprietary position for novel therapeutics and novel formulations and uses of existing and new compounds across multiple
therapeutic areas. We also plan to rely on data exclusivity, market exclusivity and patent term extensions when available.

Patent
Portfolio

We
have an extensive multi-national portfolio of intellectual property rights directed to our drug candidates, and their targeted use and
development in specific patient populations and in specific therapeutic indications. Our portfolio consists of over 20 patent families
across issued patents and pending patent applications. We have also filed over 50 patent applications directed to our proprietary drug
programs together with biomarkers and sensitivity parameters, and over 12 additional patent applications directed to our RADR®
platform. These filings include patent applications directed to LP-300 and additional patent applications directed to new manufacturing
methods for novel, synthetic illudins, and gene signatures and biomarker profiles indicating sensitivity to LP-100, LP-184, LP-284 and
synthetic illudins.

●
Our
patent family directed to LP-100 has patents that expire as early as August 2026, and patent applications, if granted, that would
expire as late as May 2040.

41

●
Our
patent family directed to LP-184 has patents that expire as early as August 2026, and patent applications, if granted, that would
expire as late as May 2044.

●
Our
patent family directed to LP-300 has patents that expire as early as March 2028, and patent applications, if granted, that would
expire as late as February 2047.

Our
patent family directed to LP-284 has patents that expire as early as August 2038, and patent applications, if granted, that would
expire as late as May 2042.

We
typically file a non-provisional patent application or a PCT within 12 months of filing the corresponding provisional patent application.
While we intend to timely file non-provisional patent applications relating to our provisional patent applications, we cannot predict
whether any of our existing or future patent applications for our existing or future drug candidates will result in the issuance of patents
that effectively protect these candidates, or if any of our issued patents or if any of our licensor’s issued patents will effectively
prevent others from commercializing competitive products. Patent protection for the composition of matter of the LP-300 compound itself
is unavailable because the compound was first identified many years ago. For more information regarding the risks related to our intellectual
property, see “Risk Factors – Risks Related to Our Intellectual Property.”

RADR®
Platform

We
do not own or in-license any patents on our RADR® platform, but we have filed at least four patent applications directed
to our RADR® platform and rely on trade secrets and confidential procedures directed to protecting:

●
our
A.I. and machine learning and training methodologies for our specific purposes in oncology drug development and drug rescue,

●
our
curation and normalization of select data from both public and proprietary data sources, and

●
our
developing insights that can be modeled to cover biological processes as algorithms inside our RADR® platform.

LP-100

Our
portfolio directed to LP-100 consists of at least two families of in-licensed patents that were filed in 2006. The patents include European,
Japanese and US patents. US Patent No. 7655695 relates to acylfulvene analogs that are directed to tumor solid tumor growth inhibition.
The nominal expiration for our patents directed to LP-100 is August 2026 and does not account for any applicable patent term adjustments
or extensions. We have also filed multiple patent applications directed to LP-100 that, if granted, would expire as late as May 2040.

LP-184
& other Novel, Synthetic Illudin Derivatives

Our
portfolio directed to LP-184 consists of over 15 families of patents and patent applications, including PCT applications. US Patent No.
7655695 relates to acylfulvene analogs that are directed to solid tumor growth inhibition. The patent applications include claims directed
to use of LP-184, synthetic illudin analogs or derivatives to treat glioblastoma or other CNS cancers as either a mono or combination
therapy, to treat rhabdoid tumors, brain cancer, brain metastases, and pancreatic cancer also as either a mono or combination therapy.
Our portfolio also includes patent applications directed to our proprietary drug programs together with biomarkers and sensitivity parameters.
The nominal expiration for patents and patent applications directed to LP-184 ranges from 2026 to as late as 2044 and does not account
for any applicable patent term adjustments or extensions. We intend to nationalize our patent applications in the US, Australia, Canada,
EU, China, and Japan.

We
have in-licensed patents from AF Chemicals related to the composition of matter of LP-184. We have also developed additional intellectual
property for this class of compounds related to the development of novel synthetic routes and the preparation of certain illudin derivatives
having therapeutic value. Additionally, we have filed patent applications on the use of LP-184 and these novel synthetic illudin derivatives
in the treatment of glioblastoma and other CNS cancers.

42

LP-284
& other Novel, Synthetic Illudin Derivatives

Our
portfolio directed to LP-284 consists of at least four patent and patent application families. US Patent No. 7655695 relates to acylfulvene
analogs that are directed to solid tumor growth inhibition and US Patent No. 11739043 covers the compound itself. Other patent applications
are directed to using LP-284 to treat leukemia and blood cancers and other cancers (as either a mono or combination therapy). The nominal
expiration for patents and patent applications directed to LP-284 ranges from 2026 to as late as 2042 and does not account for any applicable
patent term adjustments or extensions. We intend file or nationalize our patent applications in the US, Australia, Canada, EU, China,
and Japan.

LP-300

Our
portfolio directed to LP-300 consists of at least four families of owned patents. A more recent PCT patent application filed in 2020
is directed to treatment of non-small cell lung cancer (NSCLC) in nonsmokers and never smoking patients using disodium 2,2’-dithio-bis-ethane
sulfonate (dimensa) and has been nationalized in the US, Canada, Brazil, Mexico, EU, China, Japan and Australia. The nominal expiration
for NSCLC related patents and patent applications directed to LP-300 ranges from 2028 to as late as 2047 and does not account for any
applicable patent term adjustments or extensions.

We
filed an additional PCT application directed to LP-300 and its application to NSCLC, as well as biomarkers that correlate to heightened
response or sensitivity to LP-300.

Confidentiality
& Trade Secrecy

We
enter into non-disclosure and confidentiality agreements with parties who have access to confidential or patentable aspects of our research
and development output, such as our employees, collaborators, contract research organizations, contract manufacturers, consultants, advisors
and other third parties. It is possible, however, that any of these parties may breach the agreements and disclose such output before
a patent application is filed, thereby jeopardizing our ability to seek patent protection. These agreements in general provide that all
confidential information developed or made known during the course of an individual or entities’ relationship with us must be kept
confidential during and after the relationship. These agreements also generally provide that all inventions resulting from work performed
for us or relating to our business and conceived or completed during the period of employment or assignment, as applicable, shall be
our exclusive property. It is also possible that third parties may develop substantially equivalent proprietary information, platforms
or compounds, or otherwise gain access to our trade secrets.

Trademarks

We
own various trademarks, applications and unregistered trademarks in the United States and other commercially important markets, including
our company name, our A.I. platforms (e.g. our RADR platform and our withZeta platform), and certain compounds in development. Our trademark
portfolio is designed to protect the brands for our Company, our A.I. platform and our portfolio of compounds.

Other
Intellectual Property

We
believe that our intellectual property rights on the RADR® platform are valuable and important to our business. Our patent
position relating to the RADR platform is generally uncertain and involves complex legal and factual questions, which is consistent with
patent claims regarding intellectual property of this nature. We rely on a combination of trademarks, copyrights, trade secrets, license
agreements, confidentiality procedures, non-disclosure agreements, employee disclosure, and invention assignment agreements, and other
legal and contractual rights to establish and protect our proprietary rights.

43

Competition

We
exist at the intersection of rapidly moving, global industries, namely, the biotechnology industry and the A.I. drug development industry.
This is a unique and rapidly moving category with a variety of business models being developed globally. The pharmaceutical and biotechnology
industries are characterized by rapidly advancing technologies, intense competition and a strong emphasis on intellectual property. A.I.
is disrupting and changing all industries, including the biotechnology industry. Although these are competitive industries, we believe
we are uniquely positioned due to our focus on oncology drug development, prediction of patient response, use of computational biology,
and the ability to both rescue and develop compounds.

We
face potential competition from many different sources, including major pharmaceutical and biotechnology companies, academic institutions
and governmental agencies, and public and private research institutions.

Many
of the companies against which we may compete have significantly greater financial resources and expertise in research and development,
manufacturing, preclinical studies, conducting clinical trials, obtaining regulatory approvals and marketing approved products than we
do. Smaller or early-stage companies may also prove to be significant competitors, particularly through collaborative arrangements with
large and established companies. Mergers and acquisitions in the pharmaceutical, biotechnology and diagnostic industries may result in
even more resources being concentrated among a smaller number of our competitors. These competitors also compete with us in recruiting
and retaining qualified scientific and management personnel and establishing clinical trial sites and patient registration for clinical
trials, as well as in acquiring technologies complementary to, or necessary for, our programs.

Our
commercial opportunity could be reduced or eliminated if our competitors develop and commercialize medicines that are safer, more effective,
have fewer or less severe side effects, and are more convenient or less expensive than any medicines we may develop. Our competitors
also may obtain FDA or other regulatory approval for their medicines more rapidly than we may obtain approval for ours, which could result
in our competitors establishing a strong market position before we are able to enter the market. In addition, our ability to compete
may be affected in many cases by insurers or other third-party payors seeking to encourage the use of generic medicines.

Any
drug candidates we successfully develop will compete with current and new therapies that may become available in the future. The key
competitive factors affecting the success of all of our drug candidates, if approved, are likely to be their efficacy, combinability,
safety profile, convenience, cost, the effectiveness of companion diagnostics in guiding the use of related therapeutics, if any, the
level of generic competition, level of promotional activity, intellectual property protection, and the availability of reimbursement
from government and other third-party payors. If any drug candidates under development are approved for the indications in which we are
currently planning clinical trials, they will compete with the drugs discussed below and will likely compete with other drugs in development.

Artificial
Intelligence and Drug Development

We
believe our proprietary RADR® platform gives us a significant competitive advantage for using AI to both: 1) select, model
and license drugs with a well-tolerated safety profile, and 2) quickly and cost-effectively advance drugs towards market by selecting
biologically relevant mechanisms of action and their associated biomarkers of activity. In January 2026, we introduced withZeta.AI,
our novel generative AI platform built to empower researchers and clinicians to dramatically improve the quality and reduce the time
of rare cancer research. Recently, there has been an increase in the use of AI for drug development, and for improved biomarker signature
creation correlated to drug response. Due to this recent increase, we face increasing competition in both: 1) developing new drugs, and
2) biomarker signature development. This includes competition with respect to the pool of already existing drug candidates that may be
amenable for patient stratification. Our competition in AI-driven drug development for oncology includes, but is not limited to, the
following:

-
Oncology-focused clinical stage companies: Candel Therapeutics, Pyxis Oncology, Foghorn Therapeutics, Prelude Therapeutics,
Warewolf Therapeutics, Xilio Therapeutics, Ikena Oncology, Atossa Therapeutics, Elevation Oncology, Bolt Biotherapeutics.

-
AI-focused drug developers with proprietary pipelines: AbCellera, Atomwise, InSilico Medicine, Iktos, Verge Genomics,
Recursion Pharmaceuticals, Schrodinger, and Roivant Sciences.

44

Pancreatic
Cancer

There
are approved standards of care agents for treating pancreatic cancer that are dominated by FOLFIRINOX (consisting of leucovorin calcium
(folinic acid), fluorouracil, irinotecan, and oxaliplatin) and gemcitabine-based cytotoxic chemotherapeutic regimens. In February 2024
the FDA approved irinotecan liposome (Onivyde, Ipsen Biopharmaceuticals, Inc.) with oxaliplatin, fluorouracil, and leucovorin, for the
first-line treatment of metastatic pancreatic adenocarcinoma. However, these regimens cause dose limiting toxicities. Liposomal irinotecan
(Onivyde®) in combination with 5-FU and LV is recommended in patients that progressed on gemcitabine therapy. In a small subset of
patients exhibiting genetic mutations such as those with neurotrophic receptor tyrosine kinase (NTRK) gene fusions, breast cancer gene
(BRCA) 1/2 mutations, or patients with elevated microsatellite instability (MSI)-DNA mismatch repair (MMR) status, recently approved
targeted therapies such as Vitrakvi and Rozlytrek (approximately 1% of pancreatic cancer patients), poly ADP-ribose polymerase (PARP)
inhibitor Lynparza (approximately 5-8% of pancreatic cancer patients) and Keytruda (approximately 1-2% of pancreatic cancer patients)
are currently included in treatment guidelines. On December 4, 2024, the FDA granted accelerated approval to zenocutuzumab-zbco (Bizengri,
Merus N.V.) for adults with advanced, unresectable, or metastatic non-small cell lung cancer (NSCLC) or pancreatic adenocarcinoma, both
harboring a neuregulin 1 (NRG1) gene fusion. For eligible patients, paclitaxel (Abraxane®) or docetaxel has been used in the third-line
setting in combination with gemcitabine. We believe that currently, no adequate treatment options are available for as much as 80% of
advanced stage pancreatic cancer patients.

New
agents are also being actively developed for the potential treatment of pancreatic cancer. The competition we may face regarding LP-184
for the potential treatment of pancreatic cancer includes without limitation the following agents that have not yet received marketing
approval for the treatment of pancreatic cancer: the chemotherapeutic agent-glufosfamide; the tyrosine kinase inhibitor-Masiviera (masitinib);
RAS inhibitors MRTX1133 and RMC-6236; the PARP inhibitor fluzoparib; Interleukin 1 receptor antibody nadunolimab; 5’ Nucleotidase
Inhibitor quemliclustat; transforming growth factor beta-2 inhibitor trabedersen; and anti PDL-1 antibody spartalizumab.

Glioblastoma

The
standard treatment for glioblastoma includes radiation and chemotherapy with temozolomide. Based on an article in the journal Genes and
Diseases (Temozolomide resistance in glioblastoma multiforme, Genes Dis., 2016 May 11;3(3):198-210) and other publications, at
least fifty percent of temozolomide treated patients do not respond to this treatment, and others often form resistance to temozolomide
based regimens. Bevacizumab is frequently used for recurrent glioblastoma.

New
agents are also being actively developed for the potential treatment of glioblastoma. The competition we may face regarding LP-184 for
the potential treatment of glioblastoma includes without limitation the following: the chemotherapeutic agents Berubicin, and the protein
kinase inhibitors Stivarga (Regorafenib), DB102 (Enzastaurin hydrochloride) and BDTX-1535 and DNA Damage Repair pathway inhibitors such
as PARP inhibitors. There are also several immunotherapies in late-stage development for glioblastoma, including oncolytic viruses and
tumor cell vaccines.

Triple
Negative Breast Cancer

The
absence of ER, PR, HER2 markers predisposes TNBC to rapid metastasis, treatment resistance, and a high recurrence rate. In addition,
the absence of these receptors limits treatment options for TNBC patients. While TNBC can resist hormone therapy, and immunotherapy in
many instances, TNBC is often sensitive to chemotherapeutic agents and radiotherapy.

Standard
treatment options for TNBC include:

●
Chemotherapy:
Chemotherapy is often the primary systemic treatment for TNBC. Anthracycline-based regimens (such as doxorubicin and epirubicin)
and taxane-based regimens (such as paclitaxel and docetaxel) are commonly used. Platinum-based drugs like cisplatin or carboplatin
may also be included in the treatment regimen for some patients.

45

●
Surgery:
Surgery is usually recommended to remove the tumor, and may involve a lumpectomy or a mastectomy. In some cases, lymph node dissection
may also be performed to check for the spread of cancer to nearby lymph nodes.

●
Radiation
Therapy: Radiation therapy is often given after surgery to reduce the risk of cancer recurrence. It may also be used as part of the
primary treatment for patients who opt for breast-conserving surgery (lumpectomy) instead of mastectomy.

●
Immunotherapy:
In recent years, immunotherapy has shown promising results in the treatment of TNBC, particularly in patients whose tumors express
programmed death-ligand 1 (PD-L1). Pembrolizumab, a PD-1 inhibitor, has been approved for use in combination with chemotherapy as
first-line treatment for metastatic TNBC with PD-L1 expression.

●
PARP
Inhibitors: Poly (ADP-ribose) polymerase (PARP) inhibitors, such as olaparib and talazoparib, have been approved for the treatment
of advanced TNBC with germline BRCA mutations.

If
an early-stage TNBC is small enough to be removed by surgery, then breast-conserving surgery or a mastectomy with a check of the lymph
nodes may be done. In certain cases, such as with a large tumor or if the lymph nodes are found to have cancer, radiation may follow
surgery. Chemotherapy after surgery (adjuvant chemotherapy) can reduce the chances of the cancer coming back. For women who have a BRCA
mutation and at surgery are found to have a tumor larger than 2cm but no bigger than 5cm OR 1 to 3 axillary lymph nodes with cancer,
the targeted PARP inhibitor olaparib might be given for a year after adjuvant chemo. When given this way, it can help some women live
longer. Chemotherapy is often given before surgery (neoadjuvant chemotherapy) by itself or with pembrolizumab (Keytruda) to shrink a
large tumor and/or lymph nodes with cancer. If cancer is still found in the tissue removed by surgery after neoadjuvant chemotherapy
has been given, a few options exist: (i) An oral chemotherapy drug called capecitabine may be prescribed for 18 to 24 weeks. (ii) Additional
pembrolizumab after surgery (adjuvant treatment) can reduce the chances of the cancer coming back. (iii) Olaparib may be given for one
year to women who have a BRCA mutation to help lower the chance of the cancer recurring.

If
TNBC recurs locally, cannot be removed with surgery, and makes the PD-L1 protein, immunotherapy with the drug pembrolizumab along with
chemotherapy is an option. Similarly, for advanced TNBC in which the cancer cells show high levels of gene changes called microsatellite
instability (MSI) or changes in any of the mismatch repair (MMR) genes (MLH1, MSH2, MSH6, and PMS2), immunotherapy with the drug pembrolizumab
might be used. Pembrolizumab might also be an option for TNBC that has a high tumor mutational burden (TMB-H) which is a measure of the
number of gene mutations (changes) inside the cancer cells. Cells that have many gene mutations (a high TMB) might be more likely to
be recognized as abnormal and attacked by the body’s immune system. For advanced or recurrent TNBC that has failed at least 2 other
treatment regimens, the antibody-drug conjugate sacituzumab govitecan (Trodelvy) might be an option. Regardless of the stage of TNBC,
participation in a clinical trial of new or investigational treatments for TNBC is also a frequent option since TNBC tends to have a
poor prognosis compared to other types of breast cancer.

Prostate
Cancer

New
agents are being actively developed to treat specific subtypes of prostate cancer. Our approach is to leverage A.I. and biomarker data
to discover subtypes of prostate cancer and treatments for those subtypes of cancer. We believe our approach and our compounds take advantage
of this improved characterization of prostate cancer.

There
are approved standard of care agents for treating solid tumor prostate cancer, but there are a lack of approved therapeutic options for
non-metastatic castration-resistant prostate cancer (“nmCRPC”) patients and castration-resistant disease in metastatic hormone-naïve
prostate cancer (“mHNPC”). The competition we may face in regards to LP-100 and one of the indications of LP-184, specifically
mCRPC, includes without limitation the following drugs:

●
Astellas/Pfizer’s
Xtandi (enzalutamide), Johnson & Johnson’s Zytiga (abiraterone acetate), Clovis Oncology’s Rubraca (rucaparib), GSK’s
Zejula (niraparib), AstraZeneca’s Lynparza (olaparib), and Novartis’ Pluvicto (Lu-PSMA-617) are approved for treatment
of metastatic castration-resistant prostate cancer (mCRPC).

●
Xtandi
Zytiga and Androgen Deprivation Therapy (“ADT”) to treat mHNPC and nmCRPC, respectively.

●
Pfizer
has tested Talazoparib and Enzalutamide to treat mCRPC

We
believe LP-184 is unique and has promise for potential use in multiple proposed biomarker profile targeted indications where there are
unmet treatment needs.

46

Non
Small Cell Lung Cancer (NSCLC)

We
believe LP-300 may have an advantage to approved drugs on the market by serving as a well-tolerated agent in combination with
multiple existing standards of care drugs for portions of the NSCLC patient population. Beyond traditional chemotherapies
(carboplatin/ pemetrexed and/or cisplatin/paclitaxel), NSCLC treatments with potential use for the never smoker patient population
include targeted small molecules and biologics, which include, without limitation, the approved EGFR inhibitors erlotinib,
gefitinib, afatinib, and osimertinib and monoclonal antibody amivantamab-vmjw; the approved ALK inhibitors brigatinib, ceritinib,
crizotinib, alectinib, and ensartinib; the approved MET inhibitor tepotinib; the approved RET inhibitors pralsetinib and
selpercatinib; and the approved immune checkpoint inhibitors pembrolizumab, atezolizumab, and ramucirumab. Many of these agents are
used in specific NSCLC subtypes either as single agents or in various combinations. Patients with NSCLC due to driver mutations
receive treatment with tyrosine kinase inhibitors (TKI’s). Most patients treated with TKI’s will
eventually develop resistance to treatment, therefore requiring additional therapeutic options. H002, a fourth generation EGFR
inhibitor entering phase 1/ 2 trials may have potential for treatment of NSCLC subtypes with various EGFR activating mutations that
are common among never smokers and that also underlie resistance to other therapies.

Government
Regulation

Government
authorities in the United States at the federal, state and local level and in other countries regulate, among other things, the research,
development, testing, manufacture, quality control, approval, labeling, packaging, storage, record-keeping, promotion, advertising, distribution,
post-approval monitoring and reporting, marketing and export and import of drug and biological products. Generally, before a new drug
can be marketed, considerable data demonstrating its quality, safety and efficacy must be obtained, organized into a format specific
for each regulatory authority, submitted for review and approved by the regulatory authority.

U.S.
Drug Development

In
the United States, the FDA regulates drugs under the Food, Drug, and Cosmetic Act (“FDCA”). Drugs also are subject to other
federal, state and local statutes and regulations. The process of obtaining regulatory approvals and the subsequent compliance with appropriate
federal, state, local and foreign statutes and regulations requires the expenditure of substantial time and financial resources. Failure
to comply with the applicable U.S. requirements at any time during the product development process, approval process or post-market may
subject an applicant to administrative or judicial sanctions. These sanctions could include, among other actions, the FDA’s refusal
to approve pending applications, withdrawal of an approval, a clinical hold, untitled or warning letters, product recalls or market withdrawals,
product seizures, total or partial suspension of production or distribution, injunctions, fines, refusals of government contracts, restitution,
disgorgement and civil or criminal penalties. Any agency or judicial enforcement action could have a material adverse effect on us.

Our
drug candidates are considered small molecule drugs and must be approved by the FDA through the NDA process before they may be legally
marketed in the United States. The process generally involves the following:

●
completion
of extensive preclinical studies in accordance with applicable regulations;

●
submission
to the FDA of an IND, which must become effective before human clinical trials may begin;

●
approval
by an independent institutional review board (“IRB”), or ethics committee at each clinical trial site before each trial
may be initiated;

●
performance
of adequate and well-controlled human clinical trials in accordance with applicable IND regulations, good clinical practice (“GCP”),
requirements and other clinical trial-related regulations to establish substantial evidence of the safety and efficacy of the investigational
product for each proposed indication;

47

●
submission
to the FDA of an NDA;

●
a
determination by the FDA within 60 days of its receipt of an NDA to accept the filing for review;

●
satisfactory
completion of a FDA pre-approval inspection of the manufacturing facility or facilities where the drug will be produced to assess
compliance with cGMP, requirements to assure that the facilities, methods and controls are adequate to preserve the drug or biologic’s
identity, strength, quality and purity;

●
potential
FDA audit of the preclinical study and/or clinical trial sites that generated the data in support of the NDA filing;

●
FDA
review and approval of the NDA, including consideration of the views of any FDA advisory committee, prior to any commercial marketing
or sale of the drug in the United States; and

●
compliance
with any post-approval requirements, including the potential requirement to implement a Risk Evaluation and Mitigation Strategy (“REMS”),
and the potential requirement to conduct post-approval studies.

The
data required to support an NDA are generated in two distinct developmental stages: preclinical studies and clinical trials. The preclinical
and clinical testing and approval process requires substantial time, effort and financial resources, and we cannot be certain that any
approvals for any future drug candidates will be granted on a timely basis, or at all.

Preclinical
Studies and IND

Preclinical
studies generally involve laboratory evaluations of drug chemistry, formulation and stability, as well as studies to evaluate toxicity
in animals, which support subsequent clinical testing. The sponsor must submit the results of the preclinical studies, together with
manufacturing information, analytical data, any available clinical data or literature and a proposed clinical protocol, to the FDA as
part of the IND. An IND is a request for authorization from the FDA to administer an investigational product to humans, and must become
effective before human clinical trials may begin.

Preclinical
studies include laboratory evaluation of product chemistry and formulation, as well as in vitro and animal studies to assess the
potential for adverse events and in some cases to establish a rationale for therapeutic use. The conduct of preclinical studies is subject
to federal regulations and requirements, including GLP regulations for safety/toxicology studies. An IND sponsor must submit the results
of the preclinical tests, together with manufacturing information, analytical data, any available clinical data or literature and plans
for clinical studies, among other things, to the FDA as part of an IND. Some long-term preclinical testing, such as animal tests of reproductive
adverse events and carcinogenicity, may continue after the IND is submitted. An IND automatically becomes effective 30 days after receipt
by the FDA, unless before that time the FDA raises concerns or questions related to one or more proposed clinical trials and places the
trial on clinical hold. In such a case, the IND sponsor and the FDA must resolve any outstanding concerns before the clinical trial can
begin. As a result, submission of an IND may not result in the FDA allowing clinical trials to commence.

Clinical
Trials

The
clinical stage of development involves the administration of the investigational product to healthy volunteers or patients under the
supervision of qualified investigators, generally physicians not employed by or under the trial sponsor’s control, in accordance
with GCP requirements, which include the requirement that all research subjects provide their informed consent for their participation
in any clinical trial. Clinical trials are conducted under protocols detailing, among other things, the objectives of the clinical trial,
dosing procedures, subject selection and exclusion criteria and the parameters to be used to monitor subject safety and assess efficacy.
Each protocol, and any subsequent amendments to the protocol, must be submitted to the FDA as part of the IND. Furthermore, each clinical
trial must be reviewed and approved by an IRB for each institution at which the clinical trial will be conducted to ensure that the risks
to individuals participating in the clinical trials are minimized and are reasonable in relation to anticipated benefits. The IRB also
approves the informed consent form that must be provided to each clinical trial subject or his or her legal representative, and must
monitor the clinical trial until completed. There also are requirements governing the reporting of ongoing clinical trials and completed
clinical trial results to public registries.

48

A
sponsor who wishes to conduct a clinical trial outside of the United States may, but need not, obtain FDA authorization to conduct the
clinical trial under an IND. If a foreign clinical trial is not conducted under an IND, the sponsor may submit data from the clinical
trial to the FDA in support of an NDA. The FDA will accept a well-designed and well-conducted foreign clinical trial not conducted under
an IND if the trial was conducted in accordance with GCP requirements and the FDA is able to validate the data through an onsite inspection,
if deemed necessary, and the practice of medicine in the foreign country is consistent with the United States.

Clinical
trials in the United States generally are conducted in three sequential phases, known as Phase 1, Phase 2 and Phase 3, and may overlap.

●
Phase
1 clinical trials generally involve a small number of healthy volunteers or disease-affected patients who are initially exposed to
a single dose and then multiple doses of the drug candidate. The primary purpose of these clinical trials is to assess the metabolism,
pharmacologic action, tolerability and safety of the drug.

●
Phase
2 clinical trials involve studies in disease-affected patients to determine the dose and dosing schedule required to produce the
desired benefits. At the same time, safety and further pharmacokinetic and pharmacodynamic information is collected, possible
adverse effects and safety risks are identified and a preliminary evaluation of efficacy is conducted.

●
Phase
3 clinical trials generally involve a large number of patients at multiple sites and are designed to provide the data necessary to
demonstrate the effectiveness of the product for its intended use, its safety in use and to establish the overall benefit/risk relationship
of the product and provide an adequate basis for product approval. These trials may include comparisons with placebo and/or other
comparator treatments. The duration of treatment is often extended to mimic the actual use of a product during marketing.

Post-approval
trials, sometimes referred to as Phase 4 clinical trials, are conducted after initial marketing approval. These trials are used to gain
additional experience from the treatment of patients in the intended therapeutic indication. In certain instances, the FDA may mandate
the performance of Phase 4 clinical trials as a condition of approval of an NDA.

Progress
reports detailing the results of the clinical trials, among other information, must be submitted at least annually to the FDA and written
IND safety reports must be submitted to the FDA and the investigators for serious and unexpected suspected adverse events, findings from
other studies suggesting a significant risk to humans exposed to the drug, findings from animal or in vitro testing that suggest
a significant risk for human subjects and any clinically important increase in the rate of a serious suspected adverse reaction over
that listed in the protocol or investigator brochure.

Phase
1, Phase 2 and Phase 3 clinical trials may not be completed successfully within any specified period, if at all. The FDA or the sponsor
may suspend or terminate a clinical trial at any time on various grounds, including a finding that the research subjects or patients
are being exposed to an unacceptable health risk. Similarly, an IRB can suspend or terminate approval of a clinical trial at its institution
if the clinical trial is not being conducted in accordance with the IRB’s requirements or if the drug has been associated with
unexpected serious harm to patients. Additionally, some clinical trials are overseen by an independent group of qualified experts organized
by the clinical trial sponsor, known as a data safety monitoring board or committee. This group provides authorization for whether a
trial may move forward at designated check-points based on access to certain data from the trial. Concurrent with clinical trials, companies
usually complete additional animal safety studies and also must develop additional information about the chemistry and physical characteristics
of the drug as well as finalize a process for manufacturing the product in commercial quantities in accordance with cGMP requirements.
The manufacturing process must be capable of consistently producing quality batches of our drug candidates. Additionally, appropriate
packaging must be selected and tested and stability studies must be conducted to demonstrate that our drug candidates do not undergo
unacceptable deterioration over their labeled shelf life.

49

NDA
Review Process

Following
completion of the clinical trials, data is analyzed to assess whether the investigational product is safe and effective for the proposed
indicated use or uses. The results of preclinical studies and clinical trials are then submitted to the FDA as part of an NDA, along
with proposed labeling, chemistry and manufacturing information to ensure product quality and other relevant data. In short, the NDA
is a request for approval to market the drug for one or more specified indications and must contain proof of safety and efficacy for
a drug.

The
application must include both negative and ambiguous results of preclinical studies and clinical trials, as well as positive findings.
Data may come from company-sponsored clinical trials intended to test the safety and efficacy of a product’s use or from a number
of alternative sources, including studies initiated by investigators. To support marketing approval, the data submitted must be sufficient
in quality and quantity to establish the safety and efficacy of the investigational product to the satisfaction of FDA. FDA approval
of an NDA must be obtained before a drug may be marketed in the United States.

Under
the Prescription Drug User Fee Act (“PDUFA”), as amended, each NDA must be accompanied by a user fee. The FDA adjusts the
PDUFA user fees on an annual basis. According to the FDA’s fiscal year 2022 fee schedule, effective through September 30, 2022,
the user fee for an application requiring clinical data, such as an NDA, was approximately $3.11 million. PDUFA also imposes an annual
program fee for each marketed human drug ($369,413 in 2022) and an annual establishment fee on facilities used to manufacture prescription
drugs. Fee waivers or reductions are available in certain circumstances, including a waiver of the application fee for the first application
filed by a small business. Additionally, no user fees are assessed on NDAs for products designated as orphan drugs, unless the product
also includes a non-orphan indication.

The
FDA reviews all submitted NDAs before it accepts them for filing, and may request additional information rather than accepting the NDA
for filing. The FDA must make a decision on accepting an NDA for filing within 60 days of receipt. Once the submission is accepted for
filing, the FDA begins an in-depth review of the NDA. Under the goals and policies agreed to by the FDA under PDUFA, the FDA has 10 months,
from the filing date, in which to complete its initial review of a new molecular-entity NDA and respond to the applicant, and six months
from the filing date of a new molecular-entity NDA designated for priority review. The FDA does not always meet its PDUFA goal dates
for standard and priority NDAs, and the review process is often extended by FDA requests for additional information or clarification.

Before
approving an NDA, the FDA will conduct a pre-approval inspection of the manufacturing facilities for the new product to determine whether
they comply with cGMP requirements. The FDA will not approve the product unless it determines that the manufacturing processes and facilities
are in compliance with cGMP requirements and adequate to assure consistent production of the product within required specifications.
The FDA also may audit data from clinical trials to ensure compliance with GCP requirements. Additionally, the FDA may refer applications
for novel drug products or drug products which present difficult questions of safety or efficacy to an advisory committee, typically
a panel that includes clinicians and other experts, for review, evaluation and a recommendation as to whether the application should
be approved and under what conditions, if any. The FDA is not bound by recommendations of an advisory committee, but it considers such
recommendations when making decisions on approval. The FDA likely will reanalyze the clinical trial data, which could result in extensive
discussions between the FDA and the applicant during the review process. After the FDA evaluates an NDA, it will issue an approval letter
or a Complete Response Letter. An approval letter authorizes commercial marketing of the drug with specific prescribing information for
specific indications. A Complete Response Letter indicates that the review cycle of the application is complete and the application will
not be approved in its present form. A Complete Response Letter usually describes all of the specific deficiencies in the NDA identified
by the FDA. The Complete Response Letter may require additional clinical data, additional pivotal Phase 3 clinical trial(s) and/or other
significant and time-consuming requirements related to clinical trials, preclinical studies or manufacturing. If a Complete Response
Letter is issued, the applicant may either resubmit the NDA, addressing all of the deficiencies identified in the letter, or withdraw
the application. Even if such data and information are submitted, the FDA may decide that the NDA does not satisfy the criteria for approval.
Data obtained from clinical trials are not always conclusive and the FDA may interpret data differently than we interpret the same data.

50

Orphan
Drugs

Under
the Orphan Drug Act, the FDA may grant orphan designation to a drug or biological product intended to treat a rare disease or condition,
which is generally a disease or condition that affects fewer than 200,000 individuals in the United States, or more than 200,000 individuals
in the United States and for which there is no reasonable expectation that the cost of developing and making the product available in
the United States for this type of disease or condition will be recovered from sales of the product.

Orphan
drug designation must be requested before submitting an NDA. After the FDA grants orphan drug designation, the identity of the therapeutic
agent and its potential orphan use are disclosed publicly by the FDA. Orphan drug designation does not convey any advantage in or shorten
the duration of the regulatory review and approval process.

If
a product that has orphan designation subsequently receives the first FDA approval for the disease or condition for which it has such
designation, the product is entitled to orphan drug exclusivity, which means that the FDA may not approve any other applications to market
the same drug for the same indication for seven years from the date of such approval, except in limited circumstances, such as a showing
of clinical superiority to the product with orphan exclusivity by means of greater effectiveness, greater safety or providing a major
contribution to patient care or in instances of drug supply issues. However, competitors may receive approval of either a different product
for the same indication or the same product for a different indication but that could be used off-label in the orphan indication. Orphan
drug exclusivity also could block the approval of one of our products for seven years if a competitor obtains approval before we do for
the same product, as defined by the FDA, for the same indication we are seeking approval, or if a drug candidate is determined to be
contained within the scope of the competitor’s product for the same indication or disease. If one of our products designated as
an orphan drug receives marketing approval for an indication broader than that which is designated, it may not be entitled to orphan
drug exclusivity. Orphan drug status in the European Union has similar, but not identical, requirements and benefits.

Expedited
Development and Review Programs

The
FDA has a fast track program that is intended to expedite or facilitate the process for reviewing new drugs that meet certain criteria.
Specifically, new drugs are eligible for fast track designation if they are intended to treat a serious or life-threatening condition
and preclinical or clinical data demonstrate the potential to address unmet medical needs for the condition. Fast track designation applies
to both the product and the specific indication for which it is being studied. The sponsor can request the FDA to designate the product
for fast track status any time before receiving NDA approval, but ideally no later than the pre-NDA meeting with the FDA.

Any
product submitted to the FDA for marketing, including under a fast track program, may be eligible for other types of FDA programs intended
to expedite development and review, such as priority review and accelerated approval. Any product is eligible for priority review if
it treats a serious or life-threatening condition and, if approved, would provide a significant improvement in safety and effectiveness
compared to available therapies.

A
product may also be eligible for accelerated approval, if it treats a serious or life-threatening condition and generally provides a
meaningful advantage over available therapies. In addition, it must demonstrate an effect on a surrogate endpoint that is reasonably
likely to predict clinical benefit or on a clinical endpoint that can be measured earlier than irreversible morbidity or mortality (“IMM”),
which is reasonably likely to predict an effect on IMM or other clinical benefit. As a condition of approval, the FDA may require that
a sponsor of a drug or biologic receiving accelerated approval perform adequate and well-controlled post-marketing clinical trials. If
the FDA concludes that a drug or biologic shown to be effective can be safely used only if distribution or use is restricted, it may
require such post-marketing restrictions as it deems necessary to assure safe use of the product.

51

Additionally,
a drug may be eligible for designation as a breakthrough therapy if the product is intended, alone or in combination with one or more
other drugs or biologics, to treat a serious or life-threatening condition and preliminary clinical evidence indicates that the product
may demonstrate substantial improvement over currently approved therapies on one or more clinically significant endpoints. The benefits
of breakthrough therapy designation include the same benefits as fast track designation, plus intensive guidance from the FDA to ensure
an efficient drug development program. Fast track designation, priority review, accelerated approval and breakthrough therapy designation
do not change the standards for approval, but may expedite the development or approval process.

Post-Approval
Requirements

Following
approval of a new product, the manufacturer and the approved product are subject to continuing regulation by the FDA, including, among
other things, monitoring and record-keeping requirements, requirements to report adverse experiences and comply with promotion and advertising
requirements, which include restrictions on promoting drugs for unapproved uses or patient populations, known as “off-label use,”
and limitations on industry-sponsored scientific and educational activities. Although physicians may prescribe legally available drugs
for off-label uses, manufacturers may not market or promote such uses. Prescription drug promotional materials must be submitted to the
FDA in conjunction with their first use. Further, if there are any modifications to the drug, including changes in indications, labeling
or manufacturing processes or facilities, the applicant may be required to submit and obtain FDA approval of a new NDA or NDA supplement,
which may require the development of additional data or preclinical studies and clinical trials.

The
FDA may also place other conditions on approvals including the requirement for REMS, to assure the safe use of the product. A REMS could
include medication guides, physician communication plans or elements to assure safe use, such as restricted distribution methods, patient
registries and other risk minimization tools. Any of these limitations on approval or marketing could restrict the commercial promotion,
distribution, prescription or dispensing of products. Product approvals may be withdrawn for non-compliance with regulatory standards
or if problems occur following initial marketing.

The
FDA may withdraw approval if compliance with regulatory requirements and standards is not maintained or if problems occur after the product
reaches the market. Later discovery of previously unknown problems with a product, including adverse events of unanticipated severity
or frequency, or with manufacturing processes, or failure to comply with regulatory requirements, may result in revisions to the approved
labeling to add new safety information; imposition of post-market studies or clinical studies to assess new safety risks or imposition
of distribution restrictions or other restrictions under a REMS program. Other potential consequences include, among other things:

●
restrictions
on the marketing or manufacturing of the product, complete withdrawal of the product from the market, or product recalls;

●
fines,
warning letters, or holds on post-approval clinical studies;

●
refusal
of the FDA to approve pending applications or supplements to approved applications;

●
applications,
or suspension or revocation of product license approvals;

●
product
seizure or detention, or refusal to permit the import or export of products; or

●
injunctions
or the imposition of civil or criminal penalties.

The
FDA strictly regulates marketing, labeling, advertising and promotion of products that are placed on the market. Drugs may be promoted
only for the approved indications and in accordance with the provisions of the approved label. The FDA and other agencies actively enforce
the laws and regulations prohibiting the promotion of off-label uses, and a company that is found to have improperly promoted off-label
uses may be subject to significant liability.

52

Other
U.S. Regulatory Matters

Manufacturing,
sales, promotion and other activities following product approval are also subject to regulation by numerous regulatory authorities in
the United States in addition to the FDA, including the Centers for Medicare & Medicaid Services, other divisions of the Department
of Health and Human Services, the Department of Justice, the Drug Enforcement Administration, the Consumer Product Safety Commission,
the Federal Trade Commission, the Occupational Safety & Health Administration, the Environmental Protection Agency, and state and
local governments.

For
example, in the United States, sales, marketing and scientific and educational programs also must comply with state and federal fraud
and abuse laws, false claims laws, transparency laws, government price reporting, and health information privacy and security laws. These
laws include the following:

●
the
federal Anti-Kickback Statute, which makes it illegal for any person, including a prescription drug manufacturer (or a party acting
on its behalf), to knowingly and willfully solicit, receive, offer or pay any remuneration that is intended to induce or reward referrals,
including the purchase, recommendation, order or prescription of a particular drug, for which payment may be made under a federal
healthcare program, such as Medicare or Medicaid. Moreover, the ACA provides that the government may assert that a claim including
items or services resulting from a violation of the federal Anti-Kickback Statute constitutes a false or fraudulent claim for purposes
of the civil False Claims Act;

●
the
federal false claims and civil monetary penalties laws, including the civil False Claims Act that can be enforced by private citizens
through civil whistleblower or qui tam actions, prohibit individuals or entities from, among other things, knowingly presenting,
or causing to be presented, to the federal government, claims for payment that are false or fraudulent or making a false statement
to avoid, decrease or conceal an obligation to pay money to the federal government;

●
the
Federal Health Insurance Portability and Accountability Act of 1996 (“HIPAA”), prohibits, among other things, executing
or attempting to execute a scheme to defraud any healthcare benefit program or making false statements relating to healthcare matters;

●
HIPAA,
as amended by the Health Information Technology for Economic and Clinical Health Act and their implementing regulations, also imposes
obligations, including mandatory contractual terms, with respect to safeguarding the privacy, security and transmission of individually
identifiable health information;

●
the
federal Physician Payments Sunshine Act requires applicable manufacturers of covered drugs, devices, biologics and medical supplies
for which payment is available under Medicare, Medicaid or the Children’s Health Insurance Program, with specific exceptions,
to annually report to CMS information regarding payments and other transfers of value to physicians and teaching hospitals as well
as information regarding ownership and investment interests held by physicians and their immediate family members; and

●
analogous
state and foreign laws and regulations, such as state anti-kickback and false claims laws which may apply to sales or marketing arrangements
and claims involving healthcare items or services reimbursed by non-governmental third-party payors, including private insurers,
state laws that require biotechnology companies to comply with the biotechnology industry’s voluntary compliance guidelines
and the relevant compliance guidance promulgated by the federal government and may require drug manufacturers to report information
related to payments and other transfers of value to physicians and other healthcare providers or marketing expenditures, state laws
that require biotechnology companies to report information on the pricing of certain drug products, and state and foreign laws that
govern the privacy and security of health information in some circumstances, many of which differ from each other in significant
ways and often are not preempted by HIPAA, thus complicating compliance efforts.

Pricing
and rebate programs must also comply with the Medicaid rebate requirements of the U.S. Omnibus Budget Reconciliation Act of 1990 and
more recent requirements in the ACA. If products are made available to authorized users of the Federal Supply Schedule of the General
Services Administration, additional laws and requirements apply. Products must meet applicable child-resistant packaging requirements
under the U.S. Poison Prevention Packaging Act. Manufacturing, sales, promotion and other activities also are potentially subject to
federal and state consumer protection and unfair competition laws.

53

The
distribution of pharmaceutical products is subject to additional requirements and regulations, including extensive record-keeping, licensing,
storage and security requirements intended to prevent the unauthorized sale of pharmaceutical products.

The
failure to comply with any of these laws or regulatory requirements subjects firms to possible legal or regulatory action. Depending
on the circumstances, failure to meet applicable regulatory requirements can result in significant civil, criminal and administrative
penalties, including damages, fines, disgorgement, individual imprisonment, exclusion from participation in government funded healthcare
programs, such as Medicare and Medicaid, integrity oversight and reporting obligations, contractual damages, reputational harm, diminished
profits and future earnings, injunctions, requests for recall, seizure of products, total or partial suspension of production, denial
or withdrawal of product approvals or refusal to allow a firm to enter into supply contracts, including government contracts.

U.S.
Patent-Term Restoration and Marketing Exclusivity

Depending
upon the timing, duration and specifics of FDA approval of any future drug candidates, some of our U.S. patents may be eligible for limited
patent term extension under the Hatch-Waxman Act. The Hatch-Waxman Act permits restoration of the patent term of up to five years as
compensation for patent term lost during product development and FDA regulatory review process. Patent-term restoration, however, cannot
extend the remaining term of a patent beyond a total of 14 years from the product’s approval date. The patent-term restoration
period is generally one-half the time between the effective date of an IND or the issue date of the patent, whichever is later, and the
submission date of an NDA plus the time between the submission date of an NDA or the issue date of the patent, whichever is later, and
the approval of that application, except that the review period is reduced by any time during which the applicant failed to exercise
due diligence. Only one patent applicable to an approved drug is eligible for the extension and the application for the extension must
be submitted prior to the expiration of the patent. The USPTO, in consultation with the FDA, reviews and approves the application for
any patent term extension or restoration. In the future, we may apply for restoration of patent term for our currently owned or licensed
patents to add patent life beyond its current expiration date, depending on the expected length of the clinical trials and other factors
involved in the filing of the relevant NDA.

Market
exclusivity provisions under the FDCA also can delay the submission or the approval of certain applications. The FDCA provides a five-year
period of non-patent marketing exclusivity within the United States to the first applicant to gain approval of an NDA for a new chemical
entity. A drug is a new chemical entity if the FDA has not previously approved any other new drug containing the same active moiety,
which is the molecule or ion responsible for the action of the drug substance. During the exclusivity period, the FDA may not accept
for review an abbreviated new drug application (“ANDA”), or a 505(b)(2) NDA submitted by another company for another version
of such drug where the applicant does not own or have a legal right of reference to all the data required for approval. However, an application
may be submitted after four years if it contains a certification of patent invalidity or non-infringement. The FDCA also provides three
years of marketing exclusivity for a NDA, 505(b)(2) NDA or supplement to an existing NDA if new clinical investigations, other than bioavailability
studies, that were conducted or sponsored by the applicant are deemed by the FDA to be essential to the approval of the application,
for example, new indications, dosages or strengths of an existing drug. This three-year exclusivity covers only the conditions of use
associated with the new clinical investigations and does not prohibit the FDA from approving ANDAs for drugs containing the original
active agent. Five-year and three-year exclusivity will not delay the submission or approval of a full NDA. However, an applicant submitting
a full NDA would be required to conduct or obtain a right of reference to all of the preclinical studies and adequate and well-controlled
clinical trials necessary to demonstrate safety and effectiveness.

European
Union Drug Development

Similar
to the United States, the various phases of preclinical and clinical research in the European Union are subject to significant regulatory
controls. Although the EU Clinical Trials Directive 2001/20/EC has sought to harmonize the EU clinical trials regulatory framework, setting
out common rules for the control and authorization of clinical trials in the EU, the EU Member States have transposed and applied the
provisions of the Directive differently. This has led to significant variations in the member state regimes. Under the current regime,
before a clinical trial can be initiated it must be approved in each of the EU countries where the trial is to be conducted by two distinct
bodies: the National Competent Authority (“NCA”), and one or more Ethics Committees (“ECs”). Under the current
regime all suspected unexpected serious adverse reactions to the investigated drug that occur during the clinical trial have to be reported
to the NCA and ECs of the Member State where they occurred.

54

The
EU clinical trials legislation currently is undergoing a transition process mainly aimed at harmonizing and streamlining clinical-trial
authorization, simplifying adverse-event reporting procedures, improving the supervision of clinical trials and increasing their transparency.
Recently enacted Clinical Trials Regulation EU No 536/2014 ensures that the rules for conducting clinical trials in the EU will be identical.
In the meantime, Clinical Trials Directive 2001/20/EC continues to govern all clinical trials performed in the EU.

European
Union Drug Review and Approval

In
the European Economic Area (“EEA”), which is comprised of the 27 Member States of the European Union (including Norway and
excluding Croatia), Iceland and Liechtenstein, medicinal products can only be commercialized after obtaining a Marketing Authorization
(“MA”). There are two types of marketing authorizations.

●
The
Community MA is issued by the European Commission through the Centralized Procedure, based on the opinion of the Committee for Medicinal
Products for Human Use (“CHMP”), of the EMA, and is valid throughout the entire territory of the EEA. The Centralized
Procedure is mandatory for certain types of products, such as biotechnology medicinal products, orphan medicinal products, advanced-therapy
medicines such as gene-therapy, somatic cell-therapy or tissue-engineered medicines and medicinal products containing a new active
substance indicated for the treatment of HIV, AIDS, cancer, neurodegenerative disorders, diabetes, auto-immune and other immune dysfunctions
and viral diseases. The Centralized Procedure is optional for products containing a new active substance not yet authorized in the
EEA, or for products that constitute a significant therapeutic, scientific or technical innovation or which are in the interest of
public health in the EU.

●
National
MAs, which are issued by the competent authorities of the Member States of the EEA and only cover their respective territory, are
available for products not falling within the mandatory scope of the Centralized Procedure. Where a product has already been authorized
for marketing in a Member State of the EEA, this National MA can be recognized in another Member States through the Mutual Recognition
Procedure. If the product has not received a National MA in any Member State at the time of application, it can be approved simultaneously
in various Member States through the Decentralized Procedure. Under the Decentralized Procedure an identical dossier is submitted
to the competent authorities of each of the Member States in which the MA is sought, one of which is selected by the applicant as
the Reference Member State (“RMS”). The competent authority of the RMS prepares a draft assessment report, a draft summary
of the product characteristics (“SPC”), and a draft of the labeling and package leaflet, which are sent to the other
Member States (referred to as the Member States Concerned) for their approval. If the Member States Concerned raise no objections,
based on a potential serious risk to public health, to the assessment, SPC, labeling or packaging proposed by the RMS, the product
is subsequently granted a national MA in all the Member States (i.e., in the RMS and the Member States Concerned).

Under
the above described procedures, before granting the MA, EMA or the competent authorities of the Member States of the EEA make an assessment
of the risk-benefit balance of the product on the basis of scientific criteria concerning its quality, safety and efficacy. Similar to
the U.S. patent term-restoration, Supplementary Protection Certificates (“SPCs”) serve as an extension to a patent right
in Europe for up to five years. SPCs apply to specific pharmaceutical products to offset the loss of patent protection due to the lengthy
testing and clinical trials these products require prior to obtaining regulatory marketing approval.

Coverage
and Reimbursement

Sales
of our products will depend, in part, on the extent to which our products will be covered by third-party payors, such as government health
programs, commercial insurance, and managed healthcare organizations. There is significant uncertainty related to third-party payor coverage
and reimbursement of newly approved products. In the United States, for example, principal decisions about reimbursement for new products
are typically made by CMS. CMS decides whether and to what extent a new product will be covered and reimbursed under Medicare, and private
third-party payors often follow CMS’s decisions regarding coverage and reimbursement to a substantial degree. However, no uniform
policy of coverage and reimbursement for drug products exists. Accordingly, decisions regarding the extent of coverage and amount of
reimbursement to be provided for any of our products will be made on a payor-by-payor basis.

55

Increasingly,
third-party payors are requiring that drug companies provide them with predetermined discounts from list prices and are challenging the
prices charged for medical products. Further, such payors are increasingly challenging the price, examining the medical necessity and
reviewing the cost effectiveness of medical drug candidates. There may be especially significant delays in obtaining coverage and reimbursement
for newly approved drugs. Third-party payors may limit coverage to specific drug candidates on an approved list, known as a formulary,
which might not include all FDA-approved drugs for a particular indication. We may need to conduct expensive pharmaco-economic studies
to demonstrate the medical necessity and cost effectiveness of our products. As a result, the coverage determination process is often
a time-consuming and costly process that will require us to provide scientific and clinical support for the use of our products to each
payor separately, with no assurance that coverage and adequate reimbursement will be obtained.

In
addition, in most foreign countries, the proposed pricing for a drug must be approved before it may be lawfully marketed. The requirements
governing drug pricing and reimbursement vary widely from country to country. For example, the European Union provides options for its
member states to restrict the range of medicinal products for which their national health insurance systems provide reimbursement and
to control the prices of medicinal products for human use. A member state may approve a specific price for the medicinal product or it
may instead adopt a system of direct or indirect controls on the profitability of the company placing the medicinal product on the market.
There can be no assurance that any country that has price controls or reimbursement limitations for pharmaceutical products will allow
favorable reimbursement and pricing arrangements for any of our products. Historically, products launched in the European Union do not
follow price structures of the United States and generally prices tend to be significantly lower.

Healthcare
Reform

The
United States government, state legislatures, and foreign governments have shown significant interest in implementing cost containment
programs to limit the growth of government-paid healthcare costs, including price-controls, restrictions on reimbursement, and requirements
for substitution of generic products for branded prescription drugs. For example, in March 2010, the Patient Protection and Affordable
Care Act of 2010, as amended by the Health Care and Education Reconciliation Act of 2010 (collectively, the “ACA”), was passed
which substantially changed the way healthcare is financed by both the government and private insurers, and significantly impacts the
U.S. pharmaceutical industry. The ACA contains provisions that may reduce the profitability of drug products through increased rebates
for drugs reimbursed by Medicaid programs, extension of Medicaid rebates to Medicaid managed care plans, mandatory discounts for certain
Medicare Part D beneficiaries and annual fees based on pharmaceutical companies’ share of sales to federal health care programs.
The Medicaid Drug Rebate Program requires pharmaceutical manufacturers to enter into and have in effect a national rebate agreement with
the HHS Secretary as a condition for states to receive federal matching funds for the manufacturer’s outpatient drugs furnished
to Medicaid patients. The ACA made several changes to the Medicaid Drug Rebate Program, including increasing pharmaceutical manufacturers’
rebate liability by raising the minimum basic Medicaid rebate on most branded prescription drugs from 15.1% of average manufacturer price
(“AMP”), to 23.1% of AMP and adding a new rebate calculation for “line extensions” (i.e., new formulations, such
as extended release formulations) of solid oral dosage forms of branded products, as well as potentially impacting their rebate liability
by modifying the statutory definition of AMP. The ACA also expanded the universe of Medicaid utilization subject to drug rebates by requiring
pharmaceutical manufacturers to pay rebates on Medicaid managed care utilization and by enlarging the population potentially eligible
for Medicaid drug benefits. The Centers for Medicare & Medicaid Services (“CMS”), have proposed to expand Medicaid rebate
liability to the territories of the United States as well. Additionally, for a drug product to receive federal reimbursement under the
Medicaid or Medicare Part B programs or to be sold directly to U.S. government agencies, the manufacturer must extend discounts to entities
eligible to participate in the 340B drug pricing program. The required 340B discount on a given product is calculated based on the AMP
and Medicaid rebate amounts reported by the manufacturer.

56

Some
of the provisions of the ACA have yet to be implemented, and there have been judicial and Congressional challenges to certain aspects
of the ACA Congress has recently considered legislation that would repeal or repeal and replace all or part of the ACA. While Congress
has not passed comprehensive repeal legislation, two bills affecting the implementation of certain taxes under the ACA have passed. On
December 22, 2017, the Tax Cuts and Jobs Act (the “Tax Act”) was enacted, which includes a provision repealing, effective
January 1, 2019, the tax-based shared responsibility payment imposed by the ACA on certain individuals who fail to maintain qualifying
health coverage for all or part of a year that is commonly referred to as the “individual mandate.” The Bipartisan Budget
Act of 2018 (the “BBA”), among other things, amended the ACA, effective January 1, 2019, to close the coverage gap in most
Medicare Part D drug plans. In July 2018, CMS published a final rule permitting further collections and payments to and from certain
ACA-qualified health plans and health insurance issuers under the ACA risk adjustment program in response to the outcome of federal district
court litigation regarding the method CMS uses to determine this risk adjustment. On December 14, 2018, a Texas U.S. District Court Judge
ruled that the ACA is unconstitutional in its entirety because the “individual mandate” was repealed by Congress as part
of the Tax Act. On December 18, 2019, the United States Court of Appeal for the Fifth Circuit ruled that the “individual mandate”
of the ACA is unconstitutional, but remanded the case to the U.S. District Court to reconsider whether the entire ACA is unconstitutional.
In June 2021, the Supreme Court concluded that the challenge to the ACA should be dismissed. It is unclear how this decision, subsequent
appeals and decisions, and other efforts to repeal and replace the ACA will impact the ACA.

Other
legislative changes have been proposed and adopted in the United States since the ACA was enacted. These changes included aggregate reductions
to Medicare payments to providers of up to 2% per fiscal year, effective April 1, 2013, which, due to subsequent legislative amendments,
will stay in effect through 2027 unless additional congressional action is taken. In January 2013, President Obama signed into law the
American Taxpayer Relief Act of 2012, which, among other things, reduced Medicare payments to several providers, and increased the statute
of limitations period for the government to recover overpayments to providers from three to five years. These new laws may result in
additional reductions in Medicare and other healthcare funding, which could have a material adverse effect on customers for our drugs,
if approved, and accordingly, our financial operations.

Additionally,
there has been heightened governmental scrutiny recently over the manner in which drug manufacturers set prices for their marketed products,
which has resulted in several Congressional inquiries and proposed and enacted federal and state legislation designed to, among other
things, bring more transparency to product pricing, review the relationship between pricing and manufacturer patient programs, and reform
government program reimbursement methodologies for drug products. For example, At the state level, legislatures have increasingly passed
legislation and implemented regulations designed to control pharmaceutical and biological product pricing, including price or patient
reimbursement constraints, discounts, restrictions on certain product access and marketing cost disclosure and transparency measures,
and, in some cases, designed to encourage importation from other countries and bulk purchasing.

Moreover,
the Medicare Prescription Drug, Improvement, and Modernization Act of 2003 (“MMA”), established the Medicare Part D program
to provide a voluntary prescription drug benefit to Medicare beneficiaries. Under Part D, Medicare beneficiaries may enroll in prescription
drug plans offered by private entities that provide coverage of outpatient prescription drugs. Unlike Medicare Part A and B, Part D coverage
is not standardized. While all Medicare drug plans must give at least a standard level of coverage set by Medicare, Part D prescription
drug plan sponsors are not required to pay for all covered Part D drugs, and each drug plan can develop its own drug formulary that identifies
which drugs it will cover and at what tier or level. However, Part D prescription drug formularies must include drugs within each therapeutic
category and class of covered Part D drugs, though not necessarily all the drugs in each category or class. Any formulary used by a Part
D prescription drug plan must be developed and reviewed by a pharmacy and therapeutic committee. Government payment for some of the costs
of prescription drugs may increase demand for products for which we receive marketing approval. However, any negotiated prices for our
products covered by a Part D prescription drug plan likely will be lower than the prices we might otherwise obtain. Moreover, while the
MMA applies only to drug benefits for Medicare beneficiaries, private third-party payors often follow Medicare coverage policy and payment
limitations in setting their own payment rates.

57

Employees

As
of the date of this report, we employ a total of 16 employees. None of our employees are represented by a labor union or covered under
a collective bargaining agreement. We believe that we maintain strong relations with our employees.

We
also engage outside consultants to assist with research and development, clinical development and regulatory matters, business development,
operations and other functions from time to time.

Human
Capital Resources.

Our
employees drive our mission, and we place a high level of importance on employee engagement and corporate culture. Fostering and maintaining
a strong, healthy culture is a key strategic focus for us, and we regularly engage in independent third-party surveys to gauge the satisfaction
and engagement of our team.

Our
compensation approach is aimed at attracting, retaining, motivating and rewarding superior employees who operate in a highly competitive
and technologically challenging environment. The structure of our compensation aims to balance incentives for both short-term and long-term
performance.

Some
examples of the benefits we offer include medical insurance, dental insurance, vision insurance, and an unlimited paid-time off policy.

A
substantial portion of our employees are focused on leading and advancing our drug development, biology and data science efforts. As
we progress our product candidates and grow and expand our team, we intend to continue to place a significant focus on our human capital
resources.

Available
Information

We
maintain a website at www.lanternpharma.com. The contents of our website are not incorporated in, or otherwise to be regarded as part
of, this Annual Report on Form 10-K. We make available, free of charge on our website, access to our Annual Report on Form 10-K, our
Quarterly Reports on Form 10-Q, our Current Reports on Form 8-K and amendments to those reports filed or furnished pursuant to Section
13(a) or 15(d) of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), as soon as reasonably practicable
after we file or furnish them electronically with the Securities and Exchange Commission (“SEC”).

Copies
of our Annual Report on Form 10-K, our Quarterly Reports on Form 10-Q, our Current Reports on Form 8-K and other filings we make with
the SEC are also available at the SEC’s Public Reference Room at 100 F Street, N.E., Washington, D.C. 20549. Please call the SEC
at 1-800-SEC-0330 for further information on the Public Reference Room. Our SEC filings are also available on the SEC’s website
at www.sec.gov. Statements contained in this Annual Report on Form 10-K concerning the contents of any contract or any other documents
are not necessarily complete. If a contract or document has been filed as an exhibit to this Annual Report on Form 10-K, please see the
copy of the contract or document that has been filed. Each statement in this this Annual Report on Form 10-K relating to a contract or
document filed as an exhibit is qualified in all respects by the filed exhibit.