NYSE: MAIA

We
were incorporated in Delaware in August 2018, and have operations in Chicago, Illinois, with some of our team members setup virtually
and working remotely in California, North Carolina, and New Jersey, among others. Our principal executive office is located at 444 West
Lake Street, Suite 1700, Chicago, IL 60606, and our phone number is (312) 416-8592. In July 2021, we established a wholly-owned Australian
subsidiary, MAIA Biotechnology Australia Pty Ltd., to conduct various preclinical and clinical activities for the development of our
product candidates. ln April 2022, we established a wholly owned Romanian subsidiary, MAIA Biotechnology Romania S.R.L. to conduct various
preclinical and clinical activities for the development of our product candidates. Our website address is www.MAIABiotech.com. The information
contained on our website is not incorporated by reference into this prospectus supplement, and you should not consider any information
contained on, or that can be accessed through, our website as part of this prospectus supplement or in deciding whether to purchase our
securities.

Our
Lead Product Candidate

Ateganosine
is a telomere-targeting agent currently in clinical development to evaluate its activity in NSCLC. Telomeres, along with the enzyme telomerase,
play a fundamental role in the survival of cancer cells and their resistance to current therapies. Ateganosine is being developed as
a second- or later line of treatment for NSCLC for patients that have progressed beyond the standard-of-care regimen of existing checkpoint
inhibitors.

In
2019, our research team discovered that ateganosine produced telomere modifications and disruption, which ultimately induced cancer-specific
innate and adaptive immune responses against immunologically “cold” or tumor types that were unresponsive to immune checkpoint
inhibitors. This hypothesis was tested and demonstrated in syngeneic and humanized mouse models. Ateganosine administered to mice in
low doses and followed by an immune-checkpoint inhibiting agent, such as an anti-PD-1 or anti-PD-L1 compound, induced complete tumor
regression with no tumor recurrence during the 14 weeks of observation. Further, no toxicities were reported in the tumor-free mice.
These new findings were published in the peer-reviewed research scientific journal, Cancer Cell in July 2020. Based on these recent discoveries,
a new therapeutic approach has been designed to advance ateganosine in patients with advanced
NSCLC.

2

Our
regulatory strategy includes a filing of an Investigational New Drug application (IND) with the United States Food and Drug Administration
(U.S. FDA or FDA). This was granted and will allow U.S. sites to participate in the THIO-101 NSCLC trial. The human safety data generated
in Australia and Europe constituted the basis of the IND application. Although we plan to rely solely on the safety and efficacy data
we generate in our own clinical trials in support of our planned New Drug Application (NDA) filing, and do not plan to rely on clinical
data generated by unaffiliated third parties, we take added confidence in the potential tolerability of ateganosine in light of the fact
that the ateganosine dose selected of 180 mg/cycle is 14 times lower than the maximum tolerated dose tested in the earlier clinical trials
sponsored by the National Cancer Institute (NCI) in the 1970s. The THIO-101 Phase 2 trial is a proof-of-concept study that may be modified
depending on interim results to include both primary and secondary endpoints and be consistent with previously approved cancer treatments.
In September 2022, we submitted a pre-IND meeting request to the FDA to discuss, among other elements, the existing non-clinical and
clinical data to support the conduct of our planned THIO-101 Phase 2 trial under an IND to include patients from the U.S. MAIA received
feedback in-line with the proposed plans from the FDA regarding its manufacturing, preclinical and clinical development plan. MAIA also
obtained guidance from the FDA on the assessment of its safety and efficacy in the THIO-101 Phase 2 trial that was incorporated in the
U.S. IND application. The U.S. IND was granted in 2023.

The
THIO-101 study protocol was amended in December 2024 to increase the number of patients enrolled in an expansion arm to further evaluate
efficacy of the treatment in third-line NSCLC patients resistant to checkpoint inhibitor and chemotherapy. The study may undergo modification
of the statistical analysis, a change in the trial design, and/or primary endpoints. Based on the clinical data we aim to generate in
the THIO-101 study and assuming ateganosine achieves its intended clinical effect with a manageable safety profile at one of the doses
tested in the study, we expect to seek early FDA guidance on the possibility of utilizing one or more of FDA’s expedited programs
for serious conditions, such as fast track designation (FTD), breakthrough therapy designation, priority review and/or accelerated approval
designation. Accelerated approval status does not guarantee an accelerated review or marketing approval by the FDA. In July 2025, the
FDA granted fast track designation for ateganosine and we intend to utilize the incentives of the Fast Track Program to expedite the
development and review of ateganosine.

On
April 11, 2023, we announced positive topline data related to the completion of Part A, safety lead-in portion of the THI0-101 trial
which showed that administration of ateganosine, at the highest dose of 360 mg/cycle in sequential combination with Regeneron’s
anti-PD-1 therapy, Libtayo® was well tolerated with no dose limiting toxicities or significant treatment-related adverse
events reported.

On
April 18, 2023, we published data in Hepatocellular Carcinoma (HCC) models: as monotherapy, ateganosine achieved complete and durable
responses in HCC, the dominant histology in primary liver cancer (90%), in in vivo models. When combined with
Libtayo®, duration of response was further potentiated. Even upon rechallenge with two times more cancer cells and no
additional treatment, tumor growth was completely prevented. Administration of ateganosine alone and in combination with Libtayo®
generated anticancer immune memory.

On
April 20, 2023, we announced preliminary survival data from Part A of THIO-101. The first two patients enrolled in Part A of the study
continued to be alive, approximately 10 and 9 months respectively, from treatment initiation. Both patients have advanced Stage IV metastatic
disease and are heavily pretreated, receiving third and fourth line of therapy respectively after previously failing treatment with an
immune checkpoint inhibitor. They continue to be progression free following their last dose of ateganosine, 7 and 6 months respectively,
with no new treatment. The current treatment options in patients with advanced relapsed or refractory NSCLC who failed two or more therapy
regimens are limited and show minimal benefit. Furthermore, discontinuation of treatment is rapidly followed by physical decline and
death, therefore seeing patients with such survival and no disease progression in this clinical setting, is noteworthy. In real-world
clinical practice, observed survival in such heavily pretreated patients is 3-4 months.

3

On
June 20, 2023, we announced updates in enrollment in THIO-101 in Europe. To that date, 29 patients have been dosed in THIO-101. With
the addition of sites in Hungary, Poland, and Bulgaria in March 2023, THIO-101 has rapidly increased the number of patients enrolled
and dosed with ateganosine. Thirteen sites were activated with another two new additional sites ready to open shortly afterward.

On
July 10, 2023, we announced updates on preliminary survival data in the Part A safety lead-in of THIO-101. The first 2 patients enrolled
in the study continued to be alive, approximately 12.2 and 11.5 months respectively, from treatment initiation. Both patients have advanced
Stage IV metastatic disease and failed 2 prior lines of therapy, including one line with an immune CPI, and platinum-based
chemotherapy. Following the conclusion of study treatment, they have remained free of disease progression for 10.2 and 8.5 months, respectively,
without requiring any additional therapy.

On
July 11, 2023, we announced updates on disease control data in the part A safety lead-in of THIO-101. Of the first 11 patients enrolled
in THIO-101 to complete at least 1 post baseline response assessment, 9 (82%) met the primary endpoint of disease control (defined as
a Complete Response, Partial Response, or Stable Disease per RECIST 1.1). All patients enrolled have previously failed 2 or more prior
lines of treatment including an immune CPI and platinum-based chemotherapy for advanced NSCLC.

On
October 24, 2023, we reported unprecedented interim disease control rate (DCR) of 100% in second-line treatment that far surpasses standard
of care (SoC) DCR of 53-64%, presented at ESMO 2023. DCR is far stronger than overall response rate (ORR) in predicting overall survival
benefit, as shown in a recent meta-analysis of 74 clinical trials worldwide in NSCLC.

On
December 19, 2023, we announced dose selection for THIO-101, a Phase 2 clinical trial evaluating its lead asset, ateganosine, in sequential
combination with Regeneron’s anti-PD-1 cemiplimab (Libtayo®) in patients with advanced NSCLC. During the dose-finding stage of THIO-101, patients were administered either 60mg, 180mg, or 360mg of ateganosine per cycle,
followed by 350mg of cemiplimab (Libtayo®). The selected dose, 180mg/cycle, presented better safety profile and outperformed
the other doses in the key measures of efficacy for NSCLC trials. Subsequently, all future trial participants will be treated with ateganosine
180mg/cycle.

On
January 17, 2024, we announced new interim data for our ongoing THIO-101 Phase 2 trial in NSCLC. In the
latest available data from THIO-101 (November 13, 2023), 60 patients had been dosed with ateganosine in sequential combination with Libtayo®.
The patients received either 60mg, 180mg, or 360mg of ateganosine per dose, and 42 had at least one post baseline assessment completed.
The observed disease control was well sustained compared to previous scans.

On
February 7, 2024, we announced publication of international Patent Cooperation Treat (PCT) application titled “Dinucleotides and
Their Use in Treating Cancer.” The new dinucleotides disclosed in the patent application are telomere-targeting molecules, such
as ateganosine fragments or other ateganosine analogues. These compounds are key next-generation telomere-targeting agents, an important
extension of MAIA’s innovative cancer treatment platform. The PCT system streamlines the process for obtaining patent protection
globally. Under the PCT, applicants can seek patent protection in a large number of countries.

On
February 22, 2024, we announced completion of enrollment in Phase 2 THIO-101 go-to-market clinical trial. The trial reached the enrollment
target of 41 patients for the 180mg/dose on February 19, 2024. As of the latest data available for the trial, 79 patients had received
either 60mg (24 patients), 180mg (41 patients) or 360mg (14 patients). The original trial design targeted up to 182 patients, including
all patients in the safety lead-in and 41 patients in each of the 3 tested doses (60mg, 180mg, and 360mg). Following the selection of
180 mg/cycle as the optimal dose in December 2023, all patients were subsequently enrolled at the 180mg/cycle dose and trial enrollment
was completed ahead of schedule.

4

On
March 6, 2024, we announced interim efficacy data for THIO-101 Phase 2 trial in NSCLC. In the latest data available (January 8, 2024),
the overall response rate (ORR), characterized as partial or complete response to therapy, was 38% (3 out of 8 patients) in the efficacy
evaluable population for combination ateganosine 180mg + cemiplimab in third-line treatment for NSCLC patients who failed treatment with
immune checkpoint inhibitors in prior lines of therapy, with or without chemotherapy.

On
March 27, 2024, we evaluated additional clinical data from its Phase 2 clinical trial, THIO-101. At such time, a total of 68 patients
have been dosed and had a post-baseline scan in MAIA’s Phase 2 clinical trial, THIO-101, evaluating ateganosine in sequential combination
with an immune checkpoint inhibitor in patients with advanced NSCLC. Preliminary efficacy across all lines of therapy in this March 2024
data cut were consistent with previous reports including: (i) 75% of patients receiving ateganosine 180mg as third-line therapy for NSCLC
have surpassed the overall survival (OS) threshold of 5.8 months; (ii) 88% of patients in the same setting (3L, 180mg)
also crossed the 2.5 months progression free survival (PFS) threshold and have shown ORR of 38%, greatly improving on current
chemo treatment that have ORRs of around 6-10%; and (iii) across all third-line patients, DCR of 85% remained superior to current chemotherapy
options, which ranges from 25-35% DCR.

On
June 4, 2024, we announced new preliminary efficacy data from the Phase 2 THIO-101 clinical trial. The updated included that as of
April 30, 2024: (i) all evaluable patients had completed ≥1 post-baseline assessment; (ii) third-line treatment across all doses
had shown DCR of 85% for ateganosine, 65% of patients crossed the 5.8 month OS threshold identified in literature, 85% of
patients crossed the 2.5 month PFS threshold, median survival follow-up time was 9.1 months; and (iii) third-line treatment with
ateganosine 180mg had shown median PFS of 5.5 months, 78% OS rate at 6 months, 38% ORR, 75% of patients crossed the 5.8 month OS
threshold, 88% of patients crossed the 2.5 month PFS threshold and median survival follow-up time observed was 9.1
months.

On
June 6, 2024, we announced MAIA highlights and key achievements year-to-date, including: (i) exceptional measures of efficacy by lead
drug ateganosine in Phase 2 clinical trial, with 38% ORR in third-line (3L) setting (ateganosine 180mg) compared to ~6% for currently
available treatments in a similar population and 5.5 months median progression-free survival (PFS) (3L, ateganosine 180mg); and (ii)
secured continued insider investment through independent board members’ participation in private placement equity financings, with
funding of more than $12M year-to-date.

On
June 7, 2024, we announced the validation of clinical and regulatory pathways for viable therapies leveraging the cell’s telomeric
functions as evidenced by the FDA approval of imetelstat, a treatment for low- to intermediate-risk hematologic malignancies (myelodysplastic
syndromes) from Geron Corporation, illuminating the role of telomere targeting as a viable therapeutic strategy for cancer treatment.

On
July 23, 2024, we announced treatment updates from our Phase 2 clinical trial of ateganosine. As of June 12, the latest clinical cut-off
date: (i) 6 patients remain on treatment following at least 12 months of therapy; (ii) treatment with ateganosine followed by cemiplimab
has been well tolerated throughout the trial, with lower toxicity compared to standard-of-care treatments; and (iii) the longest-treated
patients have completed 21 cycles of ateganosine sequenced with cemiplimab.

On
September 10, 2024, we announced updates from our lead clinical candidate ateganosine, in our Phase 2 clinical trial, THIO-101. The updates
included: (i) As of August 1, 2024, 16 patients had survival follow-up surpassing 12 months, including 9 in third line treatment (3L);
(ii) Interim median survival follow-up in 3L was 10.6 months.; and (iii) ateganosine’s substantial survival benefit in third line
surpasses comparable standard-of-care overall survival of 5.8 months.

On
December 3, 2024, we announced the amendment of the 2021 clinical supply agreement with Regeneron for the expansion portion of THIO-101,
its Phase 2 clinical trial evaluating ateganosine in sequential administration with cemiplimab (Libtayo®). The new expansion
will further assess the efficacy of MAIA’s lead asset, ateganosine, sequenced with immune checkpoint inhibitor (CPI) Libtayo®
(cemiplimab) for advanced non-small cell lung cancer (NSCLC) patients receiving third-line therapy who were resistant to previous checkpoint
inhibitor treatments and chemotherapy. The original 2021 agreement between MAIA and Regeneron was designed to supply the original THIO-101
trial through the dose selection and safety evaluation process.

On
December 16, 2024, we announced that the FDA has designated ateganosine for the treatment of pediatric-type diffuse high-grade gliomas
(PDHGG) as a drug for a “rare pediatric disease” (RPDD). Upon FDA approval of a future new drug application in PDHGG, MAIA
would be eligible to receive a priority review voucher that can be redeemed by drug developers for FDA priority review of a different
product or transferred or sold to another sponsor.

5

On
January 7, 2025, we announced that we had entered into a clinical supply agreement with global oncology company BeiGene to assess the
efficacy of ateganosine, its small molecule telomere-targeting anticancer agent, in combination with BeiGene’s immune CPI tislelizumab in three cancer indications. The single arm pivotal Phase 2 trials will study the drug combination in HCC, SCLC and CRC. Under the terms of the collaboration, MAIA will sponsor and
fund the planned clinical trials and BeiGene will provide tislelizumab. MAIA maintains global development and commercial rights to ateganosine
and is free to develop the programs in combination with other agents and in other indications. Since May 2025, BeiGene has changed its
company name to BeOne Medicines.

On
February 4, 2025, we announced positive updated data from THIO-101 Phase 2 clinical trial evaluating its lead clinical candidate, ateganosine,
sequenced with Regeneron’s immune CPI cemiplimab (Libtayo®) in patients with advanced NSCLC who failed two or more standard-of-care therapy regimens. As of January 15, 2025, third line (3L) data updates showed
that: (i) median overall survival (OS) of 16.9 months for the 22 NSCLC patients who received at least one dose of ateganosine (the intent-to-treat
population) in parts A and B of the trial. (ii) The analysis demonstrated a 95% confidence interval (CI) lower bound of 12.5 months and
a 99% CI lower bound of 10.8 months. (iii) The treatment has been generally well-tolerated to date in this heavily pre-treated population.

On
February 26, 2025, we announced the trial design for the expansion of its THIO-101 pivotal Phase 2 trial in NSCLC. The expansion of the study will assess overall response rates (ORR) in advanced NSCLC patients receiving third line (3L) therapy
who were resistant to previous checkpoint inhibitor treatments (CPI) and chemotherapy. The THIO-101 study in 3L will enroll up to 48
patients with two arms: Arm 1, continuing the evaluation of ateganosine sequenced with Libtayo® (cemiplimab); and Arm
2, evaluating ateganosine as a monotherapy, to further gain experience of ateganosine in the contribution of components. Treatment cycles
for patients in both arms will administer ateganosine on 3 consecutive days, followed by immune activation on day 4. Arm 1 will administer
Libtayo on day 5. The Company plans to enroll an additional 100 patients for the registration phase of the trial. MAIA expects to conduct
the trials in the U.S. and select countries in Europe and Asia.

On
February 27, 2025, we announced plans to initiate a Phase 3 pivotal trial in 2025, named THIO-104, to evaluate the efficacy of ateganosine
administered in sequence with a checkpoint inhibitor (CPI) in third-line non-small cell lung cancer (NSCLC) patients who are resistant
to checkpoint inhibitors and chemotherapy. The multicenter, open-label, pivotal Phase 3 trial is designed to provide a direct comparison
to chemotherapy in a 1:1 randomization of up to 300 patients.

On
March 18, 2025, we announced that the United States Adopted Names (USAN) Council had approved “ateganosine” as the nonproprietary
(generic) name for its lead molecule a telomere-targeting anticancer agent in clinical development as a first-in-class treatment for
advanced non-small cell lung cancer (NSCLC). The company chose a name inspired by the mechanism of action of THIO: altering telomeric
guanosine of the cancer cells. The generic name ateganosine is a unique and consistent identity that aims to support clear communication
between healthcare providers, patients and researchers. MAIA will retain the name THIO in its clinical trial designations (THIO-101,
THIO-102, THIO-103, THIO-104).

On
March 20, 2025, we announced the publication of preclinical data for our lead proprietary telomere-targeting ateganosine dimer in
the peer-reviewed scientific journal Naunyn-Schmiedeberg’s Archives of Pharmacology. In a preclinical study, ateganosine and
its new described dimer form were found to be potent inhibitors of Glutathione S-transferase Pi (GSTP1), a key enzyme implicated in
cancer progression and chemoresistance and a highly important factor for the detoxification of cancer cells. The findings suggest
that the dimerized form of ateganosine could enhance chemotherapeutic efficacy by effectively targeting GSTP1 and reducing drug
resistance. The article, titled “Investigation of the inhibitory effects of the telomere-targeted compounds on glutathione
S-transferase P1,” was published on February 15, 2025.

On
June 5, 2025, we announced updated data from its THIO-101 pivotal Phase 2 clinical trial. As of May 15, 2025, third line (3L) data showed
median overall survival (OS) of 17.8 months for the 22 NSCLC patients who received at least one dose of ateganosine (the intent-to-treat
population) in parts A and B of the trial. The updated analysis continues to demonstrate a 95% confidence interval (CI) lower bound of
12.5 months and a 99% CI lower bound of 10.8 months. The Company also mentioned that treatment had been generally well-tolerated to date
in this heavily pre-treated population.

6

On
June 5, 2025, we announced that a new partial response (PR) was identified in a patient after 20 months of treatment in our Phase 2 THIO-101
clinical trial. A partial response is defined as a decrease in tumor size of at least 30%.

On
June 18, 2025, we announced its entry into a clinical master supply agreement with Roche for future studies investigating the combination
of MAIA’s telomere targeting agent ateganosine (THIO), sequenced with Roche’s checkpoint inhibitor (CPI), atezolizumab (Tecentriq®),
for the treatment of multiple hard-to-treat cancers.

On
June 24, 2025, we announced the appointment of two prominent oncologists to its Scientific Advisory Board (SAB), Claudia Fulgenzi, MD,
and David J. Pinato, MD, MRCP (UK), PhD. Both are specialists in hepatocellular carcinoma (HCC), a tumor type to be studied in future
clinical trials of MAIA’s lead candidate ateganosine (THIO) sequenced with a checkpoint inhibitor.

On
July 9, 2025, we announced the dosing of the first patient in Taiwan in the expansion phase of our THIO-101 Phase 2 trial for advanced
non-small cell lung cancer (NSCLC). The trial’s entry into another continent marks a key milestone for MAIA, opening a significantly
larger patient pool for its evaluations of ateganosine (THIO). MAIA also announced that screening for the trial is ongoing in Europe
and Asia.

On
July 17, 2025, we announced the publication of preclinical data from its second generation ateganosine prodrugs platform in Nucleic Acids
Research (NAR), a leading open-access peer-reviewed scientific journal. The study, titled “Novel Telomere-Targeting Dual-Pharmacophore
Dinucleotide Prodrugs for Anticancer Therapy,” details MAIA’s lead ateganosine (THIO)-derived second-generation prodrugs
as promising new molecules in its strategy for enhancing cancer treatment and overcoming drug resistance. The manuscript with the data
was published on June 26, 2025, in Volume 53, Issue 12 of the NAR journal.

On
July 28, 2025, we announced that the U.S. Food and Drug Administration (FDA) has granted Fast Track designation for ateganosine (THIO,
6-thio-dG or 6-thio2’-deoxyguanosine) for the treatment of non-small cell lung cancer (NSCLC). Ateganosine is currently being evaluated
in a pivotal Phase 2 THIO-101 clinical trial evaluating its anti-tumor activity when followed by a checkpoint inhibitor.

On
August 13, 2025, we announced that the European Patent Office granted a patent broadly covering a portfolio of ateganosine-based analogues
for telomere targeting anticancer therapy and methods of using ateganosine (THIO) alone or before administration of checkpoint inhibitors
(CPIs). The patent, titled “Mercaptopurine Ribonucleoside Analogues for Altering Telomerase Mediated Telomere,” was invented
by MAIA’s Chief Scientific Officer Sergei M. Gryaznov, PhD and Scientific Advisory Board member Jerry W. Shay, PhD. MAIA’s
global patent and patent-pending estate covers several areas including telomerase mediated telomere altering compounds and treatment
of therapy-resistant cancers. Further, ateganosine’s immunogenic treatment strategy, which focuses on sequential combination with
checkpoint inhibitors, has been filed worldwide. MAIA’s IP portfolio for ateganosine currently comprises 10 issued patents worldwide
including Europe (validated in 19 countries) along with 24 pending patent applications.

On
August 27, 2025, we announced that a manuscript detailing developments in its Phase 2 THIO-101 clinical trial was accepted and published
in the international peer-reviewed open access scientific journal, Cells, in a special issue, “Cellular Mechanisms of Anti-Cancer
Therapies.” The manuscript, titled “Perioperative Management of Non-Small Cell Lung Cancer in the Era of Immunotherapy,”
was authored by a group of oncology researchers in Turkey and the U.S. including MAIA scientists Sergei Gryaznov, Ph.D., Chief Scientific
Officer and Ilgen Mender, Director of Biology Research, along with MAIA Scientific Advisory Board members Z. Gunnur Dikmen, M.D., Ph.D.
and Saadettin Kiliçkap, M.D., M.Sc.

On
September 11, 2025, we highlighted positive efficacy data from its Phase 2 clinical trial, THIO-101, including that as of June 30, 2025:
(i) estimated median progression free survival (PFS) in third-line treatment (180 mg dose) was 5.6 months; (ii) Estimated median overall
survival (OS) was 17.8 months, with a 95% confidence interval (CI) lower bound of 12.5 months and a 99% CI lower bound of 10.8 months,
consistent with the prior data readout (May 15, 2025); (iii) Across patients of all treatment lines, 2 patients have completed 33 cycles
of therapy, highlighting ateganosine’ potential for extended dosing, which usually translates into longer patient survival.

7

On
October 23, 2025, we announced that as of September 17, 2025, a patient that began therapy in March 2023 has shown survival of 30
months, or 912 days, an outstanding measure relative to many of the high-risk cancers. The patient with thirty month survival
received therapy every three weeks and concluded treatment upon reaching the maximum treatment duration of 2 years based on protocol
requirements.

On
October 27, 2025, we announced that we have enrolled five patients from Taiwan and Turkey in the expansion phase of its THIO-101 Phase
2 trial.

On
November 20, 2025, we announced Romania as an additional country to begin screening patients for the expansion phase of its THIO-101
Phase 2 clinical trial which evaluates ateganosine sequenced with an immune checkpoint inhibitor as a third-line treatment for non-small
cell lung cancer (NSCLC).

On
November 21, 2025, we announced that we have enrolled 12 patients from Taiwan, Turkey, Hungary and Poland in the expansion phase
of its THIO-101 Phase 2 trial.

On
December 11, 2025, we announced that the first patient has been dosed in THIO-104 Phase 3 pivotal trial evaluating the efficacy of ateganosine
administered in sequence with a checkpoint inhibitor (CPI) as a third-line treatment for advanced non-small cell lung cancer (NSCLC).
The multicenter, open-label trial is designed to assess overall survival for ateganosine sequenced with a CPI compared to investigator’s
choice of chemotherapy in a 1:1 randomization of up to 300 patients. MAIA has received regulatory approval to screen patients in Taiwan,
Turkey, select European Medicines Agency (EMA) countries, and Georgia. Screening and enrollment are now underway.

On
January 20, 2026, we provided a corporate update on 2025 achievements and highlighted key targeted milestones and growth catalysts for
2026. The targeted milestones include: (i) initial measures of efficacy from Phase 3 study, with interim disease control rates (DCR),
overall response rates (ORR) and progression free survival (PFS) analysis of ateganosine compared to the control arm will support regulatory
discussions; (ii) expected conclusion of Part C of Phase 2 study, which will provide additional clinical efficacy data to support regulatory
review for commercial approval; (iii) Plan to engage in regulatory interactions with the FDA to expand ongoing FDA dialogue under the
Fast Track designation, including discussions around trial enhancements and prospects for Accelerated Approval and Priority Review; (iv)
clinical development of second-generation molecules planned to start in Phase 1 trials, with additional small molecules fully developed
in-house with better expected efficacy compared to ateganosine.

In
addition to NSCLC, HCC, SCLC and CRC we plan to conduct clinical trials evaluating ateganosine (THIO) in sequential combination with
an immune checkpoint inhibitor in several other cancer indications, including solid tumors, such as breast, prostate, gastric, pancreatic
and ovarian cancers.

Our
Science—Driven Telomere Targeting Approach

Telomeres
are regions of repetitive DNA nucleotide sequences that are associated with specialized proteins at the ends of linear chromosomes in
cells. Ateganosine’s mechanism of action comprises telomere targeting and induction of anti-cancer immunogenicity. The enzyme telomerase
recognizes ateganosine’s metabolite formed in situ and incorporates it into the structure of the cancer cell’s telomeres,
creating a faulty structure, which breaks apart the telomere spatial structure. As a result, the ateganosine-modified telomeric structure
unwinds, recognized as DNA damage, and the cancer cells die. We believe ateganosine transforms “cold” tumors into “hot”
tumors rendering them responsive to immunotherapy (checkpoint inhibitors) and this process takes place promptly within 24 to 72 hours.
We also believe we can improve the immunotherapy efficacy and we can restore the immunotherapy efficacy in patients who have progressed
or developed resistance to prior immunotherapy.

Telomere
maintenance is a fundamental biologic process for cell proliferation and resilience in cancer cells and thus represents one of the key
therapeutic targets for cancer treatment. Telomerase is an enzyme that is present in a majority of human cancer cells (over 85% in the
aggregate), across various tumor types. In contrast, its activity is detected in less than 1% of normal cells. Ateganosine has only been
shown to be active in cancer cells that are telomerase positive (TERT+) and actively dividing. Cancer cells are constantly telomerase
positive due to an uncontrolled division process, while a relatively small number of normal cells are telomerase positive only transiently.
Therefore, ateganosine activity is expected to be highly specific to cancer cells versus normal cells. Cancer-specific disturbance of
telomeric structure, mediated by telomerase, is likely to lead to disruption in the cell cycle, followed by a very rapid and telomere-length
independent cell death. Ateganosine was observed in preliminary in vitro and in vivo studies to induce cancer-specific telomere disruption,
by using the enzyme telomerase which differentiates ateganosine from all other available cancer therapies currently in clinical use.
We are also currently developing potential next-generation small molecule telomere modifying agents with the goal of identifying additional
proprietary drug candidates, across multiple cancer types. We have generated eighty-two (82) new telomere-targeting compounds of which
sixty (60) compounds have been evaluated in vitro. Currently, seven (7) molecules have been selected for further evaluation in additional
in vitro and in vivo models.

8

Human
clinical trials prior to approval are typically conducted in three sequential Phases that may overlap or be combined. In Phase 1, the
drug or biologic is initially introduced into healthy human subjects and tested for safety, dosage tolerance, absorption, metabolism,
distribution and excretion. In Phase 2, the drug or biologic is evaluated in a limited patient population to identify possible adverse
effects and safety risks, to preliminarily evaluate the efficacy of the product for specific targeted diseases and to determine dosage
tolerance, optimal dosage and dosing schedule for patients having the specific disease. In Phase 3, larger-scale clinical trials are
undertaken to evaluate clinical efficacy and safety and the overall risk/benefit ratio of the product. Post-approval studies, or Phase
4 clinical trials, may be conducted voluntarily, or as a condition of FDA’s approval of a drug. These studies may be used to confirm
preliminary efficacy results, gain additional experience from the treatment of certain patient populations, or to support additional
indications or labeling changes.

We
completed our selection process for the clinical sites for our Phase 2 study in Australia and Europe and our application to start the
Phase 2 study in Australia was approved on March 1, 2022, by the Australian Regulatory Agency—Bellberry Human Research Ethics Committee.
In July 2022, the first patient was administered with ateganosine in our Phase 2 human trial (THIO-101) in Australia. In December 2022,
regulatory authorities in three European countries, Hungary, Poland, and Bulgaria, approved the implementation of THIO-101, Phase 2 clinical
trial evaluating ateganosine in patients with NSCLC. In July 2025, we initiated an expansion of the THIO-101 trial focused on third-line
NSCLC patients who are resistant to checkpoint inhibitors and chemotherapy.

We
initiated a Phase 3 pivotal trial in 2025, named THIO-104, to evaluate the efficacy of ateganosine administered in sequence with a checkpoint
inhibitor (CPI) in third-line NSCLC patients who are resistant to checkpoint inhibitors and chemotherapy. The multicenter, open-label,
pivotal Phase 3 trial is designed to provide a direct comparison to chemotherapy in a 1:1 randomization of up to 300 patients.

In
March 2022, the FDA granted Orphan Drug Designation (ODD) to ateganosine for the treatment of HCC, in May 2022, the FDA granted the second
ODD to ateganosine for the treatment of small cell lung cancer, and in late 2023, a third ODD for Malignant Gliomas Brain Cancer. The
FDA’s Office of Orphan Products Development may grant orphan designation status to drugs and biologics that are intended for the
treatment, diagnosis or prevention of rare diseases, or conditions that affect fewer than 200,000 people in the U.S. ODD provides certain
benefits, including financial incentives, to support clinical development and the potential for up to seven years of market exclusivity
for the drug for the designated orphan indication in the U.S. if the drug is ultimately approved for its designated indication.

In
December 2024, the FDA granted rare pediatric disease designation (RPDD) for ateganosine for the treatment of pediatric-type diffuse
high-grade gliomas (PDHGG). Upon FDA approval of a future new drug application in PDHGG, MAIA would be eligible to receive a priority
review voucher that can be redeemed or sold as an asset. Rare pediatric disease priority review vouchers (PRVs) can be redeemed by drug
developers for FDA priority review of a different product or transferred or sold to another sponsor. Since 2015, FDA priority review
vouchers have sold as assets at an average amount of $100 million.

In
July 2025, the FDA granted fast track designation (FTD) for the treatment of NSCLC. Ateganosine is currently being evaluated in a pivotal
Phase 2 THIO-101 clinical trial evaluating its anti-tumor activity when followed by a checkpoint inhibitor. The FDA Fast Track is a process
designed to facilitate development and expedite the review of drugs for treating serious conditions and filling an unmet medical need,
as in providing a therapy where none exists or which may be potentially better than available therapy. If relevant criteria are met during
the Fast Track process, a drug will be eligible for FDA Accelerated Approval and Priority Review.

9

Our
Second Generation Molecule Candidates

We
have initiated an early-stage research and discovery program aimed at identifying new compounds capable of acting through similar mechanisms
of activity as ateganosine, such as the targeting and modifying telomeric structures of cancer cells through cancer-cell intrinsic telomerase
activity. The main objective for this program is to discover new compounds with potentially improved specificity towards cancer cells
relative to normal cells and with potentially increased anticancer activity. This program may also allow us to strengthen our patent
portfolio. Although the program is in early stages and we may not be able to identify suitable compounds, we believe we will be able
to create a second generation of ateganosine-like compounds.

Our
current 2nd-generation pipeline of potential telomere-targeting agents includes seven compounds that have successfully undergone in vitro
inhibitory testing in five cancer models. The data from those studies showed a significantly lower 50% inhibitory concentration (IC50)
for those compounds compared to ateganosine. Based on those data, we have progressed those seven compounds to in vivo testing. In January
2023, we nominated one lead new molecular entity candidate (designated as MAIA-2021-20) and one back-up new molecular entity candidate
(MAIA-2022-12) for further advancement into preclinical GLP-toxicity and other studies and may advance one of these candidates into human
clinical trials upon completion of the required preclinical evaluations. A third candidate (MAIA-2021-029) was selected in June 2023.

MAIA has filed three different families of patent applications that cover
its 2nd-generation of compounds. One family (Dinucleotides and Their Use in Treating Cancer) is filed in the US, AU, BR, CA, CH, EPO,
KR, MX, JP and TW. The second family (Tumor Redox-Activated 6-thiopurine Containing Dimer Compounds) has been filed in the US, AU, BR,
CA, CN, EP, IL, JP, KR, MX, RU, and SG. The third patent application (Dinucleotides And Their Use In Treating Cancer) has been filed in
the US and under the PCT (Patent Cooperation Treaty) and will undergo national phase filings in March 2026.

OUR
PIPELINE

Our
robust pipeline includes several targeted immuno-oncology candidates for relapsed and refractory cancers.

10

Our
Therapeutic Strategy

Our
goal is to be the leader in the discovery, development and commercialization of cancer telomere targeting agents and other similar small
molecules. Our initial focus is to efficiently advance our clinical programs with ateganosine in sequential combination with a checkpoint
inhibitor for the treatment of NSCLC. Ultimately, our goal would be to position ateganosine as a patient anticancer immunity priming
treatment for all immune-activating agents used in the treatment of cancer. To date THIO-101 and THIO-104 are the only clinical trials
testing ateganosine in combination with a checkpoint inhibitor. The key elements of our strategy are to:

●
Advance
our existing clinical programs, including seeking accelerated approval for ateganosine in NSCLC as a tumor mass-reducing and simultaneously
immune system priming agent administered in advance of the immune-activating agent, cemiplimab for treatment of advanced NSCLC, and
ultimately, as a cancer treatment foundation in multiple indications and geographies. Even if granted, accelerated approval status
does not guarantee an accelerated review or marketing approval by the FDA.

●
Broaden
the clinical development of ateganosine by exploring synergistic administration prior to other standard-of care immune-therapies
including cell therapy.

●
Develop
a franchise of telomere-targeting cancer treatments.

●
Leverage
our regulatory strategy to acquire additional human data faster outside U.S. for other cancer indications.

●
Selectively
enter into strategic collaborations with pharmaceutical and biotechnology companies that have immune activating therapies.

●
Expand
our existing intellectual property portfolio.

We
will face certain challenges in implementing our business strategy including, among others, the fact that earlier development of ateganosine
was not commercially pursued. Even if ateganosine successfully advances through clinical studies and towards approval for use, we may
face early competition from generic alternatives to ateganosine after expiration of any applicable regulatory exclusivities.

Ateganosine
Market Opportunity and Unmet Medical Need

Most
cancer cells are telomerase positive (TERT+), including 57% to 100% of primary human cancers dependent upon tumor type, indicating a
significant potential therapeutic utilization for ateganosine across most of the tumor types. We believe successful targeting of telomeres
in TERT+ cancers may represent a significant potential for broad therapeutic utilization.

Tumor
Type

TERT(+)

Tumor
Type

TERT(+)

Non-Small
Cell Lung Cancer (NSCLC)

78%

Pancreatic
Cancer

95%

Colorectal
(CRC)

82-89%

Small
Cell Lung Cancer (SCLC)

100%

Hepatocellular
Carcinoma (HCC)

79-86%

Ovarian
Cancer

91%

Breast
Cancer

88%

Renal
Cell Carcinoma (RCC)

83%

Prostate
Cancer

90%

Glioblastoma
Multiforme (GBM)

75%

Bladder
Cancer

92%

Neuroblastoma

94%

Head
& Neck Squamous Cell Carcinoma (HNSCC)

86%

Lymphoma
(high grade)

100%

Gastric
Cancer

85%

Chronic
Myeloid Leukemia (CML)

71%

Melanoma

83-86%

Chronic
Lymphocytic Leukemia (CLL)

57%

Cervical
Cancer

100%

Acute
Myeloid Leukemia (AML)

73%

Sources:
A Survey of Telomerase Activity in Human Cancer – JW Shay, S Bacchetti – European Journal of Cancer, 33,5,787-791, 1997.
Telomerase Active in Human Liver Tissues; H Tahara, et al; Cancer Research 55, 2734-2736 1995; Highly /aggressive Metastatic Melanoma
Cell Unable to Maintain Telomere Length; N Viceconte et al; Cell Reports 2017; Clinical Relevance of Telomerase Status and Telomerase
Activity in Colorectal Cancer; T Femandez et al; PLOS one 2016; and Telomeres, Telomerase, and Cancer: Mechanisms, Biomarkers, and Therapeutics;
Shou et al; Experimental Hematology & Oncology 14:8 2025.

11

Our
initial development program will focus on Non-Small Cell Lung Cancer (NSCLC), Colorectal Cancer (CRC), Hepatocellular Carcinoma (HCC)
and Small Cell Lung Cancer (SCLC) in areas of clear unmet need and/or areas with deficient immunotherapy effect within each tumor type.
Each tumor type and area of unmet or undermet needs represent significant clinical and commercial opportunity. We believe that ateganosine
offers a desirable profile with significant commercial potential.

Tumor Type

Incidence

2022 (M)

5-Year

Prevalence

2022 (M)

Mortality

2022 (M)

Annual

Sales

2025 ($B)

Annual

Sales

2029 ($B) (projected)

Non-Small Cell Lung Cancer
2.1
2.7
1.5
30.8
48.9

Breast
2.3
8.1
0.7
26.2
31.1

Prostate
1.5
5.0
0.4
16.1
22.5

Colorectal
1.9
5.7
0.9
17.1
20.3

Liver
0.9
1.1
0.8
3.1
5.5

Small Cell Lung Cancer
0.4
0.5
0.3
1.9
2.4

Sources:
Global incidence, prevalence, mortality (Global Cancer Observatory / WHO); Global sales (Global Data; BioSpace).

The
table below reflects the current market for checkpoint inhibitors because there is no current market for ateganosine-like molecules.
The years in the indication columns on the table below signify the timing of FDA approval in the US for the clinical indications of interest.
Because the key element of our strategy is to develop ateganosine to work in combination with check-point inhibitors, if ateganosine
is eventually approved by the FDA for use in conjunction with check-point inhibitors, this table provides a high-level understanding
of the potential market for ateganosine in that combination. There is no assurance, however, that any potential market for ateganosine
would follow the current landscape for checkpoint inhibitor franchises.

Current
Landscape of Checkpoint Inhibitor Franchises

2024

Sales

Indications (tumor
NSCLC
SCLC
CRC
HCC

Drug
Company
($B)
types)
Year of FDA Approval

KEYTRUDA (pembrolizumab)
Merck
29.4
20
2015
2019
2017
2018

OPDIVO (nivolumab)
BMS / Ono
10.2
11
2015
2018
2017
2017

TECENTRIQ (atezolizumab)
Genentech / Roche
4.1
6
2016
2019

2020

IMFINZI (durvalumab)
AstraZeneca
4.7
5
2018
2020

2022

LIBTAYO (cemiplimab)
Regeneron
1.2
3
2021

TEVIMBRA (tislelizumab)
BeOne Medicines
0.4
4
2024

TYVYT (sintilimab)
Eli Lilly / Innovent
0.6
3

BAVENCIO (avelumab)
Pfizer / Merck AG
0.6
3

JEMPERLI (dostarlimab)
GSK
0.6
2

TOTAL

51.8

Source:
BioMed Tracker 2025

12

Intellectual
Property

Our global patent and patent-pending estate covers
several areas. Telomerase mediated telomere altering compounds and treatment of therapy-resistant cancers. Further, ateganosine’s
immunogenic treatment strategy, which focuses on sequential combination with checkpoint inhibitors has been filed worldwide. With respect
to ateganosine IP, we maintain three (3) issued US patents, nine (9) issued foreign patents and have four (4) pending US patent applications
and eleven (11) pending foreign patent applications.

Our
goal is to obtain, maintain and enforce patent protection wherever appropriate for our product candidates, formulations, processes, methods
and any other proprietary technologies, and operate without infringing on the proprietary rights of other parties, both in the United
States and in other countries. Our practice is to actively seek to obtain, where appropriate, intellectual property protection for our
current product candidates and any future product candidates, proprietary information, and proprietary technology through a combination
of patents, protection of proprietary know-how and trade secrets, and contractual arrangements, both in the United States and abroad.
However, full patent protection may not provide us with complete protection against competitors who may seek to circumvent our intellectual
property. Our success will depend on the skills, knowledge, experience and know-how of our management research and development personnel,
as well as that of our advisors, consultants, and other contractors. To help protect our proprietary know-how that is not patentable,
we seek to put in place appropriate internal policies for the management of confidential information requiring all our employees, consultants,
advisors, and other contractors to enter into confidentiality agreements that prohibit the disclosure of confidential information, and
which will require disclosure and assignment to us of the ideas, developments, discoveries, and inventions important to our business.
See “Risk Factors – Risks Related to our Intellectual Property” for additional information.

We
file for patents, both directly and in collaboration with our licensing partners, in the United States with counterparts in certain countries
in Europe and certain key market countries in the rest of the world, thereby covering the major pharmaceutical markets.

On
December 8, 2020, we entered into an amended and restated agreement (of our prior November 29, 2018 agreement) with The Board of Regents
of The University of Texas System on behalf of The University of Texas Southwestern Medical Center (collectively, UTSW). Pursuant to
the amended and restated agreement, which we refer to as the UTSW1 Agreement, we obtained (1) an exclusive, worldwide license to develop
and commercialize the following patent families, which are generally directed to methods of using ateganosine and are owned and/or controlled
by UTSW:

THIO
(ateganosine) Intellectual Property

a.)
US patent no. 10,463,685 entitled, Telomerase Mediated Telomere Altering Compounds issued in the US on November 5, 2019. The patent
claims priority to U.S. application No.14/247,967. Related foreign patents based on PCT/US2014/033330 have also issued in the following
foreign countries, CA, EPO (validated in AT, BE, CH, CZ, DE, ES, FR, GB, HU, IE, IS, IT, LI, LU, MC, NL, PL, PT), MX, NZ, and RU
(all method of use). The application is pending in BR, and SG.

b.)
6-Thio-2’-Deoxyguanosine (6-Thio-dG) Results in Telomerase Dependent Telomere Dysfunction and Cell Death in Various Models
of Therapy-Resistant Cancer Cells (Method of Use) / PCT/US2017/O34706 (WO2017/0205756), is issued in CA (patent No. 3035533), pending in the US, and EPO.

c)
Use of 6-thio-dG to Treat Therapy-Resistant Telomerase positive Pediatric Brain Tumors /

pending in the US (U.S. application No. 18/511,417) and has received a Notice of Allowance (method of use)

d)
Treatment of Drug Resistant Proliferative Diseases with Telomerase Mediated Telomere Altering Compounds, (issued in the US as patent
no.12,070,472) which was based on US application No.16/450,430. A continuation of application 16/450,430 is pending (US application
No. 18,781,413).

and
(2) a non-exclusive worldwide license to develop and commercialize related technology rights. The UTSW1 Agreement includes an
exclusive license to US patent no. 10,463,685 (expires April 8, 2034), and US patent no. 12,070,472 (having an anticipated
expiration of March 23, 2037), and patent application No. 18/511,417 (having an earliest expiration of March 22, 2039, if a patent
is granted). All patents are method of use.

13

On
December 23, 2020, we entered into a second agreement with UTSW, which granted the Company option rights in the UTSW1 Agreement and obtaining
additional license rights. This second license with UTSW, which we refer to as the UTSW2 Agreement, we obtained (1) an exclusive, worldwide
license to develop and commercialize the following UTSW patent family:

Sequential Treatment of Cancers Using 6-Thio-dG and Checkpoint Inhibitors

PCT/US2021/022090, issued in the RU, EP (validated in AL,
AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HU, IE, IS, IT, LI, LT, LU, MC, MK, MT, NL, NO, PL, PT, RO, SE, TR) (method
of use), pending in AU, BR, CA, CN, IL, JP, KR, MX, and SG.

and
(2) a non-exclusive worldwide license to develop and commercialize related technology rights. The UTSW2 Agreement includes an
exclusive license to issued US patent no. 12,097,213 (having an earliest expiration of July 28, 2041, which includes 138 days of
patent term adjustment). This patent is generally directed to methods of using ateganosine in combination with immune checkpoint
inhibitors.

On
July 13, 2022, MAIA Biotechnology filed PCT/US23/70177, US 18/352,220, and TW 112126229, Dinucleotides and their use in treating cancer,
for Dinucleotide compounds that target telomers in cancer cells and method for using the dinucleotide compounds in treating cancers alone
and in combination with other anticancer-agents and therapies, such as in combination with checkpoint inhibitors and radiation therapy.
Pending in AU, BR, CA, CH, EPO, KR, MX, JP, US, and TW.

On
May 30, 2023, MAIA Biotechnology filed PCT/US2024/031754, Tumor Redox-Activated 6-Thiopurine containing dimer compounds, for 6-thiopurine
containing compounds that target telomers in cancer cells and methods for using the compounds in treating cancers alone and in combination
with other anticancer agents and therapies. Pending in AU, BR, CA, CN, EPO, IL, KR, MX, RU, and SG.

On October 29, 2024, MAIA Biotechnology filed PCT/US2024/053473 and US
application No. 18/930,974, entitled Telomere-Targeting Phosphatidyl-THIO Conjugates, for Telomere-targeting phosphatidyl-THIO conjugates
that target telomers in cancer cells and methods for using the telomere-targeting phosphatidyl-THIO conjugates compounds to treat cancers.
The applications are pending in the PCT and US.

On
August 13, 2025, MAIA Biotechnology was granted a patent by the European Patent Office application No. 20155920.0, entitled Mercaptopurine
Ribonucleoside Analogues for Altering Telomerase Mediated Telomere, covering a portfolio of ateganosine-based analogues for telomere
targeting anticancer therapy and methods of using ateganosine alone or before administration of checkpoint inhibitors. The patent was
granted and validated in AT, BE, BG, CH, CY, DE, DK, ES, FI, FR, GB, GR, HU, IE, IT, LI, LT, MK, MT, NL, NO, PL, PT, RO, SE, SI, and
TR.

We
continually assess and refine our intellectual property strategy as we develop new technologies and therapeutic candidates. As our business
evolves, we may, among other activities, file additional patent applications in pursuit of our intellectual property acquisition and
protection strategy, to adapt to competition or to seize potential opportunities.

Our
Team

We
have assembled an experienced management team with deep research, development, and commercialization experience in the areas of telomere-related
science, immunotherapy, and across a vast array of oncology indications.

Key
Team highlights:

●
Our
team is led by our Co-founder, Chief Executive Officer and President Vlad Vitoc. He is an M.D. and M.B.A. with over 25 years of experience
in the Pharmaceuticals and Biotechnology industries. He has served on leadership teams in various oncology companies and business
units and has a track record of success at Bayer Pharmaceuticals, Astellas Pharma Inc., Cephalon Inc. and Incyte Corporation, including
development and commercialization of major oncology brands, organizational capability building, talent recruiting and development,
and functional leadership.

●
Our
Chief Scientific Officer, Sergei M. Gryaznov, is a Ph.D. who is an internationally recognized scientist and expert in the areas of
modern drug discovery and development, oncology, telomerase, immune-regulatory therapeutics, nucleosides, nucleotides, DNA and RNA
analogues, lipid and other conjugates, small molecules and nucleic acid based therapeutic agents. He is the co-inventor of a novel
telomere-by-telomerase-targeting therapeutic approach to potential cancer treatment and responsible for leading the research team
that characterized ateganosine’s telomere targeting activity.

14

●
Our
Head of Finance and principal financial and accounting officer, Jeffrey Himmelreich, has extensive finance, accounting and public
company reporting experience. Prior to his recent appointment, since September 2023, Mr. Himmelreich acted as the Company’s
Director of Accounting and Financial Reporting, where he provided oversight for the Company’s filings with the U.S. Securities
and Exchange Commission (“SEC”) and other related financial, accounting or reporting matters. From July 2021 to September
2023, Mr. Himmelreich acted as the Chief Financial Officer of Microtech Knives, Inc., a private manufacturer of hand tools. Further,
from December 2018 to July 2021, Mr. Himmelreich served as the Director of Finance and Accounting at Avadim Health Inc., a healthcare-related
private company, during which time he assisted with SEC filings of Avadim Health Inc. for a proposed initial public offering. Mr.
Himmelreich has a Bachelor of Science (B.S.) in Accounting from the Indiana University of Pennsylvania, and a Master of Business
Administration from Pennsylvania State University.

We
have engaged the following advisors, who are leading, internationally recognized experts in oncology, telomeres and telomerase research,
to be a part of our Scientific Advisory Board (“SAB”), which provides independent non-binding scientific advice to our management
team in the roles detailed below under each member’s name:

1.
Tudor
Ciuleanu, M.D., Ph.D. – Professor of Oncology (University of Medicine and Pharmacy, Cluj-Napoca, Romania)

●
Top
Key Opinion Leader (KOL) in NSCLC and CRC in Europe

●
Key
investigator in more than 90 phase 3 and Phase 2 clinical trials, including most immune therapy agents

●
One
of the best published clinical investigators (appears in most references in the National Comprehensive Cancer Network (NCCN) guidelines)

●
President
of Romanian Federation of Cancer Societies

●
Editor
for the Journal of Clinical Oncology (JCO), Romanian edition

●
On
our SAB, will lead clinical activities in Europe across tumor types – NSCLC, CRC, Gastric, HCC, Head and Neck, Urological cancers,
and Lymphomas

2.
Jerry
Shay, Ph.D. – Professor and Vice Chairman of the Department of Cell Biology (University of Texas Southwestern)

●
One
of the world leaders in the study of telomeres and telomerase

●
Scientific
co-founder of the research supporting our lead program ateganosine and an integral advisor to the program

●
Highly
influential biomedical researcher with over 30 issued patents and more than 500 peer reviewed publications

●
Southland
Financial Corporation Distinguished Chair in Geriatric Research and a Distinguish Professor at University of Texas Southwestern,
having received the University of Texas Regent’s Outstanding Teaching Award and the Minnie Steven Piper Foundation Professor
Award

●
Awarded
the Eunice Kennedy Shriver NIH Alliance Pioneer Award in 2017

●
On
our SAB, Dr. Shay will provide scientific leadership as the ateganosine co-inventor and a worldwide recognized expert in the science
of telomeres and telomerase in cancer. Dr. Shay serves as the Chairman of the SAB.

3.
David
Ashley, M.D., Ph.D. – Professor of Neuro-Oncology (Duke University)

●
Top
KOL in pediatric and adult neuro-oncology

●
Expert
in translational research and clinical development

●
Expert
in immuno-oncology, having developed and clinically tested dendritic cell vaccines and other immuno-therapeutics

●
Principal
investigator of a number of important national and international studies, both clinical and pre-clinical

●
Former
Director of two major cancer centers, The Royal Children’s Hospital Melbourne and Andrew Love Cancer Centre – Barwon
Health

●
On
our SAB, will assist in translational research in Brain Cancers for clinical development

15

4.
Gunnur
Dikmen, M.D., Ph.D. – Professor at Hacettepe University Medical Faculty, Department of Medical Biochemistry, as well as the
director of the Hacettepe University hospital’s emergency laboratory

●
Broad
range of experimental and clinical experience in molecular & cell biology and clinical biochemistry, translating research results
from bench to bedside and from academia to clinical laboratory to mentor the next generation of multidisciplinary research projects
by providing new therapeutic approaches for cancer and telomere related diseases

●
Expert
in the biology of telomeres and telomerase in the treatment of cancer

●
Under
her capacity as Secretary-General of the Turkish Biochemical Society, organized various important national and international courses
and congresses

●
On
our SAB, will assist in preclinical and translational research, across tumor types

5.
Adam
Yopp, M.D. – Associate Professor and Division Chief of Surgical Oncology and Colorectal Surgery, at Harold C. Simmons NCI-designated
Comprehensive Cancer Center at UT Southwestern Medical Center in Dallas

●
Completed
a fellowship in surgical oncology at Memorial Sloan-Kettering Cancer Center focusing on upper GI and hepatopancreatobiliary malignancy
and joined UT Southwestern in 2009

●
Director
of the Liver Tumor Program at UTSW and both his research and clinical interests are focused on the delivery of care in patients with
primary liver cancer

●
Much-recognized
key opinion leader in liver cancer

●
On
our SAB, will assist with developing ateganosine for the treatment of liver cancer

6.
Remus
Vezan, M.D., Ph.D. – Vice President, Global Clinical Development at BeOne Medicines, formerly known as BeiGene

●
Completed
his medical training (M.D. and Ph.D.) at the University of Medicine and Pharmacy Cluj, Romania and University of Bern, Switzerland

●
Seasoned
leader in drug development of novel therapeutic modalities, including cell and gene therapies, with over 20 years of academic and
biopharmaceutical industry experience, and had a seminal contribution to the development and approval of multiple products, including
TECARTUS®, YESCARTA® or IMBRUVICA®

●
On
our SAB, will assist in development and strategy for approval of ateganosine in multiple tumor types

7.
Saadettin
Kiliçkap, M.D., M.Sc – Faculty member at İstinye University Faculty of Medicine, Department of Internal Medicine,
Türkiye

●
Graduated
from Gazi University Faculty of Medicine, completed his Internal Medicine specialty training at Hacettepe University Faculty of Medicine.
Completed the education programme of Medical Oncology at Hacettepe University Oncology Institute and the Cancer Epidemiology Thesis
Master’s Program at Hacettepe University Oncology Institute Preventive Oncology Department, granting him the title of “Master
of Science”

●
Received
more than 20 oral presentations or best work awards at national congresses, has more than 240 scientific articles published in international
peer-reviewed journals and more than 50 papers presented at international congresses. He took part as principle or sub-investigator
in more than 50 national and international multicenter phase 2 and phase 3 clinical studies

●
On
our SAB, will assist in development and strategy for approval of ateganosine in multiple solid tumor types, including lung cancer,
breast cancer, melanoma, and the gastrointestinal tract

16

8.
David
J. Pinato, MD, MRCP (UK) FRCPath, MRes, PhD – Director of Developmental Cancer Therapeutics at Imperial College in London (UK).

●
David
has led the inception of a portfolio of first-in-class studies of immune checkpoint inhibitors in liver cancer, which has represented
David’s focus of research since graduation with highest honors at the University of Piemonte Orientale “A. Avogadro”
in Novara, Italy.

●
David
was a three-time recipient of a Merit Award from the American Society of Clinical Oncology (ASCO) in 2016, 2017, 2019 as well as
a fourth Merit Award jointly awarded by ASCO and by the Society for Immunotherapy of Cancer (SITC) in 2019.

●
On
our SAB, will assist with developing ateganosine for the treatment of liver cancer

9.
Claudia
A.M. Fulgenzi, M.D. – Specialist in Medical Oncology at Imperial College in London (UK)

●
Graduated
in Medicine from the University of Rome Tor Vergata in 2017 and subsequently specialized in Medical Oncology at the University Campus
Bio-Medico of Rome, Italy. During her training, Dr. Fulgenzi developed a strong interest in gastrointestinal cancers, particularly
hepatobiliary malignancies.

●
Her
contributions to the field have been recognized with several prestigious awards, including the ASCO Merit Award and the Young Investigator
Award from the International Liver Cancer Association (ILCA) in 2022, followed by another Merit Award from the American Society of
Clinical Oncology in 2023.

●
On
our SAB, will assist with developing ateganosine for the treatment of liver cancer

Our
SAB is primarily compensated by way of the grant of stock options as determined by the Company as appropriate in recognition of the specific
services or areas of expertise of each member. We are also supported by a seasoned board of directors, whose members have significant
entrepreneurial skills in company building and corporate financing as well as decades of collective leadership and board experience.

Our
Programs

Telomere
Targeting Program

Targeting
Telomeres via Telomerase Leads to Cancer Cell Death

Telomeres
are regions of repetitive nucleotide sequences that are associated with specialized proteins at the ends of linear chromosomes, that
represent a critical key therapeutic target for cancer. Telomeres are often depicted in imagery like the end of a shoelace.

Adapted
from Transcendental Meditation and lifestyle modification increase telomerase, December 6, 2015.

●
Maintenance
of telomeres is essential for unlimited cellular proliferation and confers immortality in cancer cells. Telomeres in human cells
consist of double-stranded and single-stranded repeats of the sequence TTAGGG, which terminate in a single-stranded 3´- extension
overhang of the G-rich strand. Their major function is to cap and protect the ends of chromosomes and thus to provide genetic stability.
This capping function is mediated by a special architecture in which the 3´- overhang participates with telomere-binding proteins
in a large loop structure called T-loop. The image on the right reflects the general location of telomeres as the end-cap of the
chromosomes, which are located in the nucleus of the cell.

17

The
most successful anti-cancer drugs in the market today typically interfere with only one of the specific capabilities or “hallmarks”
cancer cells use for tumor growth and progression. In contrast, our lead drug candidate, ateganosine, targets two major hallmark pathways:

●
Targeting
cancer cell telomeric DNA structure and functional integrity; and

●
Activating
the immune system that turns immunologically “cold” tumors into “hot” tumors that are responsive to therapy.
ateganosine synergizes with immune activating agents, like checkpoint inhibitors, for the potential to attack and destroy tumors.

The
chart below reflects the many different methods by which successful anti-cancer drugs might prevent tumor growth and where ateganosine
stands in relation to the other approaches.

Adapted
from Cell 2011, Volume 144, Issue 5, Pages 646-674 (DOI:10.1016/j.cell.2011.02.013)

Role
of the Enzyme Telomerase

Telomerase
is a ribonucleoprotein enzyme (reverse transcriptase) that synthesizes telomere repeats from the beginning, or de novo. In human cells,
the telomerase holoenzyme consists of a high-molecular-weight complex with a template region-containing RNA subunit, hTR, and a protein
component, the catalytic subunit human telomerase reverse transcriptase (hTERT). In most normal somatic cells, telomerase activity is
absent and telomere repeats are lost with cell division and with aging. Telomerase is especially important in fetal tissues, reproductive
cells and other tissues where extensive cell proliferation is necessary. However, most adult normal tissues are telomerase silent. Telomere
attrition, beyond a certain threshold, results in the uncapping of chromosome ends, which subsequently induces DNA damage and onset of
replicative senescence. In contrast, about 57% to 100% of all cancer cells in most tumor types have detectable telomerase activity, which
leads to the stabilization of telomeres and allows for unlimited growth potential along with disease progression. Successful targeting
of telomerase positive (TERT+) cancers represents a significant potential for therapeutic utilization in almost all tumor types.

Since
most cancer cells are reliant on telomerase for their survival, and telomerase is undetectable or only transiently present at low levels
in normal cells, telomeres of cancer cells and telomerase are attractive targets for the development of new cancer therapeutics. “Proof
of Principle” for validation of telomere structural integrity-targeting as a therapeutic concept was demonstrated in vitro in human
tumor cells using dominant negative mutant forms of hTERT. In these experiments, telomerase activity was abolished, which was associated
with continuous telomere shortening, subsequently leading to the cancer cells death. Research has also indicated that cancer cell specific
anti-telomeres and anti-telomerase therapies may have fewer side effects than more traditional treatments, such as chemotherapy or radiotherapy.
This has made anti-cancer therapies based on telomerase inhibition an area of interest in medicine. However, attempts to directly target
telomerase in clinical trials have not yet produced an approved drug, as these efforts have encountered material limitations primarily
due to increased toxicities that may result from the long lag period between initiation of anti-telomerase treatment and its therapeutic
effects.

18

Differentiated
Activity of Ateganosine, a Telomere-Targeting Agent

Ateganosine
(THIO, 6-thio-2’-deoxyguanosine or 6-thio-dG) is a small molecule telomere targeting agent that uses the enzyme telomerase for
DNA integration predominantly in the telomeric structure. Based on pre-clinical studies, ateganosine’s telomere targeting activity
is believed to be primarily cancer-specific in tumor cells with active telomerase, but not in normal cells. Based on our extensive review
of publicly-available information, to our knowledge ateganosine’s direct telomere targeting action utilizing telomerase is different
from other commercially available cancer therapies and those currently in publicly disclosed clinical trials. Telomeres, along with the
enzyme telomerase, play a fundamental role in the survival of cancer cells and their resistance to current therapies. The statements
above are not intended to give any indication that ateganosine has been proven effective or that it will receive regulatory approval.

In
non-clinical studies, published initially in 2014 along with subsequent studies, ateganosine was found to be converted, in cells, into
the substrate recognized by telomerase, and then incorporated into telomeres of the cancer cells. Once incorporated, ateganosine compromised
the cancer cell’s telomere structure and function, leading to “uncapping” of the telomeres, induction of DNA damage
responses, and rapid cancer cell death. These profound structural modifications of cancer cell telomeres were irreparable. In both in
vitro and in vivo studies, ateganosine showed a very prompt effect, causing telomere uncapping and leading to cancer cell death, independent
of the initial tumor telomere length.

The
above graphic represents an established method of action from previously conducted research in rodents that forms the scientific rationale
for further clinical studies.

In
2019, further non-clinical research in syngeneic and humanized mouse models of telomerase-expressing cancers uncovered previously unknown
telomere targeting activity of ateganosine specifically resulting from its breakdown of cancer cells. The ateganosine-containing DNA
fragments, resulting from ateganosine telomere disruption, are packed into micronuclei and are released from the treated cancer cell
into the blood stream, which enhances immune responses. An immune response was observed, attributed to stimulation of the cGAS/STING
pathways in the host APCs (Dendritic Cells, pDCs), as well as activation of NK cells and CD 8+ and CD 4+ lymphocytes in vivo. At the
same time as the T-cells activation, ateganosine treatment reduced levels of myeloid-derived suppressor cells (MDSCs) in the tumor micro-environment
(TME), which is considered important for an anticancer immune response. While ateganosine activated CD8+ T cells, it also increased the
total number of CD8+ T cells and upregulated PD-1 expression in the CD8+ T cells on per cell basis in the mouse model. This research
demonstrated how the ateganosine-produced telomere stress may have the potential to increase innate sensing and adaptive anti-tumor immunity.
In short, this immune system stimulation and TME remodeling proceeded in a specific antigen-dependent manner and induced adaptive immune
responses that eradicated remaining cancer cells in vivo.

19

The
above noted recent studies in a humanized mouse model also supported the hypothesis that sequential administration of ateganosine followed
by an anti-PD-L1type of checkpoint inhibitor may overcome resistance to checkpoint blockade in advanced cancer models, suggesting that
the combination therapy could benefit PD-L1-resistant patients.

Administration
of low doses of ateganosine, aimed to activate the immune system via ateganosine-induced telomeric DNA modification, followed by checkpoint
inhibitor therapy (anti-PD-L1 or anti-PD1), eliminated advanced tumors in preclinical models with confirmation of cancer cell type specific
immune memory. This potential for ateganosine to induce immune memory, if confirmed in human clinical trials, would be a distinct feature
of ateganosine’s mechanism of action, offering the possibility that the immune system may continue to be active against the cancer
cells over extended periods of time, potentially reducing the need for additional treatment.

These
pre-clinical results provided the basis for our new clinical therapeutic strategy for sequentially administering ateganosine as a telomere-targeted
agent first, to activate the immune system against the specific cancer, followed by immunotherapy or other immune-activating therapy.

Limitations
of Other Therapeutic Approaches

In
contrast to ateganosine, which targets telomeres, a challenge for the potential clinical application of pharmaceutically useful telomerase
inhibitors (e.g., Imetelstat), is the therapeutic window (the range of dosage of a drug or of its concentration in a bodily system that
provides safe effective therapy) and the often-observed delay between initiation of treatment and phenotypic response (called the “lag
period”). Since the antiproliferative effect of any direct telomerase inhibitor is dependent on the telomere length of any given
tumor cell, clinical response will be delayed until the telomeres become critically short, and thus can no longer protect the chromosomes,
and as a result, the cancer cell dies. This requires a significant number of cell divisions to become apparent, and treatment may have
to be given continuously for weeks to months, potentially in conjunction with other treatment modalities, to achieve an appropriate level
of efficacy.

20

Ateganosine:
A Telomere Targeting Agent

Background

Ateganosine
(THIO, 6-thio-2’-deoxyguanosine) is a synthetically-modified small molecule nucleoside that was originally designed to be an improved
chemotherapy drug developed to work around purine analog resistance, which was standard-of-care therapy in the 1970s. Sponsored by the
National Cancer Institute, ateganosine was extensively investigated in at least 19 clinical trials with over 600 cancer patient subjects
(adult and pediatric) treated, both as monotherapy or in combination with other commonly used standard agents of the time. See “Ateganosine
Clinical Trials” below for more information about these trials. A traditional treatment strategy was used where patients were treated
to maximum tolerated dose (MTD), a common approach for cancer therapy drug development. Although study results were promising, development
was abandoned in favor of other therapies.

The
previous human experience presents significant limitations as it dates to the 1970s and early 1980s when the implementation of ICH Good
Clinical Practices was not yet in effect. The published studies did not disclose certain data points in line with the current ICH Good
Clinical Practices, such as efficacy endpoints and serious adverse events, whether those endpoints were reached, whether the data was
found to be statistically significant and serious adverse events. Further, we do not know whether those prior studies were powered for
statistical significance in the way our planned studies will be powered, based generally on the results of these prior human studies,
we believe that ateganosine has a well-established safety profile, which we intend to independently demonstrate through our own clinical
studies. Moreover, all prior studies were conducted primarily in heavily pre-treated, refractory patients.

Further
detailed analysis of the body of prior ateganosine research indicates researchers were not aware of three key factors, which if they
had been known at the time, may have impacted the decision to cease development. These factors have only been discovered since 2014 (with
the most recent in 2019), as illustrated in the following graphic:

1.
Ateganosine’s
detailed telomere targeting mechanism and resulting immune activation.

2.
At
high drug exposure (MTD), ateganosine can be immunosuppressive.

3.
Proper
administration of ateganosine to activate the immune system followed by immunotherapy to achieve best response.

Telomeres
are vital DNA-structures discovered by Jack Szostak’s laboratory, for which he received the Nobel Prize in 2009, which are present
at the ends of each chromosome which protect the genome from degradation, unnecessary recombination, repair, and interchromosomal fusion.
Telomeres, along with the enzyme telomerase, are both crucial for the survival of cancer cells. Telomerase was discovered by Elizabeth
Blackburn and Carol Greider, who shared the Nobel Prize with Jack Szostak in 2009.

Ateganosine
is believed to selectively target telomerase positive (TERT+) cancer cells, where the enzyme is activated, versus normal cells. 57% to
100% of primary human cancers are TERT+ dependent upon tumor type, indicating a significant potential therapeutic utilization for ateganosine
in almost all tumor types. Ateganosine’s cancer-specific disturbance of telomeric structure by telomerase leads to disruption in
the cell cycle, followed by rapid cell death. Based on extensive review of publicly-available information, ateganosine’s direct
telomere targeting action utilizing telomerase is different from other commercially available cancer therapies and those currently in
publicly disclosed clinical trials.

In
2019, the MAIA research team showed that in mouse models ateganosine-produced telomere modification and disruption induced cancer-specific
innate and adaptive immune response against immunologically “cold” or unresponsive tumor types. When ateganosine was administered
at low doses, in syngeneic and humanized mouse models of telomerase-expressing cancers, followed by a break to allow for the activation
of the immune system against the specific cancer, then followed by a standard-of-care immunotherapy agent like a check point inhibitor
(CPI), either PD-1 or PD-L1, complete tumor regression was observed, with no observed toxicities. These effects have been replicated
in multiple preclinical models, utilizing all leading checkpoint inhibitors or radiation therapy.

21

Based
on these studies, we hypothesized that ateganosine, administered in advance of immune-activating therapies (e.g., checkpoint inhibitors,
radiation therapy, etc.), at dose levels significantly lower than the levels evaluated in previous clinical trials, will “prime”
the tumor environment and initiate an overall anti-tumor immune response. This represents an entirely new therapeutic approach for ateganosine
and forms the basis for the new clinical strategy for planned future trials.

Ateganosine
Preclinical Development

The
following summarizes the relevant preclinical studies. Extensive preclinical studies have been performed to validate ateganosine’s
primary mechanism of action: targeting telomeres directly and causing cancer cell death via telomerase-mediated DNA damage.

To
our knowledge, ateganosine alone has shown significant telomere targeting activity in numerous non-small cell lung cancer (NSCLC) and
multiple other cancer-based cell lines in vitro and in vivo, including but not limited to small cell lung cancer (SCLC), melanoma, colorectal
cancer (CRC), glioblastoma multiforme (GBM), diffuse intrinsic pontine glioma (DIPG), neuroblastoma, pancreatic, hepatocellular carcinoma
(HCC), as well as head and neck cancer, breast cancer and prostate cancer.

In
vitro: in summary, EC50 values (the concentrations at which half of the total number of cancer cells are dead) were approximately
0.4 µM to 1.5 µM. ateganosine was not cytotoxic in normal, untransformed telomerase-negative cells at concentrations up to
100 µM.

In
vivo: in summary, the doses that resulted in cancer cell death were in the range of 2.5 - 5.0 mg/kg, depending on the tumor type
and the schedule of the drug administration ranging from 1 to 3 days per cycle.

In
March 2022, the FDA granted Orphan Drug Designation (ODD) to ateganosine for the treatment of HCC, in May 2022, the FDA granted the second
ODD to ateganosine for the treatment of small cell lung cancer, and in late 2023, a third ODD for Malignant Gliomas Brain Cancer). The
FDA’s Office of Orphan Products Development may grant orphan designation status to drugs and biologics that are intended for the
treatment, diagnosis or prevention of rare diseases, or conditions that affect fewer than 200,000 people in the U.S. ODD provides certain
benefits, including financial incentives, to support clinical development and the potential for up to seven years of market exclusivity
for the drug for the designated orphan indication in the U.S. if the drug is ultimately approved for its designated indication.

In
December 2024, the FDA granted rare pediatric disease designation (RPDD) for ateganosine for the treatment of pediatric-type diffuse
high-grade gliomas (PDHGG). Upon FDA approval of a future new drug application in PDHGG, MAIA would be eligible to receive a priority
review voucher that can be redeemed or sold as an asset. Rare pediatric disease priority review vouchers (PRVs) can be redeemed by drug
developers for FDA priority review of a different product or transferred or sold to another sponsor. Since 2015, FDA priority review
vouchers have sold as assets at an average amount of $100 million.

In
July 2025, the FDA granted fast track designation (FTD) for the treatment of NSCLC. Ateganosine is currently being evaluated in a pivotal
Phase 2 THIO-101 clinical trial evaluating its anti-tumor activity when followed by a checkpoint inhibitor. The FDA Fast Track is a process
designed to facilitate development and expedite the review of drugs for treating serious conditions and filling an unmet medical need,
as in providing a therapy where none exists or which may be potentially better than available therapy. If relevant criteria are met during
the Fast Track process, a drug will be eligible for FDA Accelerated Approval and Priority Review (FDA decision within six months).

Ateganosine
in Sequential Administration in Advance of Checkpoint Inhibitors (CPIs) Therapy

In
vivo, ateganosine, at 3 mg/kg/dose, (which corresponds to a 20 mg/patient/day low-dose), administered followed by a one-day break,
followed by an immune checkpoint inhibitor (either anti-programmed cell death protein 1 (PD-1) or anti-programmed death ligand 1 (PD-L1)
products), resulted in complete tumor regression in NSCLC and CRC syngeneic mouse tumor models.

At
this low dose, ateganosine was able to transform immunologically “cold’ tumors, (tumors that do not respond to the CPI treatment),
into immunologically “hot” tumors, which then responded well to the following sequential treatment with a CPI. These potent
anti-tumor phenotypic effects were also accompanied by the efficient induction of the tumor-specific CD8+ cells, as well as CD4+, and
natural killer (NK)-cells (Mender, 2020b).

These
responses were achieved through telomerase-dependent and cancer cell specific activation of a) DNA damage responses, and b) cGAS/STING
pathways by ateganosine. This body of research represents the basis for the new immune-activation treatment strategy.

22

The
following represents key highlights from ateganosine preclinical research:

●
Ateganosine
has been tested in multiple preclinical studies evaluating various tumor types in vitro including in lung, colorectal, prostate,
breast, ovarian, head and neck, brain, melanoma, and liver cancer. Ateganosine has also been tested in in vivo mouse models of lung,
colorectal, brain, melanoma, liver and brain cancers. In the below graphic, the left panel depicts cancer cell colony formation in
vitro assay results conducted with various types of telomerase positive cancers, namely prostate, breast, ovarian, colon, brain,
head and neck. In the control column, cancer cells grew. In the second column, with the telomerase inhibitor BIBR, the cancer cells
also grew. In the third column, in which the telomere targeting agent ateganosine was administered at a concentration of 2.5µM,
cancer cell growth was visibly inhibited. In the fourth column, in which ateganosine was administered at a concentration of 5µM,
cancer cells were also visibly inhibited. The same concentrations of ateganosine were also administered in vivo in rodent models
(mice), caring tumors, derived from either brain, or liver, or melanoma, or neuroblastoma, or colorectal cancer cells were treated
with ateganosine (at 2 mg/kg to 5 mg/kg doses), significant reduction in tumor masses resulting from the treatment with ateganosine
was observed. Note that ateganosine’s activity seen in preclinical models has yet to be demonstrated in humans.

●
Ateganosine
demonstrated potential to selectively cause cancer cell death with active enzyme telomerase versus normal cells in vitro. The below
graphic illustrates formation of telomeric damage foci (TIFs) in telomerase activity-positive cancer cells, but not in normal non-cancerous
cells, resulting from application of ateganosine. These data indicate molecular mechanism of ateganosine that targets telomeric DNA
of cancer cells through their telomerase enzymatic activity. At the same time, normal cells, that are devoid of telomerase activity,
are not affected by ateganosine.

Mender
I. et al., Cancer Discovery (2015)

23

*TIF
– telomere damages induced foci

*TRF2
– protein associated with telomeres

*
Gamma-H2AX – protein associated with induction of DNA damage

*CRC
– colorectal cancer

*hTERT
– protein components of telomerase enzyme

●
Ateganosine,
as a single agent, showed in vitro telomere targeting activity in cancer cells that are resistant to tyrosine kinase inhibitors (TKIs),
checkpoint inhibitors, IL-2, IFNα, YERVOY®(ipilimumab) and a host of chemotherapies. The below graphic, in NSCLC
and Melanoma models respectively, demonstrates in vivo telomere targeting activity of ateganosine in mice models of lung cancer,
derived from PERC16 cells, and melanoma derived from WM4265 cells. Both cell lines are resistant to multiple standard-of-care drug
compounds, as listed in the Figure legends.

*i.p.
– intraperitoneal injection

*IL-2
– cytokine interleukin 2

*IFN-a
– interferon alfa

●
Ateganosine
was observed to penetrate the blood-brain barrier and inhibits tumor growth, inducing in-tumor telomere dysfunction and cancer cell
death, in in vitro models of difficult to treat pediatric brain cancer, where no therapy exists. In the below graphic, this is shown
through presence of Caspase-3 enzyme which is associated with cell death. Sengupta, S. et al. Induced telomere damage to treat telomerase
expressing therapy-resistant pediatric brain tumors. Mol Cancer Therapeutics, 17(7): 1504-1514, 2018.

*TIF
– telomere damage induced foci

*MB004
– brain cancer cell line

24

●
Ateganosine
transformed “cold” tumors into “hot” tumors that were responsive to immunotherapy. Ateganosine utilized a
telomere targeting pathway that synergized with checkpoint inhibitors and other immune-activating therapies. The tumor-specific immune
activation, resulting from ateganosine’s primary mode of action, overcame resistance to current check point inhibitor (CPI)
standard-of-care therapy, as illustrated in the following Colorectal Cancer model. The below graphic demonstrates telomere targeting
activity of ateganosine alone, and in sequential combination with immune checkpoint inhibitor (anti-PD-L1 compound, atezolizumab),
in mice model of colorectal cancer, derived from MC-38 cells. Two doses of ateganosine are shown to control tumor growth while anti-PD-L1
agent. Sequential administration of ateganosine (2 days), followed by administration of the anti-PD-L1 agent, demonstrates disappearance
of tumor cells.

●
Immunological
memory was observed in mouse models, where the immune system continued to be active against the specific treated tumor cell type
for 100 days post-tumor inoculation. The below graphic demonstrates that the tumor-free animals that were treated with the sequential
combination of ateganosine and anti-PD-L1 compound were followed for 70 days, with no observed tumor recurrence. Subsequently, animals
were re-challenged with 10 times more MC38 cancer cells. Cancer growth was not observed in these animals, demonstrating induction
of anti-tumor-protecting memory after sequential administration of ateganosine and anti-PD-L1 agent; ref: Mender, I., et al. Telomere
stress potentiates STING-dependent anti-tumor immunity. Cancer Cell, 38,3, 400-411.E6, September 14, 2020.

25

Moreover,
due to the cGAS/STING activation caused by ateganosine, telomere targeting activity was observed in numerous preclinical tumor models
when ateganosine was administered followed by immune activating therapy such as immune checkpoint inhibitors (anti-PD-L1 or anti-PD-1
antibody). A summary of the pharmacological aspects of the investigational product and, where appropriate, its significant metabolites
studied in animals, should be included. Such a summary should incorporate studies that assess potential therapeutic activity (e.g. efficacy
models, receptor binding, and specificity) as well as those that assess safety (e.g., special studies to assess pharmacological actions
other than the intended therapeutic effect(s)). The results of all relevant nonclinical pharmacology, toxicology, pharmacokinetic, and
investigational product metabolism studies should be provided in summary form. This summary should address the methodology used, the
results, and a discussion of the relevance of the findings to the investigated therapeutic and the possible unfavorable and unintended
effects in humans.

It
is therefore hypothesized that ateganosine, administered in advance of immune-activating therapies (e.g., checkpoint inhibitors, radiation
therapy, etc.), at dose levels significantly lower than the levels evaluated in previous clinical trials, will “prime” the
tumor environment and initiate an overall anti-tumor immune response. If confirmed through additional clinical studies, this could represent
an entirely new therapeutic approach for ateganosine and form the basis for the new clinical strategy for planned future trials.

Ateganosine
(THIO) Clinical Trials

We
plan to rely solely upon our self-generated clinical safety and efficacy data, if favorable, in support of our anticipated NDA filing
for ateganosine. However, ateganosine, as a compound, was the subject of investigation in numerous clinical trials in the 1970s to the
early-80s in a variety of solid tumors and hematological malignancies. The compound was evaluated in at least nineteen (19) Phase 1 to
Phase 3 clinical trials with over 600 patients treated by major cancer institutions and cancer cooperative groups. Ateganosine was studied
in combination with common agents in use at the time, including methyl-CCNU or mitomycin, two widely used alkylating agents to treat
a variety of cancers and leukemias. Studies utilizing ateganosine as a single agent have been published in peer-reviewed journals. As
part of the existing data base of clinical experience with the drug, we expect to reference the older NCI studies in the public domain
as well as reference NCI’s original IND filing in support of an IND filing, pursuant to FDA regulations.

The
following tables summarize the ateganosine single agent peer-reviewed published data available from the previous clinical trials.

Phase
1

Study

Tumor
Type

Regimen/Dose
Schedule

Evaluable
Subjects

Description
of

Observed
Adverse Events

Responses

C76-92

Pediatric
Acute Leukemia who received prior

6-mercaptopurine
(6-MP) or 6-thioguanine

Ateganosine
(THIO) 200 to 2,250 mg/m2 given every 12 hours for 3 doses every 2 weeks

Maximum
tolerated dose (MTD) was determined to be 1,750 mg/m2given every 12 hours for 3 doses every 2 weeks

31

Reversible
urate nephropathy, elevations of liver enzymes, nausea and vomiting, alopecia, and skin reactions

Therapeutic
Responses observed in 6/23 (26%) patients comprised of

2
complete responses and 4 partial responses

Source:
Higgins, G. R., Jamin, D. C., Shore, N. A., Momparler, R., Hartman, G. and Siegel, S. E. (1985). “Phase I evaluation of beta-2’-deoxythioguanosine
in pediatric patients with leukemia.” Cancer Treat Rep 69(6): 699-701t

26

Phase
2 – Single Agent Studies

Protocol
Tumor Type

Regimen/Dose

Schedule

Evaluable

Subjects

ORR

(Overall

Response)

PR

(Partial

Response)

CR

(Complete

Response)

Observed

Adverse Events

SEG-248
Total Patients

117
27 (23%)
11 (9%)
16 (14%)
Leukopenia

Thrombocytopenia

Skin rash

Alopecia (reversible)

Nausea and vomiting

Acute Myelocytic Leukemia (AML)
300 mg/m2 daily for 5 days
17
4 (24%)
1 (6%)
3 (18%)

400 mg/m2 daily for 5 days
49
10 (20%)
6 (12%)
4 (8%)

Blastic transformation of chronic myelogenous leukemai (BTL)
300 mg/m2 daily for 5 days
11
3 (27%)
-
3 (27%)

400 mg/m2 daily for 5 days
26
6 (23%)
3 (12%)
3 (12%)

Acute Lymphocytic Leukemia (ALL)
300 mg/m2 daily for 5 days
4
2 (50%)
-
2 (50%)

400 mg/m2 daily for 5 days
10
2 (20%)
1 (10%)
1 (10%)

EST 4273 (ECOG)
Colorectal

(prior 5-FU chemotherapy)
Ateganosine (THIO) 100 mg/m2 daily for 5 days every 3 weeks

vs

MeCCNU 175 mg/m2

every 8 weeks
61
3 (5%)
3 (5%)
-
Leukopenia, thrombocytopenia, nausea and vomiting

55
5 (9%)
5 (9%)
-

Omura,
G. A., Vogler, W. R., Smalley, R. V., Maldonado, N., Broun, G. O., Knospe, W. H., et al. (1977b). “Phase II Study of beta-2’-deoxythioguanosine
in adult acute leukemia. (Study SEG-248)” Cancer Treat Rep 61(7): 1379-1381 Douglass, H. O., Jr., Lavin, P. T., Woll, J., Conroy,
J. F. and Carbone, P. (1978). “Chemotherapy of advanced measurable colon and rectal carcinoma with oral 5-fluorouracil, alone or
in combination with cyclophosphamide or 6-thioguanine, with intravenous 5-fluorouracil or beta-2’-deoxythioguanosine or with oral
3(4-methyl-cyclohexyl)-1(2-chlorethyl)-1-nitrosourea: A Phase II-III study of the Eastern Cooperative Oncology Group (EST 4273).”
Cancer 42(6): 2538-2545

The
previous human experience presents significant limitations as it dates to the 1970s and early 1980s when the implementation of ICH Good
Clinical Practices was not yet in effect. The published studies did not disclose certain data points in line with the current ICH Good
Clinical Practices, such as efficacy endpoints and serious adverse events, whether those endpoints were reached, whether the data was
found to be statistically significant and serious adverse events. Further, we do not know whether those prior studies were powered for
statistical significance in the way our planned studies will be powered. Based generally on the results of these prior human studies,
we believe that ateganosine has a well-established safety profile, which we intend to independently demonstrate through our own clinical
studies. Moreover, all prior studies were conducted primarily in heavily pre-treated, refractory patients.

27

Notwithstanding
these limitations, the available data provides substantial information on the clinical experience with and clinical profile of ateganosine
with an exposure exceeding 600 subjects (adult and pediatric) at doses significantly higher than those intended for investigation in
the current program and new treatment strategy. All studies were conducted in heavily pre-treated/refractory patients, most of whom were
pre-treated with other standards of care including chemotherapy.

To
date, ateganosine has not received marketing approval in any country; therefore, there is no marketing experience to be reported.

The
planned clinical trials will assess a novel ateganosine therapeutic strategy: - evaluate the safety and efficacy of low potentially immunogenic
doses of ateganosine administered to activate the immune system against the tumor to be treated, followed by standard-of-care immunotherapy
(checkpoint inhibitor) or other immune activating therapies.

Ateganosine
Developmental Initiatives and Objectives

Phase
2 and 3 Programs

Our
primary short-term objective is to assess this approach in a Proof-of-Concept study outlined below.

This
first study is a dose-finding, Phase 2 clinical trial evaluating both safety and efficacy of ateganosine sequenced with cemiplimab in
patients with advanced NSCLC who progressed or showed no clinical benefit to first line treatment containing an immune checkpoint inhibitor.
This trial, designated as THIO-101 study is our first human clinical trial to test the immune system activation demonstrated in preclinical
animal models: lower doses of ateganosine administered prior to a checkpoint inhibitor treatment reverses drug resistance, enhance and
prolong immune responses in patients with advanced lung cancer who did not respond or progressed after a prior cancer treatment which
contained another immune checkpoint inhibitor.

The
trial design has two primary objectives: (1) safety of ateganosine administered as a priming immune system agent prior to cemiplimab
administration and (2) clinical efficacy of ateganosine using Overall Response Rate (ORR) as the primary clinical endpoint. An expansion
arm has been amended to the trial protocol on December 2024 to further assess the efficacy of ateganosine in combination with cemiplimab
in third-line NSCLC patients who are resistant to chemotherapy and checkpoint inhibitors.

The
following chart sets forth the design of the THIO-101 trial:

28

This
Phase 2 “dose-finding” trial is designed to assess the safety, mechanism of activity, and immune system activation of three
ateganosine doses tested out in separate arms administered in parallel. Each dosing arm will be further evaluated for efficacy based
on Overall Response Rate (ORR), Duration of Response (DoR) and Progression Free Survival (PFS) to determine to optimal (safe and effective)
dose of ateganosine administered in sequence with cemiplimab. Dose selection was completed in November 2023 and and enrollment was completed
in February 2024, but monitoring and assessment of dosed subjects are ongoing as patients continue to with the postbaseline scans and
data matures. In July 2025, an expansion of the THIO-101 trial was initiated focused on third-line NSCLC patients who are resistant to
checkpoint inhibitors and chemotherapy. The expansion will enroll up to 48 patients with two arms: Arm 1, continuing the evaluation of
ateganosine sequenced with Libtayo® (cemiplimab); and Arm 2, evaluating ateganosine as a monotherapy, to further gain experience
of ateganosine in the contribution of components.

A
Phase 3 pivotal trial, named THIO-104, initiated in 2025 to evaluate the efficacy of ateganosine administered in sequence with a checkpoint
inhibitor (CPI) in third-line NSCLC patients who are resistant to checkpoint inhibitors and chemotherapy. The multicenter, open-label,
pivotal Phase 3 trial is designed to provide a direct comparison to chemotherapy in a 1:1 randomization of up to 300 patients.

The
following chart sets forth the design of the THIO-104 trial:

In
an effort to obtain FDA and/or EMEA approval of ateganosine in combination with other standard of care approved cancer immunotherapies,
we will have to conduct head-to-head studies which will compare standard of care treatment alone to standard of care treatment combined
with ateganosine. In such studies, we would have to show that ateganosine added to standard of care therapies adds a significant treatment
benefit by slowing down tumor progression and increasing the overall survival of the cancer patients.

In
addition, we are actively evaluating other regulatory strategies and pathways that have the potential to accelerate and/or expand the
study of ateganosine administered in sequence with an immune-checkpoint inhibitor in other solid tumor indications.

29

In
the event ateganosine demonstrates early clinical efficacy, we plan to expand our clinical development program in multiple tumor types
and assess several regulatory approval pathways utilizing our other development programs. The clinical development plan includes the
initiation of an additional “basket trial” in multiple cancer types. This study uses a special design which allows different
cancer indications to be studied under the same single trial umbrella. Some of the indications considered are:

●
colorectal
cancer (CRC)

●
hepatocellular
carcinomas (HCC)

●
small-cell
lung cancer (SCLC)

●
melanoma

●
breast
cancer

●
pancreatic
cancer

●
glioblastoma
multiforme (GBM)

●
ovarian
cancer

●
prostate
cancer

Ultimately,
we envision positioning ateganosine as the foundational priming treatment for all immune-activating agents over time based upon ateganosine’s
tumor-specific immune-activation approach that enables key clinical strategies that could dramatically expand the immunotherapy market.

Second
Generation of Telomere Targeting Agents

We
have initiated an early-stage research and discovery program aimed at identifying new compounds capable of acting through the same mechanism
of action as ateganosine, such as targeting and modifying telomeric structures of cancer cells through cancer-cell intrinsic telomerase
activity. The main objective for this program is to discover compositionally new compounds with potentially improved specificity towards
cancer cells relative to normal cells, and to assess telomere targeting activity in comparison with ateganosine. This program may also
allow us to strengthen our patent portfolio. Although the program is in early stages and we may not be able to identify suitable compounds,
we believe we will be able to create or discover a second generation of ateganosine-like compounds.

Strategic
Collaborations and Key Agreements

Through
our licensing agreements with The University of Texas Southwestern Medical Center (“UTSW”), we have commercial rights to
certain U.S. patents, as well as their foreign counterparts, for the use of ateganosine in treating telomerase-expressing lung and colon
cancer cells. We are currently using this technology to study a treatment regimen comprising the use of ateganosine treatment followed
by cemiplimab treatment in NSCLC. In addition, we have licensed a number of pending U.S. and foreign patent applications from UTSW directed
to other indications, and we are continuing to pursue discussions with several companies to develop other treatment regimens using ateganosine
for additional cancer indications.

Clinical
Supply Agreements

In
2021, we entered into a clinical supply agreement with Regeneron Pharmaceuticals, Inc. (Regeneron) to supply cemiplimab for the THIO-101
study. Regeneron will contribute the drug supply without cost, which represents a significant direct cost savings for our program. In
exchange, Regeneron will receive development exclusivity for NSCLC indication during the study period, which means that MAIA cannot study
ateganosine in NSCLC with any other PD-1 antagonist (a product sub-class of immune checkpoint inhibitors). All other tumor types remain
open, and we are in discussions with other pharmaceutical companies to evaluate additional agreements that may be appropriate to support
the expanded development of ateganosine. The supply agreement will remain in force until all of the obligations of the parties’
related to the studies contemplated by the agreement are completed, or until terminated by either party. The agreement may be terminated
in the event of unsafe use of cemiplimab, material breach, regulatory action or corruption. On December 3, 2024, we announced the amendment
of the 2021 clinical supply agreement with Regeneron for the expansion portion of THIO-101, its Phase 2 clinical trial evaluating ateganosine
in sequential administration with cemiplimab (Libtayo®). The new expansion will further assess the efficacy of MAIA’s
lead asset, ateganosine, sequenced with immune checkpoint inhibitor (CPI) Libtayo® (cemiplimab) for advanced non-small
cell lung cancer (NSCLC) patients receiving third-line therapy who were resistant to previous checkpoint inhibitor treatments and chemotherapy.
The original 2021 agreement between MAIA and Regeneron was designed to supply the original THIO-101 trial through the dose selection
and safety evaluation process.

In
January 2025, we announced a clinical supply agreement with BeOne Medicines, formerly known as BeiGene, Ltd (BeOne) to supply tislelizumab
for the upcoming THIO-102 studies in HCC, CRC and SCLC.

30

In
June 2025, we entered into a clinical master agreement with Roche for future studies investigating the combination of MAIA’s telomere-targeting
agent ateganosine (THIO), sequenced with Roche’s checkpoint inhibitor (CPI), atezolizumab (Tecentriq®), for the treatment of
multiple hard-to-treat cancers.

We
are in discussions with other pharmaceutical companies to evaluate additional agreements that may be appropriate to support the expanded
development of ateganosine. The supply agreement will remain in force until all of the obligations of the parties’ related to the
studies contemplated by the agreement are completed, or until terminated by either party. The agreement may be terminated in the event
of unsafe use of tislelizumab, material breach, regulatory action or corruption.

In
addition, our management believes that strong partnership interest will develop from other pharmaceutical companies who have checkpoint
inhibitor franchises or those with cancer immunotherapy interest. We expect to continue discussions with several companies that have
expressed interest and plan to expand discussions to capitalize on these opportunities. The checkpoint inhibitor market is large, and
our goal is to ultimately position ateganosine as the foundational priming treatment to be used prior to all checkpoint inhibitors.

The
University of Texas Southwestern Medical Center License Agreement 1

On
December 8, 2020, we entered into an amended and restated agreement (of our prior November 29, 2018 agreement) with The Board of Regents
of The University of Texas System on behalf of The University of Texas Southwestern Medical Center (collectively, UTSW). Pursuant to
the amended and restated agreement, which we refer to as the UTSW1 Agreement, we obtained (1) an exclusive, worldwide license to develop
and commercialize the following UTSW patent families generally directed to methods of using ateganosine (below) and (2) a non-exclusive
worldwide license to develop and commercialize related technology rights.

THIO (ateganosine) Intellectual Property

a.) US patent no. 10,463,685 entitled, Telomerase Mediated Telomere Altering Compounds issued in the US on November 5, 2019. The patent claims priority to U.S. application No.14/247,967. Related foreign patents based on PCT/US2014/033330 have also issued in the following foreign countries, CA, EPO (validated in AT, BE, CH, CZ, DE, ES, FR, GB, HU, IE, IS, IT, LI, LU, MC, NL, PL, PT), MX, NZ, and RU (all method of use). The application is pending in BR, and SG.

b.) 6-Thio-2’-Deoxyguanosine (6-Thio-dG) Results in Telomerase Dependent Telomere Dysfunction and Cell Death in Various Models of Therapy-Resistant Cancer Cells (Method of Use) /

PCT/US2017/034706 (WO2017/0205756) filed on 26 May 2017, is issued in CA (patent No. 3035533), and the EPO (Patent No. validated in AL, AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB,GR, HR, HU, IE, IS, IT, LI, LT, LU, LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, SM, and TR and pending in the US (serial no. 18/329,381), and EPO (application No. 17803670.3).

c.) Use of 6-thio-dG to Treat Therapy-Resistant Telomerase positive Pediatric Brain Tumors /

pending in the US (U.S. application No. 18/511,417) which has received a Notice of Allowance (method of use).

d.) Treatment of Drug-Resistant Proliferative Diseases with Telomerase Mediated Telomere Altering Compounds), issued in the US as patent no.12,070,472) which was based on US application No.16/450,430. A continuation of application 16/450,430 is pending (US application No. 18,781,413).

Under
the UTSW1 Agreement, we agreed to pay UTSW a minimal license fee, deferred license fees, milestone fees, and running royalties beginning
on the first net sale (among others). For additional details regarding our relationship with UTSW, see the section entitled “Business
— Intellectual Property —License Agreement 1 with The Board of Regents of The University of Texas System / The University
of Texas Southwestern Medical Center.” The UTSW1 Agreement includes an exclusive license to US patent no. 10,463,685 (expires April
8, 2034), and US patent no. 12,070,472 (having an earliest expiration of March 23, 2037), and 16,982,979 (having an earliest expiration
of March 22, 2039, if a patent is granted).

The
University of Texas Southwestern Medical Center License Agreement 2

31

On
December 23, 2020, we entered into a second agreement with The Board of Regents of The University of Texas System on behalf of The University
of Texas Southwestern Medical Center, which set forth the agreement between the parties pursuant to the Company exercising its option
rights in the UTSW1 Agreement and obtaining additional license rights. Pursuant this second license with UTSW, which we refer to as the
UTSW2 Agreement, we obtained (1) an exclusive, worldwide license to develop and commercialize the following UTSW patent family (below)
and (2) a non-exclusive worldwide license to develop and commercialize related technology rights.

Sequential Treatment of Cancers Using 6-Thio-dG and Checkpoint Inhibitors (Method of Use)

PCT/US2021/022090, issued in the RU, EP (validated in AL, AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HU, IE, IS, IT, LI, LT, LU, MC, MK, MT, NL, NO, PL, PT, RO, SE, TR), pending in AU, BR, CA, CN, IL, JP (received notice of allowance), KR, MX, and SG.

and (2) a non-exclusive worldwide license to develop
and commercialize related technology rights. The UTSW2 Agreement includes an exclusive license to issued US patent no. 12,097,213 (having
an earliest expiration of July 28, 2041, which includes 138 days of patent term adjustment). This patent is directed to methods of using
ateganosine in combination with immune checkpoint inhibitors.

Under
the UTSW2 Agreement, we agreed to pay UTSW a minimal license fee, deferred license fees, milestone fees, and running royalties beginning
on the first net sale (among others). For additional details regarding our relationship with UTSW, see the section entitled “Business
— Intellectual Property —License Agreement 2 with The Board of Regents of The University of Texas System /The University
of Texas Southwestern Medical Center.” The UTSW2 Agreement includes an exclusive license to pending US patent application no. 17/200,539
(having an earliest expiration of March 12, 2041, if a patent is granted).

Ateganosine
(THIO) Program

License
Agreement 1 with The Board of Regents of The University of Texas System /The University of Texas Southwestern Medical Center

On
December 8, 2020 (the “Effective Date”), we entered into an amended and restated agreement (of our prior November 29, 2018
agreement) with The Board of Regents of The University of Texas System on behalf of The University of Texas Southwestern Medical Center,
(collectively, UTSW) to develop and commercialize certain UTSW owned and/or controlled patents and related technology directed to methods
of using ateganosine (“the UTSW1 Agreement”). The license is exclusive as to worldwide Patent Rights for all uses in the
Field, which is defined as all therapeutic, prophylactic and diagnostic fields of use for all indications, including discovery and development
uses. The license is sublicensable with prior UTSW written approval consistent with the terms of UTSW1 Agreement.

The
UTSW1 Agreement includes an exclusive license to the “Patent Rights” of the worldwide patent families including all provisional
applications and any divisionals, continuations, continuations-in-part and foreign counterpart applications that are entitled to claim
priority thereto, and any patents resulting therefrom, of the following:

Title
/ PCT Application Number

a.)
Telomerase Mediated Telomere Altering Compounds / PCT/US2014/33330 (WO2014/168947), issued in the US (patent no. 10,463,685), CA,
MX, NZ and RU (all method of use) pending in BR, EPO (received an Intent to Grant), HK and SG.

b.)
6-Thio-2’-Deoxyguanosine (6-Thio-dG) Results in Telomerase Dependent Telomere Dysfunction and Cell Death in Various Models of
Therapy-Resistant Cancer Cells /

PCT/US2017/34706
(WO2017/205756), pending in the US (method of use), CA, and EPO.

c.)
Use of 6-thio-dG to Treat Therapy-Resistant Telomerase positive Pediatric Brain Tumors /PCT/US2019/023596 (WO2019/183482), pending
in the US (method of use)

d.)
Treatment of Drug Resistant Proliferative Diseases with Telomerase Mediated Telomere Altering Compounds / PCT/US2017/023858
(WO/2017/165675), issued in the US (patent no. 12,070,472) (method of use).

The
UTSW1 Agreement also grants the Company a non-exclusive worldwide license under the Technology Rights to develop, manufacture, have manufactured,
distribute, have distributed, use, offer for Sale, Sell, lease, loan and/or import Licensed Products in the Field, wherein Technology
Rights means Licensor’s rights in technical information, know-how, processes, procedures, compositions, devices, methods, formulas,
protocols, techniques, designs, drawings or data created before the Effective Date by Inventors at UTSW which are necessary or reasonably
useful for practicing Patent Rights.

32

The
UTSW1 Agreement also grants the Company the first right to negotiate an exclusive license under any patent rights covering or claiming
any improvement, which is any patentable invention and is conceived or reduced to practice solely by Dr. Jerry Shay or those under his
direct supervision at UTSW within 3 years of the Effective Date, under certain conditions.

The
term of the UTSW1 Agreement begins on the Effective Date and continue until the earliest of: (i) termination pursuant to the UTSW1
Agreement, (ii) the last date of expiration or termination of the Patent Rights; or (iii) if Technology Rights are licensed and no
Patent Rights are applicable, twenty (20) years after the Effective Date. The Company may terminate the UTSW1 Agreement for
convenience, at any time prior by providing ninety (90) days’ written notice to UTSW. UTSW may terminate the UTSW1 Agreement
if the Company (i) becomes in arrears in any payments due, and fails to make the required payment within 30 days after delivery of
written notice from UTSW, (ii) is in breach of any material non-payment provision, and does not cure such breach within 60 days
after delivery of written notice, (iii) UTSW delivers notice to the Company of three or more actual breaches in any twelve month
period, even in the event that the Company cures such breaches in the allowed period, (iv) becomes insolvent or bankrupt, then
termination is immediate.

UTSW
and/or the co-owners of certain patents have reserved the right to publish the scientific findings related to the Patent Rights and use
and to permit other academic institutions to use the licensed subject matter for teaching, research, education, and other education-related,
non-commercial purposes. The Patent Rights are also subject to any rights of the United States federal, state and/or local Government(s),
as well as nonprofit entities, if certain patents or technologies were created in the course of Government-funded or non-profit entity-funded
research.

Pursuant
to the UTSW1 Agreement, the Company paid to UTSW a nominal one-time upfront license fee. The Company is also obligated to pay all accrued
patent expenses as well as ongoing patent expenses on a scheduled basis tied to Company fund-raising through Series A funding until Company
has reimbursed all patent expenses. In the event that the Company assigns the agreement to a third party, the Company is obligated to
pay UTSW an assignment fee in the mid-six figures within 15 days of such assignment. The agreement cannot be assigned without UTSW’s
consent.

Under
the UTSW1 Agreement, the Company is obligated to use diligent efforts to bring licensed products to market through a funded, ongoing
and active research and development, manufacturing, regulatory, marketing or sales program (all as commercially reasonable) and provide
semi-annual reports to UTSW on its progress. The Company is also obligated to pay agreed upon milestone payments to UTSW. Failure of
the Company to fulfill these obligations may be treated as a material breach by UTSW.

The
only milestones that require payments under the UTSW1 Agreement include: (i) first commercial sale in the U.S. of licensed product for
treating an oncology indications ; (ii) first commercial sale in the U.S. of licensed product for treating a non-oncology indications;
(iii) first time aggregate Net Sales (as defined in the UTSW1 Agreement) of licensed product for treating an oncology indications exceeds
low-nine figure sales in a contract year; (iv) first time aggregate Net Sales of licensed product for treating a non-oncology indications
exceeds low nine-figure sales in a contract year; (v) first time aggregate Net Sales of licensed product for treating an oncology indications
exceeds low ten-figure sales in a contract year; (vi) first time aggregate Net Sales of licensed product for treating a non-oncology
indications exceeds low ten-figure sales in a contract year. There are no milestone payments required on any development or regulatory
milestones. The only required milestone payments under the UTSW1 Agreement related to commercial sales milestones, and the aggregate
amount of milestone fees payable pursuant to the UTSW1 Agreement will not exceed $112 million.

The
Company will also pay UTSW running royalties on a yearly basis as a percentage of Net Sales of the Company or its sublicensee. There
are single digit royalty rates for licensed products and licensed services covered by a Valid Claim (as defined in UTSW1 Agreement) and
dependent on whether Net Sales are greater than or less than/equal to low ten figures of sales, with Net Sales above that amount commanding
a slightly higher percentage. In each case, the royalty percentage is lower before patent issuance in each jurisdiction. In the event
that the licensed product or licensed service is not covered by a Valid Claim, the running royalty rates are reduced by a certain percentage.
The royalty obligations continue on a country-by-country basis until the later of expiration of the last Valid Claim in each country
or ten (10) years after the First Commercial Sale (as defined in UTSW1 Agreement) in each country. In the event that the Company or its
sublicensee challenges the Patent Rights, then the Company will be obligated to pay multiples of the applicable royalty rate of the Net
Sales and, should the outcome of such challenge determine that any claim of the Patent Rights challenged is both valid and infringed
then the Company will pay royalties at the rate of multiples of the applicable royalty rate of the Net Sales sold thereafter and reimburse
UTSW for all fees and costs associated with defending such challenge, including attorney’s fees and expert fees.

33

The
UTSW1 Agreement also contains an anti-stacking provision pursuant to which in the event the Company or its sublicensee pays royalties
or other payments to a third party who owns or controls intellectual property deemed necessary to develop, manufacture, have manufactured,
distribute, have distributed, use, lease, loan, import, offer for sale and/or sell any licensed products and licensed services, the Company
may reduce payments to UTSW by a certain percentage of the royalty, milestone or other payments paid to such third party. However, such
adjustment in royalty payments to UTSW may not be reduced by more than a certain percentage of the royalty obligation in any contract
year. In the event that the payment to the third party who owns or controls intellectual property deemed necessary to extend or expand
the franchise or exclusivity of a previously launched licensed product (e.g., such as a new formulation as a second generation product
containing the same compound as the previously launched Licensed Product), then the Company may reduce payments to UTSW by a certain
percentage of the royalty, milestone or other payments paid to such third party. However, such adjustment in royalty payments to UTSW
may not be reduced below a certain percentage of the royalty obligation in any contract year.

UTSW
maintains direct control over the prosecution and maintenance activities of the Patent Rights, and the Company is obligated to reimburse
past and ongoing patent expenses as noted above. UTSW will permit the Company to comment on submissions to government patent agencies,
during prosecution and will consider the Company’s comments, but UTSW retained control over all final decisions.

The
UTSW1 Agreement contains a representation that UTSW has the rights and authority to grant to Company the licensed rights and is to its
knowledge unaware of any third-party infringer or any infringement of third-party intellectual property rights. The UTSW1

Agreement
also requires the Company to indemnify UTSW and other related parties against any liabilities, damages, causes of action, suits, judgments,
liens, penalties, fines, losses, costs and expenses arising out of any product the Company produces under the UTSW1 Agreement, and requires
the Company, beginning with the earlier of the first clinical trial or commercial sale or other commercialization, to obtain liability
insurance.

The
Company will have the first and sole right but not the obligation, at its own expense, to initiate an infringement suit or other appropriate
actions against third party infringers and monetary recovery received therefrom, after the Company is reimbursed for expenses in enforcing
the Patent Rights, is shared between the Company and UTSW pursuant to a good faith negotiation between the parties at that time. If the
Company does not file suit within six months after a written request by UTSW, then UTSW may bring suit to enforce any Patent Right and
retain all recoveries from such enforcement. If UTSW pursues such infringement action, it may, as part of the resolution of such efforts,
grant nonexclusive license rights to the alleged infringer notwithstanding Licensee’s exclusive license rights.

In
accordance with the terms of the UTSW1 Agreement, on April 24, 2020 Company sublicensed all Company rights and obligations under the
UTSW1 Agreement to Company affiliate THIO Therapeutics, Inc.

License
Agreement 2 with The Board of Regents of The University of Texas System /The University of Texas Southwestern Medical Center

On
December 23, 2020 (the “Effective Date”), we entered into a second agreement with The Board of Regents of The University
of Texas System on behalf of The University of Texas Southwestern Medical Center, (collectively, UTSW), which set forth the agreement
between the parties pursuant to the Company exercising its option rights in the UTSW1 Agreement and obtaining additional license rights
(“the UTSW2 Agreement”). The license is exclusive as to worldwide Patent Rights for all uses in the Field, which is defined
as all therapeutic, prophylactic and diagnostic fields of use for all indications, including discovery and development uses. The license
is sublicensable with prior UTSW written approval consistent with the terms of UTSW2 Agreement.

34

The
UTSW2 Agreement includes an exclusive license to the “Patent Rights” of the worldwide patent family including all provisional
applications and any divisionals, continuations, continuations-in-part and foreign counterpart applications that are entitled to claim
priority thereto, and any patents resulting therefrom, of the following

Sequential Treatment of Cancers Using 6-Thio-dG and Checkpoint

Sequential
Treatment of Cancers Using 6-Thio-dG and Checkpoint Inhibitors / PCT/US2021/022090, issued in the EPO, and RU (method of use),
pending in AU, BR, CA, CN, IL,JP (has received Notice of Allowance), KR, MX, and SG.

The
UTSW2 Agreement also grants the Company a non-exclusive worldwide license under the Technology Rights to develop, manufacture, have manufactured,
distribute, have distributed, use, offer for Sale, Sell, lease, loan and/or import Licensed Products in the Field, wherein Technology
Rights means UTSW’s rights in technical information, know-how, processes, procedures, compositions, devices, methods, formulas,
protocols, techniques, designs, drawings or data created before the Effective Date by inventors at UTSW which are necessary or reasonably
useful for practicing Patent Rights.

The
terms of the UTSW2 Agreement are similar in many respects to those set forth in the UTSW1 Agreement. Pursuant to the UTSW2 Agreement,
the Company paid to UTSW a nominal one-time upfront license fee. The UTSW2 Agreement recognizes the accrual of low five-figures in patent
expenses relative to the Patent Rights of this agreement and provides for deferral of this fee and related ongoing patent expense fees
on a schedule connected to the Company’s fundraising through Series A funding. Once the Company has raised mid seven-figures, the
patent expense fees are be paid in full for all patent expenses incurred by UTSW for the Company’s licensed technologies which
accrued between December 12, 2019, and the date at which the mid seven-figures has been raised. Until the Company has reimbursed all
patent expenses it is obligated to report its fundraising progress to UTSW on a quarterly basis.

The
milestone payments are the same as in the UTSW1 Agreement wherein the milestone fees are based solely on commercial sales milestones
and are payable one time only, regardless of the number of licensed products or licensed services developed and regardless of the number
of indications or patient sub-populations treated with a licensed product(s) and regardless of whether the licensed products or licensed
services developed are within the rights granted by the UTSW1 Agreement or the UTSW2 Agreement. In other words, there are no milestone
payments required on any development, or regulatory milestones under the UTSW1 Agreement or the UTSW2 Agreement. The only required milestone
payment under the UTSW1 Agreement or the UTSW2 Agreement relate to commercial sales milestones and the aggregate amount of milestone
fees payable pursuant to the UTSW1 Agreement or the UTSW2 Agreement will not exceed $112 million. In the event the Company assigns the
UTSW2 Agreement to a third party, the Company is obligated to pay UTSW low six-figures within 15 days of such assignment, which is cumulative
of the UTSW1 Agreement assignment fee, such that if both agreements are assigned to a third party, a total of high six-figures would
be owed to UTSW. The agreement cannot be assigned without UTSW’s consent.

The
Company will also pay UTSW running royalties on a yearly basis as a percentage of Net Sales of the Company or its sublicensee. There
are mid-single digit royalty rates for licensed products and licensed services covered by a Valid Claim (as defined in UTSW2 Agreement)
and dependent on whether Net Sales are greater than or less than/equal to low ten-figures in sales, with Net Sales above that amount
commanding a slightly higher percentage. In each case, the royalty percentage is lower before patent issuance in each jurisdiction. In
the event that the licensed product or licensed service is not covered by a Valid Claim, the running royalty rates are reduced by a certain
percentage. The royalty obligations continue on a country-by-country basis until the later of expiration of the last Valid Claim in each
country or ten (10) years after the First Commercial Sale (as defined in UTSW2 Agreement) in each country. In the event that the Company
or its sublicensee challenges the Patent Rights, then the Company will be obligated to pay multiple times the applicable royalty rate
of the Net Sales and, should the outcome of such challenge determine that any claim of the Patent Rights challenged is both valid and
infringed then the Company will pay royalties at the rate of multiple times the applicable royalty rate of the Net Sales sold thereafter
and reimburse UTSW for all fees and costs associated with defending such challenge, including attorney’s fees and expert fees.

35

The
UTSW2 Agreement also contains an anti-stacking provision pursuant to which in the event the Company or its sublicensee pays royalties
or other payments to a third party who owns or controls intellectual property deemed necessary to develop, manufacture, have manufactured,
distribute, have distributed, use, lease, loan, import, offer for sale and/or sell any licensed products and licensed services, the Company
may reduce payments to UTSW by a certain percentage of the royalty, milestone or other payments paid to such third party. However, such
adjustment in royalty payments to UTSW may not be reduced by more than a minimum percentage of the royalty obligation in any contract
year. In the event that the payment to the third party who owns or controls intellectual property deemed necessary to extend or expand
the franchise or exclusivity of a previously launched licensed product (e.g., such as a new formulation as a second-generation product
containing the same compound as the previously launched Licensed Product), then the Company may reduce payments to UTSW by a certain
percentage of the royalty, milestone or other payments paid to such third party. However, such adjustment in royalty payments to UTSW
may not be reduced by more than a certain percentage obligation in any contract year.

The
Company has the development and reporting obligations as the UTSW1 Agreement and as with the UTSW1 Agreement, UTSW has reserved the right
to publish the scientific findings related to the Patent Rights and use and to permit other academic institutions to use the licensed
subject matter for teaching, research, education, and other educationally related, non-commercial purposes. The Patent Rights are also
subject to any rights of the United States federal, state and/or local Government(s), as well as nonprofit entities, if certain patents
or technologies were created in the course of Government-funded or non-profit entity-funded research.

The
obligations and rights as to patent prosecution and defense of the Patent Rights are the same as those for the UTSW1 Agreement. The term
and termination provisions of the UTSW2 Agreement is the same as the UTSW1 Agreement, however in the event that the UTSW1 Agreement is
terminated for any reason, or expires, then the UTSW2 Agreement likewise is terminated or deemed to have expired.

The
above description of UTSW1 Agreement and UTSW2 Agreement is just a summary and readers are referred to UTSW1 Agreement and UTSW2 Agreement,
which are attached hereto as Exhibits 10.2 and 10.3 respectively, for a full and complete description of the patent expenses, milestone
payments, fees and royalties payable by MAIA.

Some
of our intellectual property, including the intellectual property licensed under UTSW1 and UTSW2, has been conceived or developed through
government-funded research and thus may be subject to federal regulations providing for certain rights for the U.S. government or imposing
certain obligations on us, such as a license to the U.S. government under such intellectual property, “march-in” rights,
certain reporting requirements and a preference for U.S.-based companies, and compliance with such regulations may limit our exclusive
rights and our ability to contract with non-U.S. manufacturers. See Risks Relating to Our Intellectual Property - Intellectual property
discovered through government funded programs may be subject to federal regulations such as “march-in” rights, certain reporting
requirements and a preference for U.S.-based companies. Compliance with such regulations may limit our exclusive rights and limit our
ability to contract with non-U.S. manufacturers.

Competition

The
biotechnology industry is characterized by a rapid evolution of technologies, significant competition and strong defense of intellectual
property. While we believe that our platforms, technology, knowledge, experience, and scientific resources provide us with unique competitive
advantages, we expect to face competition from major pharmaceutical and biotechnology companies, academic institutions, governmental
agencies, and public and private research institutions, among others.

Any
therapeutic candidates that we successfully develop and commercialize will compete with currently approved therapies and new therapies
that may become available in the future. For example, current competitors in the non-small lung cancer indication are Merck, Regeneron,
Eli Lilly and Roche. There are also many other large and small companies developing products for this indication. Key product features
that, if approved, would affect our ability to effectively compete with other therapeutics include the efficacy, safety and convenience
of our therapeutics, the ease of use and effectiveness of any complementary diagnostics and/or companion diagnostics, and price and levels
of reimbursement.

Our
competitors also include large pharmaceutical and biotechnology companies, which may be developing therapeutic candidates with mechanisms
similar to our compounds or targeting the same clinical indications as our therapeutic candidates. The availability of reimbursement
from government and other third-party payors will also significantly affect the pricing and competitiveness of our therapeutic candidates.
Our competitors also may obtain FDA or other regulatory approval for their products 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.

36

Many
of the companies against which we may compete have significantly greater financial resources and expertise in research and development,
manufacturing, preclinical testing, 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. These early stage and more established 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.

Government
Regulation

Government
authorities in the United States, at the federal, state and local level, and in other countries, extensively 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 products such as those we are developing.
Any pharmaceutical candidate that we develop must be approved by the United States Food and Drug Administration, or FDA, before it may
be legally marketed in the United States and by the appropriate foreign regulatory agency before it may be legally marketed in foreign
countries.

United
States Government Regulation

In
the United States, the FDA regulates biopharmaceutical products under the Federal Food, Drug, and Cosmetic Act and the Public Health
Services Act, or PHSA, and implementing regulations.

Approval
Processes

The
process required by the FDA before a drug or biological product may be marketed in the United States generally involves the following:

●
Completion
of preclinical laboratory tests, animal studies and formulation studies according to Good Laboratory Practices or other applicable
regulations;

●
Submission
to the FDA of an Investigational New Drug Application, or an IND, which must become effective before human clinical trials may begin;

●
Performance
of several phases of adequate and well-controlled human clinical trials according to the FDA’s current good clinical practices,
or GCPs, to establish the safety and efficacy of the proposed drug or biologic for its intended use;

●
Submission
to the FDA of a New Drug Application, or an NDA, for a new drug product, or a Biologics License Application, or a BLA, for a new
biological product;

●
Satisfactory
completion of an FDA inspection of the manufacturing facility or facilities where the drug or biologic is to be produced to assess
compliance with the FDA’s current good manufacturing practice standards, or cGMP, to assure that the facilities, methods and
controls are adequate to preserve the drug’s or biologic’s identity, strength, quality and purity;

●
Potential
FDA audit of the nonclinical and clinical trial sites that generated the data in support of the NDA or BLA; and

●
FDA
review and approval of the NDA or BLA.

Failure
to comply with the applicable U.S. requirements at any time during the product development or approval process, or after approval, may
subject an applicant to administrative or judicial sanctions brought by the FDA and the Department of Justice, or DOJ, or other governmental
entities, any of which could have a material adverse effect on us. These sanctions could include:

●
refusal
to approve pending applications;

●
withdrawal
of an approval;

●
imposition
of a clinical hold;

●
warning
or untitled letters;

●
seizures
or administrative detention of product;

●
total
or partial suspension of production or distribution; or

●
injunctions,
fines, disgorgement, or civil or criminal penalties.

37

The
lengthy process of seeking required approvals and the continuing need for compliance with applicable statutes and regulations require
the expenditure of substantial resources. There can be no certainty that approvals will be granted.

Once
a biopharmaceutical candidate is identified for development, it enters the preclinical or nonclinical testing stage. Nonclinical tests
include laboratory evaluations of product chemistry, toxicity and formulation, as well as animal studies. An IND sponsor must submit
the results of the nonclinical tests, together with manufacturing information and analytical data, to the FDA as part of the IND. Some
nonclinical testing may continue even after the IND is submitted. In addition to including the results of the nonclinical studies, the
IND will also include a protocol detailing, among other things, the objectives of the clinical trial, the parameters to be used in monitoring
safety and the effectiveness criteria to be evaluated if the first phase lends itself to an efficacy determination. The IND automatically
becomes effective 30 days after receipt by the FDA, unless the FDA, within the 30-day time period, places the IND on clinical hold. In
this case, the IND sponsor and the FDA must resolve any outstanding concerns before clinical trials can begin. A clinical hold may occur
at any time during the life of an IND and may affect one or more specific studies or all studies conducted under the IND.

Clinical
trials involve the administration of the drug or biological candidate to healthy volunteers or patients having the disease being studied
under the supervision of qualified investigators, generally physicians not employed by or under the trial sponsor’s control. 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. Each protocol must be submitted to the FDA
as part of the IND. Clinical trials must be conducted in accordance with the FDA’s good clinical practices requirements. Further,
each clinical trial must be reviewed and approved by an independent institutional review board, or IRB, at or servicing each institution
at which the clinical trial will be conducted. An IRB is charged with protecting the welfare and rights of trial participants and considers
such items as whether 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 it is completed.

Human
clinical trials prior to approval are typically conducted in three sequential Phases that may overlap or be combined:

●
Phase
1. The drug or biologic is initially introduced into healthy human subjects and tested for safety, dosage tolerance, absorption,
metabolism, distribution and excretion. In the case of some products for severe or life-threatening diseases, especially when the
product may be too inherently toxic to ethically administer to healthy volunteers, the initial human testing is often conducted in
patients having the specific disease.

●
Phase
2. The drug or biologic is evaluated in a limited patient population to identify possible adverse effects and safety risks, to preliminarily
evaluate the efficacy of the product for specific targeted diseases and to determine dosage tolerance, optimal dosage and dosing
schedule for patients having the specific disease.

●
Phase
3. Clinical trials are undertaken to further evaluate dosage, clinical efficacy and safety in an expanded patient population at geographically
dispersed clinical trial sites. These clinical trials, which usually involve more subjects than earlier trials, are intended to establish
the overall risk/benefit ratio of the product and provide an adequate basis for product labeling. Generally, at least two adequate
and well-controlled Phase 3 clinical trials are required by the FDA for approval of an NDA or BLA.

Post-approval
studies, or Phase 4 clinical trials, may be conducted after initial marketing approval. These studies are used to gain additional experience
from the treatment of patients in the intended therapeutic indication and may be required by the FDA as part of the approval process.

Progress
reports detailing the results of the clinical trials must be submitted at least annually to the FDA and written IND safety reports must
be submitted to the FDA by the investigators for serious and unexpected adverse events or any finding from tests in laboratory animals
that suggests a significant risk for human subjects. 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 or its data safety monitoring board may suspend 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 or biologic has been associated with unexpected serious harm to patients.

38

Concurrent
with clinical trials, companies usually complete additional animal studies and develop additional information about the chemistry and
physical characteristics of the drug or biologic 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 the drug
or biological candidate and, among other things, must include methods for testing the identity, strength, quality and purity of the final
drug or biologic. Additionally, appropriate packaging must be selected and tested and stability studies must be conducted to demonstrate
that the drug or biological candidate does not undergo unacceptable deterioration over its shelf life.

U.S.
Review and Approval Processes

The
results of product development, preclinical studies and clinical trials, along with descriptions of the manufacturing process, analytical
tests conducted on the chemistry of the drug or biologic, proposed labeling and other relevant information are submitted to the FDA as
part of an NDA or BLA requesting approval to market the product. The submission of an NDA or BLA is subject to the payment of substantial
user fees; a waiver of such fees may be obtained under certain limited circumstances.

The
FDA reviews for completeness all NDAs and BLAs submitted before it accepts them for filing and may request additional information rather
than accepting an NDA or BLA for filing. Once the submission is accepted for filing, the FDA begins an in-depth review of the NDA or
BLA.

After
the NDA or BLA submission is accepted for filing, the FDA reviews the application to determine, among other things, whether the proposed
product is safe and effective for its intended use, and whether the product is being manufactured in accordance with cGMP to assure and
preserve the product’s identity, strength, quality and purity. The FDA reviews a BLA to determine, among other things, whether
the product is safe, pure and potent and the facility in which it is manufactured, processed, packaged or held meets standards designed
to assure the product’s continued safety, purity and potency. In addition to its own review, the FDA may refer applications for
novel drug or biological products or drug or biological 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. The FDA is not bound by the recommendations of an advisory committee, but it
considers such recommendations carefully when making decisions. During the approval process, the FDA also will determine whether special
marketing conditions or restrictions under a risk evaluation and mitigation strategy, or REMS, are necessary to assure the safe use of
the drug or biologic. If the FDA concludes that a REMS is needed, the sponsor of the NDA or BLA must submit a proposed REMS; the FDA
will not approve the NDA or BLA without a REMS, if required.

Before
approving an NDA or BLA, the FDA will inspect the facilities at which the product is to be manufactured, and may also inspect facilities
that provide raw materials for use in the product. 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.
Additionally, before approving an NDA or BLA, the FDA will typically inspect one or more clinical trial sites to assure their compliance
with cGCP during the conduct of studies of the subject drug. If during the review of the application the FDA identifies questions or
concerns regarding the application, data, manufacturing process or manufacturing facilities, it may issue a deficiency letter which the
sponsor must adequately address to the FDA’s satisfaction.

The
NDA or BLA review and approval process is lengthy and difficult, and the FDA may refuse to approve an NDA or BLA if the applicable regulatory
criteria are not satisfied or may require additional clinical data or other data and information. Even if such data and information is
submitted, the FDA may ultimately decide that the NDA or BLA does not, in its submitted form, satisfy the criteria for approval. Data
obtained from clinical trials are not always conclusive and may be susceptible to varying interpretations, which could delay, limit or
prevent regulatory approval. The FDA will issue a “complete response letter” (CRL) if the agency decides not to approve the
NDA or BLA. The complete response letter usually describes the specific deficiencies in the NDA or BLA identified by the FDA. The deficiencies
identified may be minor, for example, requiring labeling changes, or major, for example, requiring additional clinical trials. Additionally,
the complete response letter will typically include recommended actions that the applicant might take to place the application in a condition
for approval. If a complete response letter is issued, the applicant may either resubmit the NDA or BLA, addressing all of the deficiencies
identified in the letter, or withdraw the application.

39

If
a product receives regulatory approval, the approval may be for more limited conditions of use than the sponsor had proposed, such as
limitations to specific diseases or subsets of a disease, limited patient populations, second-line or third-line use limitations, limited
dosages or other limitations which could restrict the commercial value of the product. Further, the FDA may require that certain contraindications,
warnings or precautions be included in the product labeling. In addition, the FDA may require Phase 4 testing which may involve clinical
trials designed to further assess a product’s safety and effectiveness and may require testing and surveillance programs to monitor
the safety of approved products that have been commercialized.

Companion
Diagnostics

Many
drugs for cancer indications involving patient-specific genetic mutations or biomarkers are approved by FDA with limitations that the
specific genetic mutation must be confirmed in each patient by use of an FDA-approved diagnostic test, commonly referred to as a “companion
diagnostic.” The FDA issued a final guidance document in July 2014 addressing agency policy in relation to in vitro companion diagnostic
tests. The guidance explains that for some drugs and therapeutic biologics, the use of a companion diagnostic test is essential for the
safe and effective use of the product, such as when the use of a product is limited to a specific patient subpopulation that can be identified
by using the test. According to the guidance, the FDA generally will not approve such a product if the companion diagnostic is not also
approved or cleared for the appropriate indication, and accordingly the therapeutic product and the companion diagnostic should be developed
and approved or cleared contemporaneously. The FDA has also issued a Guidance, Principles for Codevelopment of an In Vitro Companion
Diagnostic Device with a Therapeutic Product (2016), which is “is intended to be a practical guide to assist therapeutic product
sponsors and IVD sponsors in developing a therapeutic product and an accompanying IVD companion diagnostic,” and a Guidance, Developing
and Labeling In vitro Companion Diagnostic Devices for a Specific Group of Oncology Therapeutic Products (2020), which “describes
considerations for the development and labeling of in vitro companion diagnostic devices (referred to as “companion diagnostics”
herein) to support the indicated uses of multiple drug or biological oncology products, when appropriate.”

As
stated in its Guidance, the FDA may decide that it is appropriate to approve such a product without an approved or cleared in vitro companion
diagnostic device when the drug or therapeutic biologic is intended to treat a serious or life-threatening condition for which no satisfactory
alternative treatment exists and the FDA determines that the benefits from the use of a product with an unapproved or uncleared in vitro
companion diagnostic device are so pronounced as to outweigh the risks from the lack of an approved or cleared in vitro companion diagnostic
device. The FDA encourages sponsors considering developing a therapeutic product that requires a companion diagnostic to request a meeting
with both relevant device and therapeutic product review divisions to ensure that the product development plan will produce sufficient
data to establish the safety and effectiveness of both the therapeutic product and the companion diagnostic. To date, no product targeting
TERT+ cancer patients has been approved by FDA, and the applicability to ateganosine of FDA’s Companion Diagnostics Guidance and
policy is yet to be determined. If a companion diagnostic is required to be developed and approved in order to receive approval of ateganosine,
the cost and length of time to fully develop and receive approval (if at all) of ateganosine may both be increased, as described in more
detail in the section Risk Factors – Risks Relating to Government Regulation. Because the FDA’s policy on companion diagnostics
is set forth only in guidance, this policy is subject to change and is not legally binding.

Expedited
Development and Review Programs

The
FDA has a Fast-Track program that is intended to expedite or facilitate the process for reviewing new drug and biological products that
meet certain criteria. Specifically, new drug and biological products are eligible for Fast Track designation if they are intended to
treat a serious or life-threatening condition and demonstrate the potential to address unmet medical needs for the condition. Fast Track
designation applies to the combination of the product and the specific indication for which it is being studied. Under a Fast Track designation,
the FDA may consider for review sections of the NDA or BLA on a rolling basis before the complete application is submitted, if (i) the
sponsor provides a schedule for the submission of the sections of the NDA or BLA, (ii) the FDA agrees to accept sections of the NDA or
BLA and determines that the schedule is acceptable, and (iii) the sponsor pays any required user fees upon submission of the first section
of the NDA or BLA.

40

Any
product submitted to the FDA for marketing approval, including those submitted under a Fast Track designation, may also 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 has the potential to provide safe and effective therapy where no satisfactory alternative therapy
exists or the new product has the potential to offer a significant improvement in the treatment, diagnosis or prevention of a disease
compared with marketed products. The FDA will attempt to direct additional resources to the evaluation of an application for a new drug
or biological product designated for priority review in an effort to facilitate the review. Additionally, a product may be eligible for
accelerated approval. Drug or biological products studied for their safety and effectiveness in treating serious or life-threatening
illnesses and that provide meaningful therapeutic benefit over existing treatments may receive accelerated approval, which means that
they may be approved on the basis of adequate and well-controlled clinical studies establishing that the product has an effect on a surrogate
endpoint that is reasonably likely to predict a clinical benefit, or on the basis of an effect on a clinical endpoint other than survival
or irreversible morbidity. As a condition of accelerated approval, the FDA generally requires that a sponsor of a drug or biological
product receiving accelerated approval perform adequate and well-controlled post-marketing clinical studies to confirm the safety and
efficacy for the approved indication. Failure to conduct such studies or conducting such studies that do not establish the required safety
and efficacy may result in revocation of the original accelerated approval. In addition, the FDA currently requires as a condition for
accelerated approval, pre-approval of promotional materials, which could adversely impact the timing of the commercial launch or subsequent
marketing of the product. Fast Track designation, priority review and accelerated approval do not change the standards for approval but
may expedite the development or approval process, and even if granted, accelerated approval status does not guarantee an accelerated
review or marketing approval by the FDA.

The
Hatch-Waxman Amendments and Generic Competition

Orange
Book Listing

Once
a drug product is approved under an NDA, the product is listed in the FDA’s publication, “Approved Drug Products with Therapeutic
Equivalence Evaluations,” commonly known as the Orange Book. An NDA-approved drug product will be designated in the Orange Book
as a Reference Listed Drug (RLD). Sponsors of approved NDA’s are required to list with the FDA patents whose claims cover the product’s
active ingredient, formulation, or an approved method of using the drug.

Patent
Term Extensions

Depending
upon the timing, duration and specifics of FDA approval of the use of our therapeutic candidates, some of our United States patents may
be eligible for limited patent term extension under the Hatch-Waxman Act. The Hatch-Waxman Act permits a patent restoration term of up
to five years as compensation for patent term lost during product development and the FDA regulatory review process. However, patent
term restoration cannot extend the remaining term of a patent beyond a total of 14 years from the product or therapeutic candidate’s
approval date. The patent term restoration period is generally one half of the time between the effective date of an IND and the submission
date of a NDA, plus the time between the submission date of a NDA 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 product
or therapeutic candidate is eligible for the extension and the application for extension must be made prior to expiration of the patent.
The United States Patent and Trademark Office (USPTO), in consultation with the FDA, reviews and approves the application for any patent
term extension or restoration. In the future, we intend to apply for restorations of patent term for some of our currently owned or licensed
patents to add patent life beyond their current expiration date, depending on the expected length of clinical trials and other factors
involved in the submission of the relevant NDA.

Abbreviated New Drug Application (ANDA)
Approval Process

The
Hatch-Waxman Amendments established an abbreviated FDA approval process for generic drugs that are shown to be pharmaceutically equivalent
and bioequivalent to drugs previously approved by the FDA through the NDA process. Approval to market and distribute these drugs is obtained
by filing an abbreviated new drug application, or ANDA, with the FDA. An ANDA provides for marketing of a drug product that has the same
active ingredients in the same strengths and dosage form as the listed drug and has been shown to be bioequivalent to the listed drug.
An ANDA is a comprehensive submission that contains, among other things, data and information pertaining to the active pharmaceutical
ingredient, drug product formulation, specifications and stability of the generic drug, as well as analytical methods, manufacturing
process validation data and quality control procedures. ANDAs are termed abbreviated because they generally do not include preclinical
and clinical data to demonstrate safety and effectiveness. Instead, a generic applicant must demonstrate that its product is bioequivalent
to the innovator drug. Drugs approved in this way are commonly referred to as “generic equivalents” to the listed drug and
can often be substituted by pharmacists under prescriptions written for the original listed drug.

41

Section
505(b)(2) NDA Approval Process

As
an alternative path to FDA approval for modifications to formulations or uses of products previously approved by the FDA, an
applicant may submit an NDA under Section 505(b)(2) of the Federal Food, Drug, and Cosmetic Act (FDCA). Section 505(b)(2) was
enacted as part of the Hatch-Waxman Amendments to the FDCA and enables the applicant to rely, in part, on the FDA’s previous
approval of a similar product, and/or published literature, in support of its application. Section 505(b)(2) permits the filing of
an NDA where at least some of the information required for approval comes from studies not conducted by, or for, the applicant and
for which the applicant has not obtained a right of reference. If the Section 505(b)(2) applicant can establish that reliance on
FDA’s previous findings of safety and effectiveness is scientifically appropriate, it may eliminate the need to conduct
certain preclinical studies or clinical trials of the new product. The FDA may also require companies to perform additional studies
or measurements, including clinical trials, to support the change from the approved reference drug. The FDA may then approve the new
product candidate for all, or some, of the label indications for which the reference drug has been approved or for any new
indication sought by the Section 505(b)(2) applicant.

ANDA
and 505(b)(2) products may be significantly less costly to bring to market than the reference listed drug, and companies that produce
generic products are generally able to offer them at lower prices. Moreover, generic versions of RLDs are often automatically substituted
for the RLD by pharmacies when dispensing a prescription written for the RLD. Thus, following the introduction of a generic drug, a significant
percentage of the sales of any branded product or reference listed drug is typically lost to the generic product.

ANDA
and 505(b)(2) NDA Patent Certification Requirements

Any
applicant who files an ANDA seeking approval of a generic equivalent version of a drug listed in the Orange Book or a Section 505(b)(2)
NDA referencing a drug listed in the Orange Book must certify to the FDA, as applicable, that (1) no patent information on the drug product
that is the subject of the application has been submitted to the FDA; (2) such patent has expired; (3) the date on which such patent
expires; or (4) such patent is invalid or will not be infringed upon by the manufacture, use or sale of the drug product for which the
application is submitted. This last certification is known as a paragraph IV certification. If an ANDA is submitted to FDA with a Paragraph
IV Certification, the generic applicant must also provide a “Paragraph IV Notification” to the holder of the NDA for the
RLD and to the owner of the listed patent(s) being challenged by the ANDA applicant, providing a detailed written statement of the bases
for the ANDA applicant’s position that the relevant patent(s) is invalid or would not be infringed. If the patent owner brings
a patent infringement lawsuit against the ANDA applicant within 45 days of the Paragraph IV Notification, FDA approval of the ANDA will
be automatically stayed for 30 months, or until 7-1/2 years after the NDA approval if the generic application was filed between 4 years
and 5 years after the NDA approval. Any such stay will be terminated earlier if the court rules that the patent is invalid or would not
be infringed. The applicant may, in certain circumstances, elect to submit a “section viii” statement with respect to a listed
method of use patent, certifying that the proposed generic labeling does not contain (or carves out) any language that would infringe
a method of use patented listed in the Orange Book for the RLD.

The
ANDA or Section 505(b)(2) application also will not be approved until any applicable non-patent exclusivity listed in the Orange Book
for the reference drug has expired as described in further detail below.

Regulatory
Exclusivities

New
Chemical Entity (NCE) Exclusivity

The
Hatch-Waxman amendments provides a period of five years of non-patent marketing exclusivity for the first approved drug containing a
new chemical entity (“NCE”) as an active ingredient. An NCE is an active moiety that has not been approved by the FDA in
any other NDA. A fixed combination drug product may receive NCE exclusivity if one of its active ingredients is an NCE, but not if
all of its active ingredients have previously been approved. An “active moiety” is defined as the molecule or ion
responsible for the drug substance’s physiological or pharmacologic action. During the five year exclusivity period, the FDA
cannot accept for filing any ANDA or 505(b)(2) NDA seeking approval of a product that contains the same active moiety, except that
the FDA may accept such an application for filing after four years if the application includes a paragraph IV certification to a
listed patent. In the case of such applications accepted for filing between four and five years after approval of the reference
drug, the thirty month stay of approval triggered by a timely patent infringement lawsuit is extended by the amount of time
necessary to extend the stay until 7-1/2 years after the approval of the reference drug NDA.

42

New
Clinical Trial (3-Year) Exclusivity

A
drug, including one approved under Section 505(b)(2), may obtain a three year period of exclusivity for a particular indication or
condition of approval, or change to a marketed product, such as a new formulation for a previously approved product, if one or more
new clinical trials (other than bioavailability studies) was essential to the approval of the application or supplemental
application and was conducted/sponsored by the applicant. Should this occur, the FDA would be precluded from approving any ANDA or
Section 505(b)(2) application for the protected modification until after that three year exclusivity period has run. However, unlike
NCE exclusivity, the FDA can accept an application and begin the review process during the exclusivity period.

Orphan
Drug Designation and Orphan Exclusivity

Under
the Orphan Drug Act, the FDA may grant Orphan Drug Designation to a therapeutic candidate intended to treat a rare disease or condition,
which is generally a disease or condition that affects either (i) fewer than 200,000 individuals in the United States, or (ii) more than
200,000 individuals in the United States and for which there is no reasonable expectation that the cost of developing and making available
in the United States a product or therapeutic candidate for this type of disease or condition will be recovered from sales in the United
States for that product or therapeutic candidate. Orphan Drug Designation must be requested before submitting a BLA. 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 or therapeutic candidate that has Orphan Drug Designation subsequently receives the first FDA approval for the disease for
which it has such designation, the approved product is entitled to orphan product exclusivity, which means that the FDA may not approve
any other marketing applications for the same drug for the same indication, except under limited circumstances, for seven years. Orphan
product exclusivity, however, could also block the approval of one of our therapeutic candidates for seven years if a competitor obtains
approval of the same drug as defined by the FDA, or if our therapeutic candidate is determined to be contained within a competitor’s
approved drug for the same indication or disease.

In
addition, an orphan drug credit is available for qualifying costs incurred between the date the FDA designates a drug as an orphan drug
and the date the FDA approves the drug.

Pediatric
Exclusivity

Pediatric
exclusivity is another type of non-patent marketing exclusivity available in the United States and, if granted, it provides for the attachment
of an additional six months of marketing protection to the term of any existing regulatory exclusivity or listed patents. Under the Best
Pharmaceuticals for Children Act, or BPCA, certain therapeutic candidates may obtain an additional six months of exclusivity if the sponsor
conducts pediatric research and submits new clinical information requested in writing by the FDA, referred to as a Written Request, relating
to the use of the active moiety of the product or therapeutic candidate in children. The data do not need to support a label change for
pediatric use; rather, the additional protection is granted if the pediatric clinical trial is deemed to have fairly responded to the
FDA’s Written Request. Although the FDA may issue a Written Request for studies on either approved or unapproved indications, it
may only do so where it determines that information relating to that use of a product or therapeutic candidate in a pediatric population,
or part of the pediatric population, may produce health benefits in that population. The issuance of a Written Request does not require
the sponsor to undertake the described trials. This is not a patent term extension, but it effectively extends the regulatory period
during which the FDA cannot approve another application.

43

Post-Approval
Requirements

Following
approval of a new drug or biologic product, the manufacturer and the approved product are subject to pervasive and continuing regulation
by the FDA, including, among other things, continuing cGMP compliance, monitoring and recordkeeping activities, reporting of adverse
experiences with the product, product sampling and distribution restrictions, complying with promotion and advertising requirements,
which include restrictions on promoting drugs for unapproved uses or patient populations (i.e., “off-label use”) and limitations
on industry-sponsored scientific and educational activities. Although physicians may prescribe legally available products for off-label
uses, manufacturers may not market or promote such uses. 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. If there are any modifications to the product, 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 a NDA supplement, which may require the applicant to
develop additional data or conduct additional preclinical studies and clinical trials.

Once
an NDA or BLA approval is granted, the FDA may withdraw the approval if compliance with regulatory requirements and standards is not
maintained or if problems occur after the product or therapeutic reaches the market. Later discovery of previously unknown problems with
a product or therapeutic candidate, including adverse events of unanticipated severity or frequency, may result in in mandatory revisions
to the approved labeling to add new safety information; imposition of post-market or clinical trials to assess new safety risks; or imposition
of distribution 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 other enforcement-related letters or clinical holds on post-approval clinical trials;

●
refusal
of the FDA to approve pending applications or supplements to approved application, or suspension or revocation of product approvals;

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

●
injunctions
or the imposition of civil or criminal penalties;

●
consent
decrees, corporate integrity agreements, debarment, or exclusion from federal health care programs; or

●
mandated
modification of promotional materials and labeling and the issuance of corrective information.

Accordingly,
a therapeutic candidate manufactured or distributed by us pursuant to FDA approvals are subject to continuing regulation by the FDA,
including, among other things:

●
cGMP
compliance requirements;

●
record-keeping
requirements;

●
reporting
of adverse experiences with the therapeutic candidate;

●
providing
the FDA with updated safety and efficacy information;

●
therapeutic
sampling and distribution requirements;

●
notifying
the FDA and gaining its approval of specified manufacturing or labeling changes; and complying with FDA promotion and advertising
requirements, which include, among other things, standards for direct-to-consumer advertising, restrictions on promoting products
for uses or in-patient populations that are not described in the product’s approved labeling, limitations on industry-sponsored
scientific and educational activities and requirements for promotional activities involving the internet.

FDA
regulations require that products be manufactured in specific approved facilities and in accordance with cGMPs. The cGMP regulations
include requirements relating to organization of personnel, buildings and facilities, equipment, control of components and drug product
containers and closures, production and process controls, packaging and labeling controls, holding and distribution, laboratory controls,
records and reports and returned or salvaged products. Therapeutic manufacturers and other entities involved in the manufacture and distribution
of approved therapeutic products are required to register their establishments with the FDA and certain state agencies and are subject
to periodic unannounced inspections by the FDA, foreign regulatory agencies, and some state agencies for compliance with cGMPs and other
laws. In addition, changes to the manufacturing process are strictly regulated, and, depending on the significance of the change, may
require FDA approval before being implemented. FDA regulations also require investigation and correction of any noncompliance with cGMP
requirements. FDA regulations also require investigation and correction of any deviations from cGMP and impose reporting and documentation
requirements upon the NDA or BLA applicant and any third-party manufacturers involved in producing the approved product. Accordingly,
manufacturers must continue to expend time, money and effort in the area of production and quality control to maintain compliance with
cGMP and other aspects of quality control and quality assurance.

44

In
addition, the distribution of prescription pharmaceutical products is subject to the Prescription Drug Marketing Act, or the PDMA,
which regulates the distribution of drugs and drug samples at the federal level and sets minimum standards for the registration and
regulation of drug distributors by the states. Both the PDMA and state laws limit the distribution of prescription pharmaceutical
product samples and impose requirements to ensure accountability in distribution. The Drug Supply Chain Security Act, or the DSCSA,
was enacted with the aim of building an electronic system to identify and trace certain prescription drugs distributed in the United
States, including most biological products. The DSCSA mandates phased-in and resource-intensive obligations for pharmaceutical
manufacturers, wholesale distributors, and dispensers over a ten year period that is expected to culminate in November 2023. From
time to time, new legislation and regulations may be implemented that could significantly change the statutory provisions governing
the approval, manufacturing and marketing of products regulated by the FDA. It is impossible to predict whether further legislative
or regulatory changes will be enacted, or FDA regulations, guidance or interpretations changed or what the impact of such changes,
if any, may be.

Regulation
Outside of the United States

In
addition to regulations in the United States, we will be subject to regulations of other jurisdictions governing any clinical trials
and commercial sales and distribution of our therapeutic candidates. Whether or not we obtain FDA approval for a product, we must obtain
approval by the comparable regulatory authorities of countries outside of the United States before we can commence clinical trials in
such countries and approval of the regulators of such countries or economic areas, such as the European Union, before we may market products
in those countries or areas. The approval process and requirements governing the conduct of clinical trials, product licensing, pricing
and reimbursement vary greatly from place to place, and the time may be longer or shorter than that required for FDA approval.

Under
European Union regulatory systems, a company can consider applying for marketing authorization in several European Union member states
by submitting its marketing authorization application(s) under a centralized, decentralized or mutual recognition procedure. The centralized
procedure provides for the grant of a single marketing authorization that is valid for all European Union member states. The centralized
procedure is compulsory for medicines derived from biotechnology, orphan medicinal products, or those medicines with an active substance
not authorized in the European Union on or before May 20, 2004 intended to treat acquired immune deficiency syndrome, cancer, neurodegenerative
disorders or diabetes and optional for those medicines containing a new active substance not authorized in the European Union on or before
May 20, 2004, medicines which are highly innovative, or medicines to which the granting of a marketing authorization under the centralized
procedure would be in the interest of patients at the European Union-level. The decentralized procedure provides for recognition by European
Union national authorities of a first assessment performed by one of the member states. Under this procedure, an identical application
for marketing authorization is submitted simultaneously to the national authorities of several European Union member states, one of them
being chosen as the “Reference Member State,” and the remaining being the “Concerned Member States.” The Reference
Member State must prepare and send drafts of an assessment report, summary of product characteristics and the labeling and package leaflet
within 120 days after receipt of a valid marketing authorization application to the Concerned Member States, which must decide within
90 days whether to recognize approval. If any Concerned Member State does not recognize the marketing authorization on the grounds of
potential serious risk to public health, the disputed points are eventually referred to the European Commission, whose decision is binding
on all member states. The mutual recognition procedure is similar to the decentralized procedure except that a medicine must have already
received a marketing authorization in at least one of the member states, and that member state acts as the Reference Member State.

As
in the United States, we may apply for designation of a therapeutic candidate as an orphan drug for the treatment of a specific indication
in the European Union before the application for marketing authorization is made.

45

Orphan
drugs in the European Union enjoy economic and marketing benefits, including up to ten years of market exclusivity for the approved indication
unless another applicant can show that its product is safer, more effective or otherwise clinically superior to the orphan-designated
product, the marketing authorization holder is unable to supply sufficient quantity of the medicinal product, or the marketing authorization
holder has given its consent.

Coverage,
Pricing 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 may be significant delays in obtaining coverage and reimbursement
for approved products, and coverage may be more limited than the purposes for which the product is approved by the FDA or regulatory
authorities in other countries. It is time consuming and expensive to seek reimbursement from third-party payors. Moreover, eligibility
for reimbursement does not imply that any product will be paid for in all cases or at a rate that covers our costs, including research,
development, manufacture, sale and distribution. Interim payments for new products, if applicable, may also not be sufficient to cover
our costs and may not be made permanent. Payment rates may vary according to the use of the product and the clinical setting in which
it is used, may be based on payments allowed for lower cost products that are already reimbursed and may be incorporated into existing
payments for other services. Net prices for products may be reduced by mandatory discounts or rebates required by third-party payors
and by any future relaxation of laws that presently restrict imports of products from countries where they may be sold at lower prices
than in the United States. In the U.S., third-party payors often rely upon Medicare coverage policy and payment limitations in setting
their own reimbursement policies, but they also have their own methods and approval process apart from Medicare coverage and reimbursement
determinations. Accordingly, one third-party payor’s determination to provide coverage for a product does not assure that other
payors will also provide coverage for the product.

Additionally,
the containment of healthcare costs has become a priority of federal and state governments and the prices of therapeutics have been a
focus in this effort. The United States government, state legislatures and foreign governments have shown significant interest in implementing
cost-containment programs, including price controls, restrictions on reimbursement and requirements for substitution of generic and biosimilar
products. Adoption of price controls and cost-containment measures, and adoption of more restrictive policies in jurisdictions with existing
controls and measures, could further limit our net revenue and results. If these third-party payors do not consider our products to be
cost-effective compared to other therapies, they may not cover our products after approval as a benefit under their plans or, if they
do, the level of payment may not be sufficient to allow us to sell our products on a profitable basis. In addition, companion diagnostic
tests require coverage and reimbursement separate and apart from the coverage and reimbursement for their companion pharmaceutical or
biological products. Similar challenges to obtaining coverage and reimbursement for the pharmaceutical or biological products apply to
companion diagnostics.

Moreover,
in some foreign countries, the proposed pricing for a product and therapeutic candidate must be approved before it may be lawfully marketed.
The requirements governing therapeutic pricing 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 therapeutic candidates. Historically, therapeutic candidates
launched in the European Union do not follow price structures of the United States and generally tend to be significantly lower.

Healthcare
Reform

In
the United States and some foreign jurisdictions, there have been, and continue to be, several legislative and regulatory changes and
proposed changes regarding the healthcare system that could prevent or delay marketing approval of product and therapeutic candidates,
restrict or regulate post-approval activities, and affect the ability to profitably sell product and therapeutic candidates that obtain
marketing approval. The FDA’s and other regulatory authorities’ policies may change, and additional government regulations
may be enacted that could prevent, limit, or delay regulatory approval of our product and therapeutic candidates. For example, in the
United States, the system for FDA to collect and expend user fees paid by manufacturers of drugs, biologics, and medical devices must
be reauthorized by statute every five years, and since 1992, each reauthorization legislation has included, to greater or lesser degrees,
various other changes to the FDA’s regulatory systems and procedures. The current legislative authority for FDA user fees expired
in September 2022, new legislation will be required for FDA to continue collecting prescription drug user fees in future fiscal years.
The reauthorization may include new legal provisions that could significantly impact our business in ways that cannot be predicted at
this time. If we are slow or unable to adapt to changes in existing requirements or the adoption of new requirements or policies, or
if we are not able to maintain regulatory compliance, we may lose any marketing approval that we otherwise may have obtained and we may
not achieve or sustain profitability, which would adversely affect our business, prospects, financial condition and results of operations.
Moreover, among policy makers and payors in the United States and elsewhere, there is significant interest in promoting changes in healthcare
systems with the stated goals of reducing drug prices, containing healthcare costs more generally, improving quality and/or expanding
access.

46

For
example, the Patient Protection and Affordable Care Act, as amended by the Health Care and Education Reconciliation Act, or collectively
the ACA, was enacted in March 2010 and has had a significant impact on the health care industry in the U.S. The ACA expanded coverage
for the uninsured while at the same time containing overall healthcare costs. It also included the BPCIA, which created an abbreviated
approval pathway for biological products that are biosimilar to or interchangeable with an FDA-licensed reference biological product.
With regard to biopharmaceutical products, the ACA, among other things, addressed a new methodology by which rebates owed by manufacturers
under the Medicaid Drug Rebate Program are calculated for drugs that are inhaled, infused, instilled, implanted or injected, increased
the minimum Medicaid rebates owed by manufacturers under the Medicaid Drug Rebate Program and extended the rebate program to individuals
enrolled in Medicaid managed care organizations, established annual fees on manufacturers of certain branded prescription drugs, and
created a new Medicare Part D coverage gap discount program.

Since
its enactment, there have been executive, judicial and Congressional challenges to certain aspects of the ACA and we expect there may
be additional challenges and amendments to the ACA in the future.

In
addition, other legislative changes have been proposed and adopted in the United States since the ACA that affect health care expenditures.
These changes include aggregate reductions to Medicare payments to providers of up to 2% per fiscal year pursuant to the Budget Control
Act of 2011, which began in 2013 and will remain in effect through 2030 unless additional Congressional action is taken. The Coronavirus
Aid, Relief, and Economic Security Act, or the CARES Act, which was signed into law on March 27, 2020, and was designed to provide financial
support and resources to individuals and businesses effected by the COVID-19 pandemic, suspended the 2% Medicare sequester from May 1,
2020 through December 31, 2020, and extended the sequester by one year, through 2030, in order to offset the added expense of the 2020
cancellation.

Additionally,
on December 20, 2019, the Further Consolidated Appropriations Act for 2020 became law (P.L. 116-94), which includes a piece of bipartisan
legislation called the Creating and Restoring Equal Access to Equivalent Samples Act of 2019 or the “CREATES Act.” The CREATES
Act aims to address the concern articulated by both the FDA and others in the industry that some brand manufacturers have improperly
restricted the distribution of their products, including by invoking the existence of a REMS for certain products, to deny generic and
biosimilar product developers access to samples of brand products. Because generic and biosimilar product developers need samples to
conduct certain comparative testing required by the FDA, some have attributed the inability to timely obtain samples as a cause of delay
in the entry of generic and biosimilar products. To remedy this concern, the CREATES Act establishes a private cause of action that permits
a generic or biosimilar product developer to sue the brand manufacturer to compel it to furnish the necessary samples on “commercially
reasonable, market-based terms.” Whether and how generic and biosimilar product developments will use this new pathway, as well
as the likely outcome of any legal challenges to provisions of the CREATES Act, remain highly uncertain and its potential effects on
our future commercial products are unknown.

Moreover,
there has been heightened governmental scrutiny over the manner in which 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. While the Trump administration put forward various proposals and executive orders
aimed at reducing drug prices, the Biden administration is likely to pursue its own proposals going forward. In August 2021, President
Biden announced his support for legislative proposals to grant Medicare the power to negotiate lower drug prices, for pharmaceutical
companies to face penalties if they raise prices faster than inflation, and to impose a new cap on how much Medicare recipients have
to spend on medications. Such proposals may be included in upcoming legislation in Congress, but the outcome of such proposals remains
uncertain.

47

Individual
states in the United States have also increasingly passed legislation and implemented regulations designed to control pharmaceutical
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.

We
cannot predict the likelihood, nature or extent of government regulation that may arise from future legislation or administrative or
executive action, either in the United States or abroad. We expect that additional state and federal health care reform measures will
be adopted in the future, any of which could limit the amounts that federal and state governments will pay for health care products and
services.

Other
Healthcare Laws

Our
current and future business operations are subject to healthcare regulation and enforcement by the federal government and the states
and foreign governments where we research, and, if approved, market, sell and distribute our therapeutic candidates. These laws include,
without limitation, state and federal anti-kickback, fraud and abuse, false claims, privacy and security, physician sunshine and drug
pricing transparency laws and regulations such as:

●
The
federal Anti-Kickback Statute prohibits, among other things, any person from knowingly and willfully offering, soliciting, receiving
or providing remuneration, directly or indirectly, to induce either the referral of an individual, for an item or service or the
purchasing or ordering of a good or service, for which payment may be made under federal healthcare programs such as the Medicare
and Medicaid programs. The federal Anti-Kickback Statute is subject to evolving interpretations. In the past, the government has
enforced the federal Anti-Kickback Statute to reach large settlements with healthcare companies based on sham consulting and other
financial arrangements with physicians. A person or entity does not need to have actual knowledge of the statute or specific intent
to violate it in order to have committed a violation. In addition, 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 civil and criminal false claims laws, including the civil False Claims Act, and civil monetary penalty laws, prohibit, among
other things, knowingly presenting or causing the presentation of a false, fictitious or fraudulent claim for payment to the U.S.
government, knowingly making, using, or causing to be made or used a false record or statement material to a false or fraudulent
claim to the U.S. government, or from knowingly making a false statement to avoid, decrease or conceal an obligation to pay money
to the U.S. government. Actions under these laws may be brought by the Attorney General or as a qui tam action by a private individual
in the name of the government. The federal government uses these laws, and the accompanying threat of significant liability, in its
investigation and prosecution of pharmaceutical and biotechnology companies throughout the U.S., for example, in connection with
the promotion of products for unapproved uses and other allegedly unlawful sales and marketing practices;

● 
The
U.S. federal Health Insurance Portability and Accountability Act of 1996, or HIPAA, includes federal, civil and criminal provisions
that prohibit among other actions, knowingly and willfully executing, or attempting to execute, a scheme to defraud any healthcare
benefit program, including private third-party payors, knowingly and willfully embezzling or stealing from a healthcare benefit program,
willfully obstructing a criminal investigation of a healthcare offense, and knowingly and willfully falsifying, concealing or covering
up a material fact or making any materially false, fictitious or fraudulent statement in connection with the delivery of or payment
for healthcare benefits, items or services. Similar to the federal Anti-Kickback Statute, a person or entity does not need to have
actual knowledge of the statute or specific intent to violate it in order to have committed a violation;

48

●
The
Physician Payments Sunshine Act, among other things, imposes requirements on manufacturers of FDA-approved drugs, devices, biologics
and medical supplies covered by Medicare or Medicaid to report, on an annual basis, to HHS information related to payments and other
transfers of value to physicians (defined to include doctors, dentists, optometrists, podiatrists, chiropractors and, beginning in
2022 for payments and other transfers of value provided in the previous year, certain advanced non-physician health care practitioners),
teaching hospitals, as well as ownership and investment interests held by physicians and their immediate family members;

●
HIPAA,
as amended by the Health Information Technology for Economic and Clinical Health Act, or HITECH, and their respective implementing
regulations impose specified requirements relating to the privacy, security and transmission of individually identifiable health
information. Among other things, HITECH makes HIPAA’s privacy and security standards directly applicable to “business
associates,” defined as independent contractors or agents of covered entities, which include certain healthcare providers,
health plans, and healthcare clearinghouses, that create, receive, maintain or transmit protected health information in connection
with providing a service for or on behalf of a covered entity. HITECH also increased the civil and criminal penalties that may be
imposed against covered entities, business associates and possibly other persons, and gave state attorneys general new authority
to file civil actions for damages or injunctions in federal courts to enforce HIPAA and seek attorney’s fees and costs associated
with pursuing federal civil actions; and

●
Analogous
state 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 which require pharmaceutical companies to comply with the pharmaceutical industry’s voluntary compliance guidelines
and the relevant compliance guidance promulgated by the federal government in addition to requiring drug and therapeutic biologics
manufacturers to report information related to payments to physicians and other healthcare providers or marketing expenditures and
pricing information; state and local laws which require the registration of pharmaceutical sales representatives; and state laws
and non-United States laws and regulations (particularly European Union laws regarding personal data relating to individuals based
in Europe) that govern the privacy and security of health information in certain circumstances, many of which differ from each other
in significant ways, thus complicating compliance efforts.

●
Ensuring
that our current and future business arrangements with third parties comply with applicable healthcare laws and regulations could
involve substantial costs. It is possible that governmental authorities will conclude that our business practices do not comply with
current or future statutes, regulations, agency guidance or case law involving applicable fraud and abuse or other healthcare laws
and regulations. If our operations are found to be in violation of any such requirements, we may be subject to significant civil,
criminal and administrative penalties, including monetary damages, fines, disgorgement, imprisonment, loss of eligibility to obtain
approvals from the FDA, exclusion from participation in government contracting, healthcare reimbursement or other government programs,
including Medicare and Medicaid, reputational harm, diminished profits and future earnings, additional reporting requirements if
we become subject to a corporate integrity agreement or other agreement to resolve allegations of non-compliance with any of these
laws, and the curtailment or restructuring of our operations.

Manufacturing

We
do not own or operate manufacturing facilities to produce any of our therapeutic candidates, nor do we have plans to develop our own
manufacturing operations in the foreseeable future. We currently depend on third-party contract manufacturers for all our required raw
materials, Active Pharmaceutical Ingredient (API), and finished products for our preclinical and clinical trials and if and when applicable,
commercialization. We currently employ internal resources to manage our manufacturing relationships with these third parties.

Manufacturers
of our products are required to comply with applicable FDA manufacturing requirements contained in the FDA’s current good manufacturing
practices, or cGMP, regulations. cGMP regulations require, among other things, quality control and quality assurance as well as corresponding
maintenance of records and documentation. Pharmaceutical product manufacturers and other entities involved in the manufacture and distribution
of approved pharmaceutical products are required to register their establishments with the FDA and certain state agencies and are subject
to periodic unannounced inspections by the FDA and certain state agencies for compliance with cGMP and other laws. Accordingly, manufacturers
must continue to expend time, money, and effort in the area of production and quality control to maintain cGMP compliance. Discovery
of problems with a product after approval may result in restrictions on a product, manufacturer or holder of an approved NDA, including
withdrawal of the product from the market. In addition, changes to the manufacturing process generally require prior FDA approval before
being implemented.

49

Regulations
- Environmental

We
are subject to various environmental laws of federal, state and local governments and foreign governments at various levels. Compliance
with existing laws has not had a material adverse effect on our capital expenditures, competitive position, financial condition or results
of operations, and management does not believe it will have such an impact in the current fiscal year. However, we cannot predict the
impact of unforeseen environmental contingencies or new or changed laws or regulations on our business.

Digital
Asset Treasury Strategy

On
October 7, 2025, we announced our launch of a new digital asset treasury strategy focused on top-tier cryptocurrency assets. On October
6, 2025, our Board of Directors authorized holdings of up to 90% of the Company’s liquid assets in various cryptocurrencies. Corporate
officers are authorized to purchase and sell Bitcoin (BTC), Ethereum (ETH), and USD Coin (USDC) initially. Management will regularly
consult with the Board on cryptocurrency transactions and holdings, cybersecurity procedures, accounting policies, risks, and material
developments. Due to cryptocurrency volatility, the Company’s digital asset
strategy is currently on hold. As
of the date of this report, the Company holds approximately $0 in digital assets.

Employees

As
of December 31, 2025, we had a total of 13 full-time employees which includes one employee employed by our Romanian subsidiary. We believe
that we maintain a satisfactory working relationship with our employees, and we have not experienced any significant labor disputes or
any difficulty in recruiting staff for our operations. None of our employees are represented by a labor union.

Human
Capital Resources

Employee
Engagement, Talent Development & Benefits. We believe that our future success largely depends upon our continued ability to attract
and retain highly skilled employees. We provide our employees with competitive salaries and bonuses, and opportunities for equity ownership.

Diversity,
Inclusion, and Culture. Much of our success is rooted in the diversity of our teams and our commitment to inclusion. We value diversity
at all levels and continue to focus on extending our diversity and inclusion initiatives across our entire workforce. We believe that
our business benefits from the different perspectives a diverse workforce brings, and we pride ourselves on having a strong, inclusive
and positive culture based on our shared mission and values.

Our
Corporate Information

We
were incorporated in Delaware in August 2018, and we have operations in Chicago, Illinois, with some of our team members setup virtually
and working remotely in California, Oregon, Massachusetts, Iowa, Ohio, Texas, North Carolina, and New Jersey. Our principal executive
office is located at 444 West Lake Street, Suite 1700, Chicago, IL 60606, and our phone number is (312) 416-8592. In July 2021, we established
a wholly owned Australian subsidiary, MAIA Biotechnology Australia Pty Ltd, to conduct various preclinical and clinical activities for
the development of our product candidates. In April 2022, we established a wholly owned Romanian subsidiary, MAIA Biotechnology Romania
S.R.L. to conduct various preclinical and clinical activities for the development of our product candidates. Our website address is www.MAIABiotech.com.
The information contained on our website is not incorporated by reference into this Annual Report on Form 10-K, and you should not consider
any information contained on, or that can be accessed through, our website as part of this Annual Report on Form 10-K or in deciding
whether to purchase our common stock.

50

Implications
of Being an Emerging Growth Company

We
are an “emerging growth company,” as defined in Section 2(a) of the Securities Act of 1933, as amended (the “Securities
Act”), as modified by the Jumpstart Our Business Startups Act of 2012, or the JOBS Act. As such, we are eligible to take advantage
of certain exemptions from various reporting requirements that are applicable to other public companies that are not emerging growth
companies including, but not limited to:

●
not
being required to comply with the auditor attestation requirements of Section 404 of the Sarbanes-Oxley Act of 2002, as amended,
or the Sarbanes-Oxley Act;

●
reduced
disclosure obligations regarding executive compensation in our periodic reports, proxy statements, and registration statements; and

●
exemptions
from the requirements of holding a non-binding advisory vote on executive compensation and stockholder approval of any golden parachute
payments not previously approved.

If
some investors find our common stock less attractive as a result of these exemptions, there may be a less active trading market for our
common stock and the price of our common stock may be more volatile.

In
addition, Section 107 of the JOBS Act also provides that an emerging growth company can take advantage of the extended transition period
provided in Section 7(a)(2)(B) of the Securities Act of 1933 (the “Securities Act”) for complying with new or revised accounting
standards. In other words, an emerging growth company can delay the adoption of certain accounting standards until those standards would
otherwise apply to private companies. We intend to take advantage of the benefits of this extended transition period.

We
will remain an emerging growth company until the earlier of (1) the last day of the fiscal year (a) following the fifth anniversary
of the completion of our initial public offering, (b) in which we have total annual gross revenue of at least $1.235 billion, or (c)
in which we are deemed to be a large accelerated filer, which means the market value of our common stock that is held by
non-affiliates exceeds $700 million as of the prior June 30, and (2) the date on which we have issued more than $1.0 billion in
non-convertible debt securities during the prior three year period. References herein to emerging growth company will have the
meaning associated with it in the JOBS Act.

Implications
of Being a Smaller Reporting Company

Additionally,
we are a “smaller reporting company” as defined in Rule 10(f)(1) of Regulation S-K. Smaller reporting companies may take
advantage of certain reduced disclosure obligations, including, among other things, providing only two years of audited financial statements.
We will remain a smaller reporting company until the last day of the fiscal year in which (1) the market value of our common stock held
by non-affiliates equals or exceeds $250 million as of the end of that year’s second fiscal quarter, or (2) our annual revenues
equaled or exceeded $100 million during such completed fiscal year and the market value of our common stock held by non-affiliates equals
or exceeds $700 million as of the end of that year’s second fiscal quarter.