OTC: CERO

The ability to enhance the
activity of T cells against human cancers through genetic engineering has been among the most significant advances in cancer therapy in
the last decade. One of the more promising therapeutic uses of T cells to emerge has been CAR-T cell technology. However promising CAR-T
cell therapy has been, its use has been largely limited to the treatment of certain hematological cancers due to lack of specific tumor-associated
antigens and CAR-T cells’ limited ability to proliferate, traffic, and circulate in solid tumors. Curative CAR-T cell therapies
for solid tumors currently do not exist, and the significance of this limitation is underscored by the prevalence of solid tumor malignancies.
The American Cancer Society estimates that solid tumor cancers accounted for more than 1.7 million of the 1.9 million people newly diagnosed
with cancer in 2022. Even in hematological malignancies with approved CAR-T cell therapies, cure rates do not exceed 60%. Nevertheless,
despite such limitations, sales of CAR-T cell therapies are anticipated to grow rapidly over the next several years and are expected to
exceed $10 billion globally by 2030.

We believe that the preferential
attributes engineered into our CER-T cell therapy enable us to overcome many of the limitations which hinder the wider application of
CAR-T technology. Our CER-T cells employ a novel targeting mechanism that targets a ligand broadly expressed on tumor cells but not healthy
cells. Specifically, CER-1236 targets the TIM-4 Ligand (“TIM-4-L”), otherwise known as phosphatidylserine (“PS”),
a critical component of the cell’s plasma membrane that has a key role in cell removal. Exposure of TIM-4-L on the outer surface
of the plasma membrane acts as an “eat-me” signal and marks abnormal, stressed and dying or dead cells for phagocytosis. The
pro-phagocytic activities of CER-T cells are designed to integrate innate immune effector functions into cytotoxic killer T cells, creating
within a single T cell the ability to directly mediate cytotoxic effects and indirectly prime other immune cells. Moreover, in preclinical
studies, we have observed that CER-1236 cells exhibit superior cross-presentation abilities compared to conventional T cells, potentially
triggering a broad complement of immune effector cells against tumors. Since externally oriented TIM-4-L is broadly expressed by numerous
cancer cell types but has very limited exposure on normal healthy cells, we envision CER-1236 as having differentiated therapeutic utility
with application across a wide array of cancer types.

We have patterned the design
of our CER-T constructs based upon many of the components found in existing conventional CAR-T cell therapies, which we believe could
shorten development timelines and enhance commercial application. The processes and protocols used to genetically modify a patient’s
T cells to produce CAR-T cells are already well recognized, as is the use of lentivirus in the manufacture of these therapies. Accordingly,
we have developed CER-T cell manufacturing processes that closely resemble those used to produce existing engineered CAR-T cells. We also
expect to benefit from the well-defined and recognized regulatory guidelines established by both U.S. and European regulatory authorities
related to CAR-T therapies and their use. In contrast to these attributes, we believe that other emerging CAR-based drug candidates which
involve immune effector cells other than T cells, such as CAR-NK and CAR-M therapies, are unlikely to enjoy similar benefits.

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In preclinical studies, we have observed CER-1236
to display attractive functional attributes, among which are:

● target-dependent
activation, cytotoxicity, anti-tumor cytokine production, and high proliferative capacity;

● phagocytosis
of tumor cells;

● distinct
transcriptome, cytokine and chemokine signatures that substantiate the complementary activity of both the innate and adaptive immune
response;

● enhanced
antigen acquisition, processing and presentation;

● no
evidence of T cell exhaustion despite repeated challenges;

● no
observed off-target or off-tumor toxicities;

● expression
and maintenance of diverse T cell populations, including naïve and memory cells, likely indicative of response persistence and durability;
and

● well
defined and scalable manufacturing protocols.

Based on the preclinical data regarding the use of CER-1236 T cells
to combat hematologic malignancies, we began our Phase 1 clinical trial in May 2025. Our initial targets are relapsed or refractory AML
patients as well as AML patients with measurable residual disease (“MRD”) and patients with mutations in TP53, a gene mutation
associated with aggressive AML. AML is a heterogenous and aggressive hematopoietic malignancy characterized by the rapid buildup of immature
myeloid cells in the bone marrow and blood. This process results in the inhibition of normal hematopoiesis, manifesting as neutropenia,
anemia, thrombocytopenia, and the clinical features of bone marrow failure. According to the American Cancer Society, AML accounts for
90% of all acute leukemias in adults, with an estimated 22,010 new cases and 11,090 estimated deaths in the United States in 2025. The
current treatment has remained largely unchanged over several decades with combination chemotherapy with cytarabine for 7 days and an
anthracycline for 3 days (“7+3”). Newer, targeted approaches that include multi-kinase domain inhibitors and antibody-drug
conjugates are now available during induction chemotherapy for certain patients. For patients that are sufficiently healthy and at unfavorable
risk, allogeneic Hematopoietic Stem Cell Transplants (“HSCTs”) are commonly performed. Despite these interventions, there
is significant unmet medical need for novel therapies, including cell therapeutic approaches. In July 2025, CER-1236 received an FDA Orphan
Drug Designation for the treatment of acute myeloid leukemia. In September 2025, CER-1236 received FDA Fast Track Designation.

Our Phase 1 AML clinical
trial is intended to evaluate the safety, potential therapeutic utility and applicable dose of CER-1236. The approved starting dose for
the clinical trial is sufficiently high that we expect to begin to see clinical activity by the second dose level cohort. Based on favorable
interim safety results and effects in one patient, the trial was expanded to include patients with Myelodysplastic Syndrome (“MDS”)
and Myelofibrosis (“MF”). Concurrent with a trial in these hematological malignancies, we intend to expand the clinical development
of CER-1236 with an additional IND submission, which has been approved, to investigate solid tumors such as NSCLC and ovarian cancer.
We believe that CER-1236 has the potential to address unmet medical needs in the targeted indications, and be differentiated from currently
available therapeutics by its safety, tolerability and efficacy. We dosed the first three patients in dose 1 of our Phase 1 AML clinical
trial in May 2025, July 2025 and September 2025. The first patient of the second dose cohort was dosed in October 2025. The four patients
completed their DLT periods without any treatment-related toxicities, and the cell therapy was observed to expand during treatment of
all four patients, with a peak of expansion between 10 to 14 days post infusion. None of the abovementioned statements regarding any of
our products in development are intended to be a prediction or conclusion of efficacy.

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Our Strategy

Our intent is to become a
leading biopharmaceutical company focused on the capital-efficient advancement of innovative anti-cancer product candidates targeting
the unmet medical need associated with aggressive and difficult-to-treat hematological malignancies and solid tumors. To accomplish this
objective, the key elements of our strategy include:

●
Advance the clinical development of CER-1236 for the treatment of AML patients. We began dosing the cohort in our Phase 1 AML clinical trial of CER-1236 in May 2025. As of March 2026, five patients have had product successfully manufactured and were treated. For the first four patients, none had any dose-limiting toxicities during the 28 day observation window, and the cell therapies in the first four patients were observed to expand during the first 14 days period post infusion. For the fifth patient, with more than seven days of follow-up completed after infusion, protocol-defined monitoring of safety, pharmacokinetic, pharmacodynamic, and clinical activity endpoints is ongoing. Based on preclinical data generated to date related to the use of CER-1236 to treat hematological cancers, we intend to initially target relapsed and refractory AML patients for clinical development. These are aggressive cancers with limited treatment options. Moreover, these cancers represent a significant unmet medical need, and to date there are no approved CAR-T cell therapies for patients diagnosed with AML. There are approximately 20,800 cases of AML diagnosed annually in the U.S.

●
Incorporate treatment of MDS and MF into clinical trial. Early safety and efficacy signals in AML patients indicated the potential for use of CER-1236 in MDS and MF, both of which are more chronic inflammatory diseases of the bone marrow. The clinical trial was amended to include patients with these diseases in the dose-escalation phase and 3 new cohorts for the dose expansion phase were added to individually address these diseases. Both of these diseases are common in aged individuals and have limited curative treatment options, especially after resistance to frontline therapy develops. There are over 10,000 cases of MDS diagnosed annually in the US, and approximately 500 MF cases per year in the US.

●
Leverage past and current CAR-T product approvals to shorten the regulatory and manufacturing pathway for CER-1236. We have designed our CER-T cells to share similar construction to currently approved CAR-T cell therapies. The processes and protocols used to produce autologous CAR-T cells are well recognized, and we expect to benefit from the well-defined regulatory guidelines established by both U.S. and European regulatory authorities related to CAR-T cell therapy manufacture. Accordingly, we have configured CER-T cell manufacturing processes to share similarities with those employed in the production of CAR-T cells.

●
Expand CER-1236 development activities to target solid tumors. We intend to expand the clinical development of CER-1236 to include solid tumors. To this end, we plan on evaluating the potential therapeutic utility of CER-1236 to treat NSCLC and ovarian cancer, indications for which efficacious treatments have proven elusive. We believe CER-1236’s differentiated mechanism of action enables the enhanced activity of a broader contingent of immune effector cells, which may allow CER-1236 to achieve success treating cancers for which currently approved CAR-T cell therapies have demonstrated little clinical benefit. We anticipate initiation of a Phase 1 study in NSCLC and ovarian cancer in the second half of 2026.

The Immune System and its Function

The immune system is a host
defense system comprising multiple structures and processes within an organism that protects against disease. As with other mammalian
species, the human immune system is segregated into two separate yet interconnected components, the innate immune system and the adaptive
immune system. The innate immune system is responsible for an immediate, non-specific response to infected or diseased cells. Triggering
its activation are pathogen-associated and damage-associated molecular patterns recognized by preconfigured pattern recognition receptors
which reside on the surface of various types of leukocytes, or white blood cells, that make up the innate immune system, including macrophages,
dendritic cells, eosinophils and natural killer (“NK”) cells. In addition to its direct participation in eliminating damaged
or diseased cells, certain components of the innate immune system function significantly as antigen-presenting cells (“APCs”)
promoting the activity of the adaptive immune system.

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The adaptive immune system
is composed of special types of leukocytes known as T and B lymphocytes, also known as T and B cells, respectively. T cells participate
primarily in the cell-mediated immune response while B cells are involved in the humoral immune response. T cells are an essential component
of the adaptive immune system, targeting specific antigens and either destroying targeted cells directly or participating in their destruction
by activating other immune cells. T cells use T cell specific receptors to recognize antigens presented via major histocompatibility complex
(“MHC”) molecules on APCs. Through this mechanism, T cells have the ability to target tumor-transformed or virus infected
cells, as well as help coordinate the activity of other immune cells.

T cells are differentiated
by the expression of protein markers on their surface. The two most prominent types of T cells are those that express CD8 molecules and
are known as CD8 T cells, and those that express CD4 molecules and are known as CD4 T cells. CD8 T cells, also referred to as cytotoxic
lymphocytes (“CTLs”), eliminate cells which they encounter that are recognized as being infected with viruses or other pathogens
or are otherwise damaged or dysfunctional through a process referred to as cell lysis, which involves the release by these killer T cells
of perforins and granzymes to compromise the integrity of the target cell’s membrane. Endogenous pathogens are broken down by mechanisms
present in virtually all cells into smaller fragments and presented to CD8 T cells in combination with an MHC Class I molecule. CD4 T
cells, also referred to as T helper cells, have limited cytotoxic activity and typically do not kill infected or dysfunctional cells or
eliminate pathogens directly. Instead, they participate in the immune response by providing signals which activate and orchestrate other
types of immune cells to perform these tasks. Professional APCs, such as dendritic cells and macrophages, process exogenous pathogens
and then present small fragments of the degraded pathogen to CD4 T cells in combination with an MHC Class II molecule, through a phenomenon
known as cross-presentation, while antigens of exogenous origin are coupled with an MHC Class I molecule to amplify CD8 T cell activity.
Antigen cross presentation is of particular importance in the immune system’s response to cancer.

Genetically Engineered T Cells

The ability to enhance the
activity of T cells against human cancers through genetic engineering has been among the most significant advances in cancer therapy in
the last decade. Advances in understanding T cells and their role in immunology, and an appreciation of their potential use to treat cancer,
has increased interest in the clinical application of T cells in recent years, with the field of adoptive immunotherapy attaining increased
prominence as a means of enhancing immune control over tumors. Modern molecular biological techniques allow scientists to introduce genes
into human T cells that enhance T cell activity, expand their numbers and infuse them back into the patient from whom they were originally
collected. We have developed a novel approach to T cell engineering which has enabled us to integrate certain desirable characteristics
of both the innate immune system and the adaptive immune system into a single therapeutic construct intended to optimize cancer therapy.
This novel cellular immunotherapy platform is designed to redirect T cells to eliminate tumors by building in engulfment pathways that
employ phagocytic programs, creating our CER-T cell therapy.

Phagocytosis is a vital cellular
process by which a phagocytic cell engulfs and internalizes a target for elimination and is a major mechanism for the removal of pathogens
and unwanted cells to maintain tissue homeostasis. The human body removes billions of cells daily through phagocytic processes. Phagocytic
removal employs specific cell clearance programs and machinery to eliminate target cells. The process is a crucial part of the innate
immune system and is distinct from the adaptive immune response which involves the generation of cytotoxic T cells to elicit antigen-specific,
cytolytic target elimination. Compared to traditional CAR-T cell approaches, which largely target the adaptive immune system, we developed
CER-T cell therapy to collaboratively mediate both cytotoxic and phagocytic mechanisms to optimize anti-tumor function. By leveraging
both immune responses, we believe CER-T cell therapy has the potential to eliminate cancer cells more effectively and with fewer side
effects than traditional CAR-T cell therapies.

The recognition of phagocytosis
as a therapeutic modality to directly clear cancer cells and initiate anti-tumor T cell immune responses has fueled interest in effectively
engaging phagocytes for use in cancer therapy. Macrophage cell engineering and macrophage-targeting approaches that enhance cytotoxic,
phagocytic and cytokine-mediated anti-tumor function are in development. Early clinical trial data from therapeutic candidates targeting
myeloid inhibitor function has demonstrated the potential to elicit clinical responses. However, the diverse pro-tumor functions of myelo-monocytic
cells may offset these efforts by supporting cancer cell survival, proliferation and the release of factors that may impede anti-tumor
immune responses. Limited in vivo proliferation and manufacturing challenges have also been hurdles in the development of macrophage-based
cellular therapy.

Experimental evidence demonstrates
the ability of CER-T cells to engulf targeted cells, employ cytolytic and non-cytolytic killing mechanisms, and exhibit pro-inflammatory
and antigen processing capabilities that augment the current capabilities of T cell immunotherapy. To that end, we believe CER-1236 cell
therapy, if approved, may become a component of standard of care treatment regimens, used as a monotherapy or in combination with both
small molecule therapeutics and biologics to direct robust tumor elimination.

The Increasing Prominence of CAR-T Technology

Immunotherapy is a treatment
that harnesses the components and mechanics of the immune system to address diseases and disorders. Cellular immunotherapy is a form of
immunotherapy that focuses on modulating or enhancing the activity of different immune cells. One of the more prominent and promising
therapeutic uses of T-cells to emerge has been CAR-T cell technology.

CAR-T therapy recognizes
specific antigens that are present on the surface of tumor cells and destroys them. The concept of CAR-T builds upon the normal biology
of CTLs, whereby naturally occurring receptors serve to activate these cells when a foreign pathogen or cancerous cell is detected. Conventional
CAR-T cell therapy involves the genetic manipulation of a patient’s T cells to enable these modified cells to express a receptor
designed to bind to a specific surface antigen. To engineer these cells, a fraction of a patient’s T cells is collected from their
blood, and a viral vector containing the genetic instructions for the CAR is used to insert those genes into the genome of the T cell
through a process known as transduction. Contained in a single viral vector are the genes encoding for each component of the CAR. Typical
CAR-T cells include the following components:

● Antigen
recognition domain. At one end of the CAR is a binding domain that is specific to a targeted antigen. This domain is exposed to the
outside of the engineered lymphocyte, where it can recognize the target antigen or antigens. The extracellular target binding domain
of CAR-T therapies currently approved by the FDA typically use a single-chain variable fragment (“scFv”), consisting of the
heavy-chain and light-chain variable regions of an antibody.

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● Extracellular
hinge domain. The hinge domain is a small structural component which extends from the outer cell membrane to the antigen recognition
domain and provides conformational flexibility to facilitate optimal binding of the antigen recognition domain to the targeted antigen
on the surface of the cancer cell.

● Transmembrane
domain. This middle portion of the CAR links the antigen recognition domain to the activating elements inside the cell. The transmembrane
domain anchors the CAR in the lymphocyte’s membrane, bridging the extracellular hinge and antigen recognition domains with the
intracellular signaling domain and provides critical stability to the CAR. In addition, the transmembrane domain may also interact with
other transmembrane proteins that enhance CAR function.

● Intracellular
signaling domain. The other end of the CAR, inside the T cell, is connected to two or more contiguous domains responsible for activating
the lymphocyte when the CAR binds to its target antigen. The first, found in almost all CAR constructs, is called CD3ξ. The CD3ξ
domain delivers an essential primary signal within the T cell and is the natural basis for activation of these lymphocytes. The current
generation of CAR-T configurations generally employ one or more costimulatory domains, such as CD28, to provide enhanced activation signals
and augment lymphocyte activity. Together, these signals result in the proliferation of the CAR-enabled T cells and selective cellular
destruction. In addition, activated CAR-T cells stimulate the local secretion of cytokines and other molecules that can recruit and activate
additional immune cells to increase target elimination.

The assembly of these core
CAR components is depicted in the schematic presented below to which certain non-coding regulatory sequences may be used to augment viral
gene expression.

Delivery of conventional CAR-T cell therapies involves a single
viral vector.

Conventional CAR-T cell therapies
often utilize a lentiviral vector for the delivery of CAR specific genes. Lentiviral particles offer a well-characterized transduction
mechanism and are recognized as efficient and convenient vehicles for gene transfer as they demonstrate broad tropism, or activity, in
a wide array of cell types, and can be used to target quiescent, or non-dividing, cells. In addition, they do not integrate close to the
promoter regions of genes with the frequency of other gene delivery alternatives and lack the immunogenicity of DNA-based vectors, characteristics
which provide for enhanced safety. The use of a lentiviral vector to facilitate ex vivo clinical gene transfer has been demonstrated to
be safe in humans for two decades with minimal genotoxicity observed in hundreds of patients following gene transfer into T cells or hematopoietic
progenitor cells.

Currently, seven CAR-T cell
therapies have been approved by the FDA for the treatment of certain types of hematological cancers. The first two, approved in 2017,
are axicabtagene ciloleucel, sold by Gilead Sciences under the brand name Yescarta, and tisagenlecleucel, sold by Novartis under the brand
name Kymriah. A third CAR-T cell therapy, brexucabtagene autoleucel, which is comparable to Yescarta and sold by Gilead under the tradename
Tecartus, was approved in 2020. Lisocabtagene matraleucel, sold by Bristol Myers Squibb under the brand name Breyanzi, received FDA approval
in February 2021 with Bristol Myers Squibb also receiving approval for idecabtagene vicleucel, sold under the tradename Abecma, in March
of that year. Janssen Biotech received FDA approval for ciltacabtagene autoleucel, brand name Carvykti, to treat adult patients with relapsed
or refractory multiple myeloma and which targets the BCMA protein expressed on cancer cells rather than CD19, the target of the other
approved CAR-T cell therapies. Most recently, Autolus Therapeutics received approval for obecabtagene autoleucel, trade name Aucatzyl,
which targets CD19 for relapsed and refractory B-cell precursor acute lymphoblastic leukemia. Each of these therapies is an autologous
therapy and is made from T cells first collected from the patient, which are then genetically modified and administered back to the same
patient. Sales of CAR-T cell therapies are anticipated to grow rapidly over the next several years and are expected to exceed $10 billion
by 2030. CAR-constructs incorporating alternate immune effector cell types, including NK cells and macrophages, are in earlier stages
of clinical development and have only recently entered clinical trials. To date, no CAR-based therapies that employ NK cells or macrophages
have received FDA approval. There are at present no FDA approved CAR T cell products for the treatment of AML.

The Limitations of Current CAR-T Technology

Much of the excitement of
cellular therapy surrounds the curative potential of adoptive transfer of genetically engineered T cells. Adoptively transferred T cells
proliferate upon their engagement with target antigens and represent a form of therapy that can be appropriately characterized as living
and expanding. Efficient targeted killing and tumor elimination may be achieved in a short period of time. However, multiple barriers
limit the efficacy of conventional CAR-T cell therapy. A high rate of side effects often accompany treatment with currently approved products,
especially in those patients with high tumor burdens. In addition, partial responses occur, often associated with immune escape of the
tumor from the CAR or the display by the T cells of an exhaustion phenotype. Moreover, while engineered CAR-T cells have shown remarkable
potential in the treatment of hematological cancers, they have not demonstrated equivalent efficacy in the treatment of solid tumors.
Curative CAR-T cell therapies for solid tumors currently do not exist and the importance of this limitation is underscored by the prevalence
of solid tumor malignances. The American Cancer Society estimates that solid tumor cancers accounted for more than 1.7 million of the
1.9 million people newly diagnosed with cancer in 2021. Even in hematological malignancies with approved CAR-T cell therapies, less toxic
orthogonal treatment approaches are needed as cure rates for CD19-targeted CAR-T cell therapies do not exceed 60%.

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Challenges to the use of
cellular therapy to address solid tumors often relate to difficulty in developing receptors directed towards targets expressed in high
frequency on cancer cells as well as overcoming the immunosuppressive microenvironments that contribute to ineffective immune responses.
The tumor stroma, made up of a dense fibrotic matrix, often surrounds solid tumors and acts as a physical barrier, which restricts CAR-T
cell access to the tumor. CAR-T cell activity may be further hindered by the tumor microenvironment (“TME”). In the TME, multiple
cell types which drive immunosuppression infiltrate solid tumors, including myeloid-derived suppressor cells, tumor-associated macrophages,
and regulatory T cells. The interaction of these cells and the tumor cells increases the expression of signaling molecules that enable
tumor cell proliferation while dampening the generation of co-stimulatory signals necessary for T cell expansion and persistence. In addition,
TME-associated immune dysfunction may result in a down regulation of MHC class I molecules, limiting proper antigen presentation and T
cell proliferation. Collectively, these attributes of solid tumors enable them to avoid normal immune surveillance. Increased engagement
of the endogenous host response is an important, if not critical, component of CAR-T cell therapy clinical success as the recruitment
into the tumor of bystander lymphocytes has been observed in tumor biopsies from patients with curative CAR-T cell therapy. Enhancing
the host’s own response to tumor cells offers an important opportunity to improve current CAR T cell responses.

CAR-T recipients may also
incur serious adverse events, perhaps the most prominent of which is cytokine release syndrome. Believed to be related to the rapid proliferation
and activation of T cells upon detection of a target antigen, severe or life-threatening cytokine release syndrome was noted in a significant
number of patients who participated in the registrational trials of FDA-approved CAR-T therapies. These serious adverse events can result
in patients requiring longer hospitalizations and more intensive medical care. The frequency and severity of observed serious adverse
events is one of the primary reasons that administration of currently approved CAR-T therapy is restricted to a select number of treatment
centers. Moreover, aside from the low-level expression of certain cancer specific neoantigens, most tumor associated antigens are also
found on normal cells which may lead to serious, if not life threatening, “on-target, off-tumor” toxicities.

We believe that the preferential
attributes engineered into our CER-T cell therapies have the potential to represent a next-generation adoptive cellular immunotherapy
approach and enable us to overcome many of the limitations which hinder the wider application of current CAR-T technology. The prophagocytic
and immunomodulatory properties of CER-T cells are designed to overcome some of the immunosuppressive elements in many solid tumors. In
addition, their anticipated superior antigen presentation properties may enhance a patient’s ongoing immune response against tumor
antigens. Lastly, healthy cells have minimal expression of TIM-4-L as compared to tumor cells, reducing the potential for on-target off-tumor
effects. In consequence, we envision CER-1236 as having a differentiated mechanism for tumor clearance that enables the potential for
enhanced activity across a broad array of hematological malignancies and solid tumors.

CER-T Cell Therapy Technology

Distinguishing our CER-1236
cell therapy candidate is the integration into a single therapeutic construct of many of the anti-tumor capabilities resident in both
the innate and the adaptive immune systems. We believe the coupling of these functions better emulates normal immune system activity which
may promote enhanced T cell activation, proliferation and durability for more robust elimination of cancerous cells and reduction in tumor
burden.

We have designed our CER-T
constructs to embrace many of the components found in conventional CAR-T cell therapies. The processes and protocols used to genetically
modify a patient’s T cells to produce CAR-T cells are well recognized, as is the use of lentivirus in the manufacture of these therapies.
Accordingly, we have constructed CER-1236 cell manufacturing processes to be similar to those of CAR-T cells. We expect to benefit from
the well-defined regulatory guidelines established by both U.S. and European regulatory authorities related to CAR-T cell therapy and
its use.

The biological foundations for CER-T cell therapy

PS, or TIM-4 ligand, is a
component of a cell’s plasma membrane and has a key role in cell removal. Under normal physiological conditions, TIM-4-L is restricted
to the inner leaflet of the phospholipid bilayer which makes up the plasma membrane of a cell. However, cellular stresses cause the externalization
of TIM-4-L to the cell surface. Exposure of TIM-4-L on the outer surface acts as an “eat-me” signal and marks abnormal, stressed
and dying or dead cells for phagocytic clearance. A variety of tumors have been shown to have constitutively increased surface TIM-4-L
as a result of altered plasma membrane regulation. Among hematologic tumors, loss-of-function mutations in the flippase chaperone transmembrane
protein 30A (“TMEM30A”), have been identified in approximately 11% of patients with diffuse large B cell lymphoma (“DLBCL”),
and this mutation was correlated with improved response to the standard therapeutic regimen suggesting the host’s immune elimination
of TIM-4-L positive tumor cells enhances tumor clearance. We are seeking to exploit the presence of TIM-4-L expressed on the outer cell
surface of both hematological malignancies and solid tumors.

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CER-1236: Our Lead Development Candidate

As externally oriented TIM-4-L
is present on many cancerous cells regardless of tumor type, we believe a single CER construct may demonstrate clinical utility in treating
an array of cancers. To that end, we have focused our development activities on optimizing the cancer killing capabilities of a specific
CER-T therapeutic design. These efforts have resulted in our lead clinical candidate, CER-1236. In preclinical studies, we have observed
CER-1236 to display attractive functional capabilities and product characteristics, among which are:

● target-dependent
activation, cytotoxicity, anti-tumor cytokine production, and high proliferative capacity;

● tumor
cell phagocytosis;

● distinct
transcriptome, cytokine and chemokine signatures that substantiate the complementary activity of both the innate and adaptive immune
response;

● enhanced
antigen acquisition, processing and presentation;

● no
evidence of T cell exhaustion despite repeated challenges;

● no
observed off-target or off-tumor toxicities;

● expression
and maintenance of diverse T cell populations, including naïve and memory cells, likely indicative of response persistence and durability;
and

● well
defined and scalable manufacturing protocols.

We have designed CER-1236
to align with components included in the current generation of conventional CAR-T configurations by fusing the external domain of TIM-4,
a phagocytic receptor, with intracellular signaling domains from T cells and innate immune cells. TIM-4 harbors endogenous phagocytic
capacity through its binding to the pro-phagocytic “eat-me” signal TIM-4-L. CER-1236’s intracellular signaling domains,
including TLR2, CD28 and CD3ξ motifs, are designed to augment both TIM-4 mediated phagocytosis and cytotoxic T cell function. Another
similarity between conventional CAR-T therapeutic formats and our CER-T design is the delivery vehicle used in transduction. As is found
in many approved CAR-T therapies, our CER-T technology also employs a lentiviral vector to facilitate gene delivery to patient-derived
T cells. A schematic of the structural elements of CER-1236 is presented below.

Schematic of CER-1236

Abbreviations: TIM-4 = ectodomain
of the T cell immunoglobulin mucin domain protein 4; TLR2 = toll-like receptor 2.

CER-1236 employs an innovative mechanism of
action

CER-1236 is an autologous
T cell therapy candidate designed to target TIM-4-L through the external domain of the prophagocytic receptor TIM-4 protein. This therapeutic
construct was developed to combine adaptive T cell killing activity with phagocytic clearance and antigen presentation activity to create
T cells with enhanced cancer immunotherapy capabilities. The approach builds on the early success of adoptive T cell transfer, which has
demonstrated the ability of T cells to proliferate, traffic, and circulate within both primary and metastatic tumors.

By enhancing phagocytic clearance
and antigen presentation activity and integrating them into T cells, we believe CER-T cells offer the potential for more effective elimination
of cancer cells. The industry’s decades-long experience with engineered T cell use provides a solid foundation for the development
of CER-1236.

As the target ligand of our
initial CER-T cell is not an antigen restricted to only certain tumors, CER-1236 T cells may provide clinical benefit across multiple
tumor types. The functional interaction of CER-1236 T cells is depicted in the illustration presented below.

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CER-1236 T cells are designed to harness the power of both the innate
and adaptive immune systems

CER-1236 expresses the external
domain of the prophagocytic receptor TIM-4 which is linked to T cell and innate immune cell intracellular signaling domains. TIM-4 is
normally expressed on subsets of macrophages and dendritic cells and harbors endogenous phagocytic capacity through its binding to and
recognition of TIM-4-L. The intracellular signaling domains in CER-1236 are designed to trigger T cell cytotoxic function and enhance
TIM-4 mediated phagocytosis. CD3ξ is the signaling component of the TCR and CD28 is a co-stimulatory domain needed for optimal activation.
The TLR2 domain is involved in both innate and adaptive immune responses and activation of TLR2 further enhances signaling through both
NF-κB and the mitogen-activated protein (“MAP”) kinase family, promoting T cell activity and phagocytic uptake. Both
CD28 and CD3ξ signaling domains are incorporated into approved CAR-T cell products. A third generation anti-CD19 CAR-T cell that incorporates
a TLR2 domain is currently in clinical development.

By virtue of the TIM-4 engulfment
receptor and the intracellular signaling domains, CER-1236 combines attributes of both T cells and phagocytic cells. In phagocytic cells,
such as macrophages and dendritic cells, recognition of TIM-4-L on the surface of apoptotic cells by native TIM-4 leads internalization
by utilizing integrin coreceptors to activate phagocytic signaling. TIM-4-mediated phagocytosis depends on activation of the RAC1 GTPase
which is similarly targeted by TLR signaling, especially TLR9 and TLR2. However, it has been shown that the intracellular portion of TIM-4
is not required for phagocytosis, and therefore the extracellular domain (“ECD”) of TIM-4 appears to function as a tether
during phagocytosis to allow intracellular signaling by other transmembrane phagocytic molecules with which it associates, such as the
integrins which are expressed ubiquitously on T cells. Since CER-1236 contains only the ECD of TIM-4, binding to TIM-4-L on tumor cells
recruits the cell-surface phagocytosis machinery, and simultaneously directly activates CER-1236 T cells through the intracellular CD3ξ
and CD28 costimulatory domains. Phagocytosis and cytokine secretion are further enhanced by the TLR2 intracellular signaling domain.

In preclinical studies, CER-1236 empowers T
cells with phagocytic and cytotoxic potency

In an in vitro evaluation
of the phagocytic potential of CER-1236, CER-transduced T cells demonstrated robust phagocytosis of TIM-4-L. CER-1236 T cells were produced
by transducing donor T cells using a lentiviral vector encoding for the chimeric receptor CER-1236, yielding a high percentage of T cells
expressing the TIM-4 receptor, in similar CD4:CD8 ratios to untransduced cells. CER-1251 T cells, which express matching intracellular
signaling domains but are unable to bind to TIM-4-L due to a mutation in the gene encoding for the TIM-4 binding site, were also produced
as a negative control.

TIM-4-L-coated agarose beads
were prelabeled with pHrodo red, a pH-sensitive dye which displays limited fluorescence at neutral pH but generates significant fluorescence
in acidic pH. The post-phagocytic fusion of phagosomes and lysosomes leads to a drop in pH which can be detected by pH-sensitive dyes.
As is illustrated in the graphic below, CER-1236 T cells co-cultured with TIM-4-L-coated beads displayed significant phagocytic activity
with up to 60% of CER-T cells acquiring a pHrodo red signal, indicative of bead capture and internalization. By contrast, untransduced
T cells and CER-1251 T cells, with a mutation in the TIM-4 binding site, demonstrated minimal phagocytosis.

8

CER-1236 displays robust, target-specific phagocytic activity

Gene expression patterns
demonstrate the combined cytotoxic and phagocytic functions of CER-1236 T cells. RNA-sequencing enables the interrogation of the transcriptional
profile of CER-1236 T cells after stimulation with TIM-4-L, with defined separation between the CER-1236 activated cells and the untransduced
and CER-1251 control T cells. As shown in the gene expression profile below, over 1,700 genes were noted to be differentially expressed
in CER-1236 stimulated T cells in comparison to CER-1251 stimulated T cells. Among these genes were those related to pathways with well-known
involvement in regulating phagocytosis, genes involved in nucleation of the ARP-WASP complex, Rho family GTPases, RAC signaling and phagosome
formation. Of note, the RhoG subfamily of GTPase has been previously implicated in TCR-driven phagocytic processes. This aggregate of
transcriptional signatures is indicative of the multi-modal immune response elicited by CER-1236 T cells.

Phagocytic and cytotoxic transcriptional signatures demonstrate
the plasticity of CER-1236 T cells

9

CER-1236 T cells were also
observed to generate potent anti-cancer responses in cell lines derived from specific hematological malignancies and solid tumors. A mantle
cell lymphoma (“MCL”) cell line that has been modified to constitutively express externalized cell surface TIM-4-L was co-cultured
with either CER-1236 T cells or untransduced T cells. Notably, CER-1236 T cells eliminated 87% of the MCL cells while the untransduced
cells demonstrated minimal cytotoxic ability. In addition, CER-1236 T cells secreted multiple cytokines, including IFNγ, granzyme
B and TNFα, all indicative of robust and sustained T cell cytotoxicity. Cytokine secretion was determined to be dependent on binding
to TIM-4-L, as CER-1251 T cells did not secrete cytokines despite exposure to cell surface TIM-4-L. Further visual evidence of the cancer-killing
capacity of CER-1236 T cells is illustrated in the staining assays depicted in the graphs presented below. In the assays with no CER-1236
T cells, significant proliferation of cancer cells was observed, as evidenced by the increase in red staining, while the growth of cancer
cells when exposed to CER-1236 T cells was limited. These results are presented in the graph to the left below.

CER-1236 T cells demonstrate potent cytotoxic responses to cancer
cells in vitro

Significant cytotoxic activity
of CER-1236 was also noted in an advanced NSCLC cell line, HCC827, which has a mutation in its epidermal growth factor receptor (“EGFR”)
gene, a cancer type accounting for between 10% and 15% of all lung adenocarcinoma cases in persons of European descent and higher among
the Asian population. As is depicted in the above, right graph, while the addition of CER-1236 demonstrates moderate cancer cell killing
activity, the addition of osimertinib, the preferred tyrosine kinase inhibitor option for first-line treatment of EGFR-mutation positive
advanced NSCLC, substantially enhanced CER-1236 T cell killing in an osimertinib concentration dependent manner. In contrast, HCC827 cells
co-cultured with untransduced T cells displayed minimal changes in cell number as compared to cells incubated in the absence of T cells,
at all drug concentrations tested. Conditional cytokine proliferation was also observed with CER-1236 T cell treatment, with IFNγ
levels over 400-fold higher in cancer cell cultures which used CER-1236 T cells, in contrast to co-cultures which used untransduced T
cells. The addition of osimertinib to co-cultures further increased IFNγ levels by more than two-fold, compared with CER-1236 treatment
alone. Similar trends were observed with TNFα and Granzyme B levels and increases in osimertinib concentrations led to dose-dependent
CER-1236 T cell proliferation. These results demonstrated that CER-1236 T cell activity could be significantly enhanced by upregulating
target expression through concomitant dosing of standard of care medication.

TIM-4-L, a lipid moiety recognized
by phagocytic cells as an “eat me” signal, has previously been shown to be aberrantly upregulated on acute promyelocytic (“APL”)
blasts, a subset of AML. To further interrogate TIM-4-L across other AML subtypes, we evaluated a panel of primary bone marrow samples
and peripheral blood from AML patients. We screened a preliminary panel of primary, treatment-naïve or on-therapy AML bone marrow
and PBMC samples by flow cytometry: (n=5 adverse, n=5 intermediate, n=1 APL, n=1 familial, n=5 N/A) (Table 1). We observed both high percent
(35.5 % ± 21.6) and geometric mean fluorescence index (“gMFI”) of cell surface TIM-4-L on a range of AML bone marrow
samples. The median gMFI of tertiles 1-3 was: T1 n=7, gMFI = 5033; T2 n=8, gMFI = 1873; T3 n=8, gMFI = 611. Of note, the two on-therapy
samples showed high percent and gMFI of cell surface TIM-4-L, with a patient receiving 5-azacytidine showing 1.8 fold TIM-4-L gMFI over
median. The second patient receiving TKI therapy showed 3.3 fold TIM-4-L gMFI over median. Healthy donor samples had much lower cell surface
TIM-4-L, with a mean gMFI of 582. Circulating AML leukemic blasts were also evaluated for cell surface TIM-4-L and showed high concordance
with BM blasts, with high levels of cell surface TIM-4-L compared to healthy donor peripheral blood mononuclear cells (“PBMCs”).

10

Table 1. AML patient characteristics

Patient:

Patient ID
Treatment Status:

Disease Status
Previous

Treatments
Patient

Age At

Collection
Gender
Race
Patient:

Ethnicity
% Blast

Cells
Risk Category
Genetic

Abnormality
Cytogenetics

200001107
Newly Diagnosed
none
67
Female
White
Non-Hispanic/Latino
91
Adverse
RUNX1
N/A

200015767
Newly Diagnosed
none
59
Female
White
Non-Hispanic/Latino
35
Adverse
TP53
N/A

200013141
Newly Diagnosed
none
69
Male
White
Non-Hispanic/Latino
75
Intermediate
VAF ASXL1 < 50%
N/A

200015300
Newly Diagnosed
none
59
Male
White

93.03

N/A

200018491
Newly Diagnosed
none
62
Female
White
Non-Hispanic/Latino
30
Adverse
TP53
N/A

130802218
Newly Diagnosed
none
71
Male
White

94.77

N/A

200018493
Newly Diagnosed
none
48
Male
White
Non-Hispanic/Latino
82
Adverse
ASXL1, FLT3-ITD
N/A

200015400
Newly Diagnosed
none
51
Male
White
Non-Hispanic/Latino
80.2
Familial
GATA2 Deficiency
N/A

130776684
Newly Diagnosed
none
38
Female
White

89.78

N/A

200055487
Newly Diagnosed
none
74
Male
White

80.9

N/A

130781611
Newly Diagnosed
none
62
Female
White

81.67
Intermediate
N/A
Normal

200015406
Newly Diagnosed
none
43
Male
White

91.37
Adverse
FLT-3 ITD
N/A

200036152
Newly Diagnosed
none
85
Female
White

70.13

200015557
Newly Diagnosed
none
69
Female
White
Non-Hispanic/Latino
84
Intermediate
DNMT3A
N/A

200019235
Stable
Azacitidine 8 cycles
71
Female
White

72.63
Intermediate
N/A
N/A

200018645
Newly Diagnosed
none
41
Male
White

76.54
APL
N/A
t(15;17)

200015508
Progressive
Imatinib 400 mg.
63
Female
White
Non-Hispanic/Latino
50
Intermediate
VAF < 50%
N/A

200019095
Newly Diagnosed
none
63
Female
White

82.65

200013114
Newly Diagnosed
none
83
Male
White

56.8

NRAS

130800395
Newly Diagnosed
none
72
Female
White

75.7
Adverse
TET2, ASXL1, TP53

200015280
Newly Diagnosed
none
67
Female
White

15.3

ETV6, BCORL, KRAS

200009820
Newly Diagnosed
none
31
Male
White

85.7

KRAS

200009056
Newly Diagnosed
none
21
Female
White

94.8
Adverse
DNMT3A, BCORL1, TP53

AML from bone marrow or PBMC have elevated cell surface TIM-4-L

11

CER-1236 T cells were also
observed to generate potent anti-cancer responses against myeloid malignancies. AML is a heterogenous, and aggressive hematopoietic malignancy
characterized by the rapid buildup of immature myeloid cells in the bone marrow and blood. We used AML cell lines depicted in the graph
below, Kasumi-1 and MV-4-11, to demonstrate cytotoxic anti-AML responses in co-culture studies with CER-1236. Similar to in vitro cytotoxicity
results observed with B cell malignancy and NSCLC cell lines, we show the addition of CER-1236 alone to AML cell lines demonstrates potent
cell killing activity. Kasumi-1 harbors a p53 mutation, marking a subset of unfavorable disease risk AML patients, while MV4-11 cells
carry a FLT-3 mutation, a proliferative AML leukemia subset. Both cell lines co-cultured with untransduced T cells displayed minimal changes
in cell number as compared to cells incubated in the absence of T cells. CER-1236 T cells secreted multiple cytokines in co-cultures with
AML cell lines, including IFNγ, granzyme B and TNFα, all indicative of robust and sustained T cell cytotoxicity.

CER-1236 T cells demonstrate robust in vivo elimination of MCL xenografts

The cancer killing capacity
of CER-1236 that was demonstrated in studies involving MCL cell lines was also noted in a mouse xenograft model. Immune deficient NOD
scid gamma (“NSG”) mice were xenografted with the human REC-1 cell line at Day -2 and then treated with 8 mg/kg ibrutinib
or vehicle and administered CER-1236 T cells daily from Day -1 to study completion. Administration of 7.5e6 CER-1236 T cells in the presence
of ibrutinib resulted in the elimination of REC-1 tumor burden in all 11 of the mice in this treatment cohort. The administration of CER-1236
T cells in the absence of ibrutinib eliminated the tumors in all nine animals treated with CER-1236 T cells alone. No tumor growth inhibition
was observed in either the vehicle-treated or ibrutinib-treated control groups. Median survival for mice receiving CER-1236 T cells with
or without co-administration of ibrutinib was not reached during the study period. The results of this study are presented in the charts
below.

A single infusion of CER-1236 T cells eliminates
tumors and improves survival

The level of CER-1236 T cells
in peripheral blood displayed robust expansion at Day 7, with or without the concomitant administration of ibrutinib. Animals that received
CER-1236 T cells demonstrated an expansion of over 400-fold as compared to Day 2 levels both in the absence and presence of ibrutinib.
High levels of CER-1236 T cells did not persist in the periphery and animals that received CER-1236 T cells showed a greater than 95%
contraction in cell count from peak numbers by Day 14 with subsequent CER-T cell expansion likely prompted by residual tumor cell encounters.
CER-1236 T cells also maintained robust proliferative capacity despite repeated in vitro antigen challenges with no evidence of T cell
exhaustion noted. These findings are illustrated in the following charts.

12

A single infusion of CER-1236 T cells generated rapid cell expansion
across repeated challenges

CER-1236 demonstrates in vivo tumor clearance in NSCLC adenocarcinoma
xenograft

We envisioned that the simultaneous
exposure to both osimertinib and CER-1236 would lead to synergistic in vivo anti-tumor responses. HCC827 NSCLC cells were inoculated into
the flanks of NSG mice. Once established, the mice were dosed with a short course of the EGFR inhibitor osimertinib to prime TIM-4-L antigen
on tumors and administered 2.5e6 CER-1236 T cells. Treatment groups that received the EGFR inhibitor alone, after initial tumor regression,
developed progressive disease, as evidenced in the below left graph. In contrast, animals infused with CER-1236 T cells demonstrated potent
anti-tumor responses in the presence of osimertinib. CER-1236 T cells expanded rapidly in the blood, with the highest expansion observed
in the osimertinib-treated cohorts, as observed in the below right graph. Importantly, no evidence of organ toxicity or weight loss was
observed with increases in body weight recorded in all groups over the course of the study. Analysis of the tumors post-infusion indicated
extensive infiltration of T cells compared to untransduced controls.

CER-1236 T cells infused to Osimertinib dosed animals showed tumor
elimination and higher levels of T cell expansion

CER-1236 T cells infused
to AML engrafted animals shows tumor elimination and T cell expansion

We engrafted NSG-MHC double
knock out mice with Kasumi-1, a TP53 mutant AML cell line. Once established, the mice were infused with a single dose of CER-1236 or control
T cells. Animals infused with CER-1236 T cells showed rapid tumor elimination and long term control. In addition, CER-1236 T cell expansion
was observed early after infusion, reaching a peak at day 7 and contracting afterwards.

13

We believe that the preclinical
models of AML, MCL, ovarian cancer and EGFR-mutation positive NSCLC demonstrate the ability of CER-1236 T cells to induce collaborative
innate-adaptive anti-tumor immune responses in both in vitro and in vivo studies. Moreover, concurrent treatment with standard-of-care
therapeutics for each of these indications increases target ligand, conditionally bolstering CER-1236 T cell function to augment anti-tumor
activity. Additionally, in antigen presentation assays, activated CER-1236 T cells exhibited superior cross-presentation ability relative
to conventional T cells, triggering specific TCR-T cell responses in an MHC class I and TLR-2 dependent manner, overcoming the limited
antigen presentation capabilities of conventional T cells. These results indicate that CER-1236 T cells have the potential to achieve
optimal tumor control by eliciting both cytotoxic effects and cross-priming.

CER-1236 T cells did not elicit safety signals in preclinical safety/toxicology
studies

Importantly, no evidence
of toxicity was observed during a safety/toxicology study conducted in mice, a clinically relevant model that has an identical structure
of TIM-4-L as humans. The effects of CER-1236 administration were evaluated at 2 doses at 3- and 28-day timepoints. No incidence of anemia,
thrombocytopenia, neutropenia or coagulation abnormalities were recorded in any condition. Hematologic indices, including hemoglobin/hematocrit,
platelets and neutrophils remained stable throughout the study. No perturbation of clinical chemistries was noted. None of the animals
experienced weight loss, morbidity or unexpected mortality. No clinically relevant tissue abnormalities were noted at either timepoint
at the high dose in any organ evaluated. Overall, these data demonstrate a lack of on-target off-tumor responses and support the safety
profile of CER-1236.

The potential for off-target
toxicity by CER-1236 was also tested against primary human cells or iPSC-derived human cells representing vital organs, including the
CNS, heart, lungs, liver, spleen, kidneys, GI tract, and gonads. CER-1236 was co-cultured with these cells and activation was monitored
by IFNγ secretion or cytotoxic effect. Over the time points tested, CER-1236 showed potent activation and cytotoxicity against AML
cells (Below, top and bottom graphs), but limited activation (Below, top graph) and no cytotoxicity (Below, bottom graph) against any
of the human cell types tested. These experiments support the lack of off-target responses by CER-1236 T cells.

14

CER-1236 Clinical Development Strategy

Based on the extensive preclinical
data that we have assembled regarding the use of CER-1236 T cells to combat cancer, we commenced our Phase 1 clinical trial in May 2025
with an initial treatment target being patients suffering from relapsed, or refractory AML as well as those subsets who are positive for
Minimal Residual Disease and the TP53 mutation. Analyses of the first two patients treated revealed no dose-limiting toxicities. In addition,
expansion of the CER-T cells was observed. We subsequently intend to expand the clinical development of CER-1236 to include solid tumors
such as NSCLC and ovarian cancer. We anticipate initiation of the Phase 1 study in NSCLC and ovarian cancer in the first quarter of 2026.
We expect these clinical trials to evaluate the safety, the potential therapeutic utility and applicable dose of CER-1236. In addition,
we anticipate that these clinical trials may provide insight into the possible use of CER-1236 to treat an array of hematologic and solid
tumors.

We believe this drug candidate
has the potential to be a therapy for the unmet needs of targeted indications, if approved, and by leveraging the innate immune system’s
phagocytic capabilities, could be differentiated by its safety, tolerability, efficacy and clinical benefit over current therapeutic approaches,
which have been observed in preclinical studies. None of the abovementioned statements regarding any of our products in development are
intended to be a prediction or conclusion of efficacy. No clinical trials on our product candidates have been completed so no conclusions
relating to such attributes can be made.

Disease backgrounds

Acute Myeloid Leukemia

AML is a cancer of the blood
and bone marrow that affects myeloid cells, cells which normally develop into the various types of mature blood cells. It is a fast-progressing
and aggressive form of blood cancer, with a median time from diagnosis to death of just 5.5 months. Despite over 20 FDA approved therapeutics
for the treatment of AML, the death rate in AML patients has only moderately diminished since the 1990s, with the disease hovering around
a 32% 5-year overall survival rate according to the National Cancer Institute. AML was diagnosed in 21,000 Americans in 2019, and there
were 11,000 AML-related deaths in the same year, according to the Leukemia and Lymphoma Society. Like most cancers, it is a terrifying
diagnosis for patients which often leads to many rounds of treatment and a complete disruption of their lives.

Figure 1: Rate of new cases of AML and associated
mortality in the United States 1992-2020

Source: NIH, National Cancer Institute

According to Alliance Global
Partners, the total AML therapeutic market is estimated to be approximately USD $2.58B as of 2024 and projected to grow at a compound
annual growth rate (CAGR) of 10.25% based on the historical growth rate, the anticipated approval of new therapeutics, and an increase
in the number of total patients to be diagnosed in the coming years. According to estimates, by 2033, the AML therapeutic market will
likely grow to over $6B+, highlighting the significant economic upside associated with any improvements to the standard of care from the
current pipeline therapeutics.

Current therapies and their limitations

Currently, there are over
20 FDA approved therapeutics in the AML space, with eight approvals having come in just two years from 2017-2019. Before then, AML was
treated with decades-old combination chemotherapy regimens, including cytarabine and anthracycline. This regimen has about a 70-80% complete
response rate of adults younger than 60 years and 40-60% of fit adults older than 60 years old. For those eligible for the chemotherapy
regimen and experiencing a complete response, many patients with adverse features (70%) undergo allogeneic HSCT which, in some patients
are “curative.” Unfortunately, a significant proportion (up to 50%) of AML patients are over the age of 65 and are “unfit”
for intensive chemotherapy, requiring different treatment approaches for medically unfit patients. The treatment landscape for older unfit
adults with AML fundamentally changed with the recent availability of new drugs, in particular the oral B-cell lymphoma 2 inhibitor venetoclax.
Venetoclax is used in conjunction with azacytidine to treat these patients, with a complete response rate of ~65%. However, the majority
of adult patients with AML experience relapse despite initially attaining complete response; a venetoclax-based doublet therapy for medically
less-fit adults carries a median survival of ~14.7 months. The prognosis for patients who are refractory to or relapse after frontline
azacitidine venetoclax is dismal with median overall survival of 2.4 months, making this an area of high unmet need. Such patients who
do not respond to frontline therapy with azacitidine or venetoclax, and the subset who do not respond to targeted therapies, e.g., IDH1/2
inhibitors, are candidates for investigational trials. To date, there are no approved cell therapeutic approaches to treat AML.

15

Myelodysplastic Syndrome

MDS is a cancer that occurs
when blood-forming stem cells become dysfunctional and fail to properly mature. This results in failure to produce red blood cells, platelets,
or white blood cells, or a combination thereof. MDS is commonly diagnosed in people in their 70s, which limits curative treatment options.
MDS has both high risk and low risk subtypes, with median survival as short as 1 year in very high risk groups or 10.6 years in very low
risk groups, making it largely a chronic disease. The only potentially curative therapy for MDS is stem cell transplantation, which is
often unavailable for elderly patients. The chemotherapeutic drugs Azacitidine and Cytarabine are commonly used to treat MDS, but are
not curative. Patients with MDS are often transfusion dependent, and either succumb to side effects of poor hematopoeisis or have their
disease advance to AML. MDS is newly diagnosed in over 10,000 Americans each year.

Myelofibrosis

Myelofibrosis is a type of cancer caused by scarring of the bone marrow,
impairing the normal maturation of healthy blood cells and leading to reduced levels of red blood cells and platelets. Myelofibrosis is
typically diagnosed in people over 50 years old. Median survival for treated MF is 7 years, although this can be shorter for higher risk
subtypes. MF is primarily treated with JAK inhibitors or bone marrow transplantation. MF is estimated to be diagnosed in 5,000 patients
per year in the US. In some cases, myelofibrosis can advance to AML.

Ovarian Cancer

The American Cancer Society
estimates for ovarian cancer in the United States for 2024 are:

● About
19,680 women will receive a new diagnosis of ovarian cancer.

● About
12,740 women will die from ovarian cancer.

Ovarian cancer is one of
the leading causes of cancer deaths among women. A woman’s risk of getting ovarian cancer during her lifetime is about 1 in 87.
The lifetime chance of a woman dying from ovarian cancer is about 1 in 130. (These statistics don’t count low malignant potential
ovarian tumors.) This cancer mainly develops in older women. About half of the women who are diagnosed with ovarian cancer are 63 years
or older. It is more common in White women than Black women.

Non-Small Cell Lung Cancer

Most lung cancer statistics
include both small cell lung cancer (“SCLC”) and NSCLC. In general, about 10% to 15% of all lung cancers are SCLC, and about
80% to 85% are NSCLC. Lung cancer (both small cell and non-small cell) is the second most common cancer in both men and women in the United
States (not counting skin cancer).

The American Cancer Society’s
estimates for lung cancer in the U.S. for 2024 are:

● About
234,580 new cases of lung cancer (116,310 in men and 118,270 in women)

● About
125,070 deaths from lung cancer (65,790 in men and 59,280 in women)

Lung cancer mainly occurs
in older people. Most people diagnosed with lung cancer are 65 or older; a very small number of people diagnosed are younger than 45.
The average age of people when diagnosed is about 70.

Lung cancer is by far the
leading cause of cancer death in the U.S., accounting for about 1 in 5 of all cancer deaths. Each year, more people die of lung cancer
than of colon, breast, and prostate cancers combined.

Overall, the chance that
a man will develop lung cancer in his lifetime is about 1 in 16; for a woman, the risk is about 1 in 17. These numbers include both people
who smoke and those who don’t smoke. For people who smoke, the risk is much higher, while for those who don’t, the risk is
lower.

● Black
men are about 12% more likely to develop lung cancer than White men. The rate is about 16% lower in Black women than in White women.

● Black
and White women have lower rates than men, but the gap is closing. The lung cancer rate has been dropping among men over the past few
decades, but only for about the past decade in women.

● Despite
their overall risk of lung cancer being higher, Black men are less likely to develop SCLC than White men.

Statistics on survival in
people with lung cancer vary depending on the type of lung cancer, the stage (extent) of the cancer when it is diagnosed, and other factors.

16

5-year relative survival rates for non-small
cell lung cancer

These numbers are based on people diagnosed
with NSCLC between 2015 and 2021.

SEER stage
5-year relative

survival rate

Localized
67 %

Regional
40 %

Distant
12 %

All SEER stages combined
32 %

Our therapeutic approach and development program

We designed our clinical development program for CER-1236 to enable
our evaluation of its therapeutic utility in treating both hematologic and solid tumors, as the capacity of a single therapeutic construct
to provide clinical benefit across this diversity of tumor types would represent a significant advance in cancer immunotherapy. Due to
the therapy’s novel mechanism of action, engaging both the innate and the adaptive immune response, and the broad expression profile
of PS on a variety of hematologic and solid tumors, we have employed an adaptive Phase 1 trial design to evaluate patient response to
CER-1236. As such, the dosing protocol is designed to emphasize a gradual increase in the delivered dose with the objective of achieving
a clinical signal, while ensuring patient safety. Our Phase 1 trial is also designed to enable an evaluation of appropriate dosing strategies
to optimize CER-T engagement and proliferation. Two patient products have been successfully manufactured and dosed. The initial patient
did not experience any dose-limiting toxicities during the 28-day observation window, and the second patient was still under observation
7 days after treatment. Pharmacokinetic data from the first patient indicates that the CER-1236 T cells successfully expanded upon infusion,
and began to contract after 2 weeks. We dosed a third patient in September 2025, which will be followed by a meeting of the dose escalation
safety committee to determine if we can advance to the next dose. The fourth patient was treated in October 2025.

We believe, subject to discussions
with the FDA and other regulatory authorities, that there may be a full development path to registration and use in the larger AML patient
populations on achieving positive safety data along with indications of therapeutic benefit in these initial trial cohorts. We believe
CER-1236 may provide significant treatment advantages over currently available therapeutics, including CAR-T therapy as a result of its
potential to enhance objective response rates and the duration of response related to the comprehensive, coordinated engagement of the
innate and adaptive immune systems and a sustained signaling environment. We believe this novel mechanism of action will enable our advance
of a single therapeutic construct to address the substantial unmet need for a safe and effective cell therapy offering an improved therapeutic
profile, despite significant competition. We subsequently anticipate initiating clinical trials for additional indications, including
the possible application of CER-1236 in the treatment of certain solid tumors such as NSCLC and ovarian cancer.

Ongoing Phase 1 trial of CER-1236 in patients
with AML

In May 2025, we initiated
our Phase 1 clinical trial designed to evaluate the safety, potential therapeutic utility and applicable dose of CER-1236 in patients
with acute myeloid leukemia (“AML”). The first-in-human, multi-center, open label, Phase 1/1b study is designed to evaluate
the safety and preliminary efficacy of CER-1236 in patients with acute myeloid leukemia that is either relapsed/refractory, or in remission
with measurable residual disease, or newly diagnosed patients with TP53 mutated MDS/AML or AML. The two-part study has begun with dose
escalation to determine highest tolerated dose and recommended dose for Phase 2, followed by an expansion phase to evaluate safety and
efficacy. Primary outcome measures include incidence of adverse events and serious adverse events, incidence of dose limited toxicities
and estimation of overall response rate, complete response, composite complete response, and measurable residual disease. Secondary outcome
measures include pharmacokinetics. To date we have successfully manufactured and administered cell products for four patients. Following
the dosing and observation period for the third patient, the dose escalation safety committee determined that the fourth patient could
receive a higher dose. The fourth patient was dosed in October 2025. The fourth patient received an initial dose of CER-1236 at twice
the initial dose of the patients in the first cohort, with a follow-on second identical dose 48 hours later. The fifth patient was dosed
in March 2026.

Trial expansion into Myelodysplastic Syndrome
and Myelofibrosis

Early safety signals observed
in the first cohort of AML patients demonstrated a unique safety profile for CER-1236 T cells that differentiated it from many other engineered
T cell products. Robust cell expansion was seen in all patients without concurrent cytokine secretion leading to CRS or ICANS. No off-tumor
effects were observed, either. This unusual safety profile and early signals in an AML patient who had progressed from MDS suggested CER-1236
could be suitable for treatment of chronic diseases of the bone marrow. The trial was expanded to include MDS and MF, both chronic diseases
with similarities to AML, into the phase 1 dose escalation and phase 2 dose expansion portions of the trial.

17

Updated Certain T-1 study design in relapsed
and refractory AML

Certain T-2 study design
in ovarian and non-small cell lung cancer

Manufacturing Strategy

The manufacture of product
candidates derived from our autologous CER-1236 T cells involves the same type of equipment, materials and protocols already used in the
manufacture of currently FDA-approved CAR-T cell therapies, which we believe will provide us numerous benefits. CER-1236 cell product
is being manufactured using an automated closed process, with product manufacture continuous from bulk harvested cells through to cryopreserved
drug product bags. There are multiple factors involved in the manufacturing process needed to ensure proper CER-T cell cryopreservation
both preceding and following freezing, including the thawing process and post-thaw handling prior to patient administration. These factors
are well understood and procedures have been identified to optimize yield, activity, stability and consistency. In addition, we may be
able to take advantage of the increasing regulatory familiarity with these established protocols. Our expected manufacturing process embraces
a fully automated, closed-system design intended to minimize exposure to potential contaminants and ensure consistent successful manufacture
of the product. The product is being manufactured in a contract manufacturing facility which maintains a quality system compliant with
current Good Manufacturing Practice (“cGMP”) requirements.

Lentivirus containing CER-1236
will be produced following a cGMP process using cGMP plasmids.

We have entered into a contract
manufacturing agreement related to the production of drug product for our clinical trials, and we anticipate entering into similar arrangements
regarding plasmid, viral vector and final drug product manufacture for drug product to be used in subsequent clinical trial phases in
the future. We intend to advance related process development work both internally and with our contract manufacturing organization (“CMO”)
partners. In the event a product candidate receives regulatory approval, we anticipate entering into contract manufacturing agreements
with one or more CMOs to support product launch and commercial manufacture.

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Intellectual Property

Intellectual property is
of vital importance in our field and in biotechnology generally. Our commercial success will depend in part on obtaining and maintaining
patent protection for our current and future product candidates. We seek to protect and enhance proprietary technology, inventions, and
improvements that are commercially important to the development of our business by seeking, maintaining, and defending our patent rights.
When available to expand market exclusivity, our strategy is to obtain or license additional intellectual property related to current
or contemplated development platforms, core elements of technology, and/or clinical candidates. We will also seek to rely on regulatory
protection afforded through inclusion in expedited development and review, data exclusivity, market exclusivity, and patent term extensions,
where available. In addition to patent protection, we also may rely on trademark registration, trade secrets, know-how, other proprietary
information, and continuing technological innovation to develop and maintain our competitive position. We seek to protect and maintain
the confidentiality of proprietary information to protect aspects of our business that are not amenable to, or that we do not consider
appropriate for, patent protection.

The term of individual patents
depends upon the legal term of the patents in the countries in which they are obtained. In most countries in which we file, including
the United States, the patent term is 20 years from the earliest date of filing a non-provisional patent application. In the United States,
a patent’s term may be lengthened by patent term adjustment, which compensates a patentee for administrative delays by the U.S.
Patent and Trademark Office (“USPTO”) in examining and granting a patent, or may be shortened if a patent is terminally disclaimed
over an earlier filed patent. In the United States, the patent term of a patent that covers an FDA-approved drug may also be eligible
for patent term extension, which permits patent term restoration as compensation for the patent term lost during the FDA regulatory review
process. The Hatch-Waxman Act permits a patent term extension of up to five years beyond the expiration of the patent. The length of the
patent term extension is related to the length of time the drug is under regulatory review. Patent term extension cannot extend the remaining
term of a patent beyond a total of 14 years from the date of product approval, only one patent applicable to an approved drug may be extended,
and only those claims covering the approved drug, a method for using it, or a method for manufacturing it may be extended. Similar provisions
are available in Europe and other foreign jurisdictions to extend the term of a patent that covers an approved drug. In the future, if
and when our product candidates receive FDA approval, we expect to apply for patent term extensions on patents covering those product
candidates. We plan to seek patent term extensions to any issued patents we may obtain in any jurisdiction where such patent term extensions
are available.

In some instances, we submit
patent applications directly to the USPTO as provisional patent applications. Corresponding non-provisional patent applications must be
filed not later than 12 months after the provisional application filing date. While we intend to timely file non-provisional patent applications
relating to our provisional patent applications, we cannot predict whether any such patent applications will result in the issuance of
patents that provide us with any competitive advantage.

We will file U.S. non-provisional
applications and Patent Cooperation Treaty (“PCT”) applications that claim the benefit of the priority date of earlier filed
provisional applications, when applicable. The PCT system allows a single application to be filed within 12 months of the original priority
date of the provisional patent application, and to designate all of the PCT member states in which national phase patent applications
can later be pursued based on the international patent application filed under the PCT. The PCT search authority performs a patentability
search and issues a non-binding patentability opinion which can be used to evaluate the chances of success for the national applications
in foreign countries prior to having to incur the filing fees. Although a PCT application does not issue as a patent, it allows the applicant
to seek protection in any of the member states through national-phase patent applications. At the end of the period of 30 months from
the first priority date of the provisional patent application, separate national phase patent applications can be pursued in any of the
PCT member states either by direct national filing, or in some cases, by filing through a regional patent organization, such as the European
Patent Office. The PCT system delays expenses, allows a limited evaluation of the chances of success for national/regional patent applications,
and enables substantial savings where applications are abandoned within the first thirty months of filing.

For all patent applications,
we determine claiming strategy on a case-by-case basis. Advice of counsel and our business model and needs are always considered. We continuously
reassess the number and type of patent applications, as well as the scope of our patent claims to pursue coverage and value for our processes
and compositions, given existing patent office rules and regulations. Further, claims may be modified during patent prosecution to meet
our intellectual property and business needs.

We have sought patent protection
in the United States and various international jurisdictions related to the CER-1236 T cell technology platform and its constructs, as
well as their use as individual cellular compositions and product candidates targeting specific diseases. We also intend to seek patent
protection related to the processes and materials used in CER-1236 T cell expression as well as its use in combination therapies. As of
December 31, 2025, our patent portfolio comprises ten different patent families filed in various jurisdictions worldwide. These patent
families include four issued patents in the United States, three of which relates to CER-1236; ten pending U.S. applications; one U.S.
provisional application; twenty-six issued patents in international jurisdictions, including patents in Europe, France, Germany, Italy,
Spain, United Kingdom, Denmark, Finland, Norway, Sweden, Switzerland, China, Japan, Hong Kong, and Mexico; and twenty-seven pending applications
in Canada, China, Europe, Hong Kong, Japan, and Korea. These patents and applications, if and when issued, are projected to expire from
2037 to 2047, absent any available patent term adjustments or extensions. We intend to pursue, when possible, further composition, method
of use, dosing, formulation, and other patent protection directed to our current and new product candidates. We may also pursue patent
protection with respect to manufacturing and drug development processes and technology.

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The following issued patents
are directed at a composition of matter and therapeutic uses and provide coverage for our CER-1236 T cell candidate:

U.S. Patent No. 11,708,423,
having an anticipated expiration date of March 26, 2039, including 186 days of patent term adjustment awarded by the USPTO;

U.S. Patent No. 12,291,557,
having an anticipated expiration date of March 10, 2042, including 1,079 days of patent term adjustment awarded by the USPTO;

U.S. Patent No. 12,303,551,
having an anticipated expiration date of March 26, 2039, subject to terminal disclaimer;

EP Patent No. 3,519,441 (validated
in the United Kingdom, France, Spain, Germany, and Italy), having an anticipated expiration date of September 26, 2037, absent any available
patent term adjustments or extensions;

EP Patent No. 3,688,032 (validation
in the United Kingdom, France, Spain, Germany, Italy, Denmark, Finland, Norway, Sweden, Switzerland) having an anticipated expiration
date of September 21, 2038, absent any available patent term adjustments or extensions;

EP Patent No. 4,376,874 (validation
in designated countries in progress) having an anticipated expiration date of July 28, 2042, absent any available patent term adjustments
or extensions;

JP Patent No. 7,730,008 having
an anticipated expiration date of September 26, 2037, absent any available patent term adjustments or extensions;

JP Patent No. 7,286,658 having
an anticipated expiration date of September 21, 2038, absent any available patent term adjustments or extensions; and

CN Patent No. ZL201880076426.1
having an anticipated expiration date of September 21, 2038, absent any available patent term adjustments or extensions.

CN Patent No. ZL201980036210.7
having an anticipated expiration date of March 27, 2039, absent any available patent term adjustments or extensions.

Competition

The biotechnology and pharmaceutical
industries have made substantial investments in recent years into the rapid development of novel immunotherapies for the treatment of
a range of pathologies, including cancers, making this a highly competitive market.

We face substantial competition
from multiple sources, including large and specialty pharmaceutical, biopharmaceutical and biotechnology companies, academic research
institutions and governmental agencies, and public and private research institutions. Our competitors compete with us based on the specific
technologies employed, and on the stage of product candidate development. In addition, many small biotechnology companies have formed
collaborations with large, established companies to (i) obtain support for their research, development, and commercialization of products,
or (ii) combine several treatment approaches to develop longer lasting or more efficacious treatments that may potentially directly compete
with our current or future product candidates.

In addition to the current
standard of care treatments for patients with cancer, numerous commercial and academic preclinical studies and clinical trials are being
undertaken by a large number of parties to assess novel technologies and product candidates in the field of immunotherapy. Results from
these studies and trials have fueled increasing levels of interest in the field of immunotherapy. Accordingly, we face competition from
numerous pharmaceutical and biotechnology entities related to the development of cellular-based therapies to treat cancer. We expect to
face competition from other companies developing TCR T therapies, such as Adaptimmune Therapeutics, plc, GlaxoSmithKline plc, MediGene
AG, TCR2 Therapeutics Inc., TScan Therapeutics Inc. and Ziopharm Oncology, Inc. We also may compete with other T cell therapy companies
with target discovery platforms, such as Adaptive Therapeutics, Inc., Immatics, N.V., 3T Biosciences, Inc., and Sana Biotechnology, Inc.,
among others. We may also compete against a significant number of companies engaged in the development of autologous and allogeneic CAR-T,
CAR-NK, TIL and T cell engager technologies including larger companies such as Gilead Sciences, Inc., Bristol-Myers Squibb Company and
Amgen, Inc. as well as smaller companies such as Nkarta Inc., Allogene Therapeutics Inc., Century Therapeutics Inc., and Fate Therapeutics
Inc., among others.

Many of our competitors,
either alone or in combination with their respective strategic partners, have significantly greater financial resources and expertise
in R&D, manufacturing, the regulatory approval process, and marketing than we do. Mergers and acquisitions activity in the pharmaceutical,
biopharmaceutical, and biotechnology sector is likely to result in greater resource concentration among a smaller number of our competitors.
Smaller or early-stage companies may also prove to be significant competitors, particularly through sizeable collaborative arrangements
with established companies. These competitors also compete with us in recruiting and retaining qualified scientific and management personnel,
establishing clinical trial sites and patient registration for clinical trials, and acquiring technologies complementary to, or necessary
for, our programs.

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Our commercial opportunity
could be reduced or eliminated if one or more of our competitors develop and commercialize products that are safer, more effective, better
tolerated, or of greater convenience or economic benefit than our proposed product offering. Our competitors also may be in a position
to obtain FDA or other regulatory approval for their products more rapidly, resulting in a stronger or dominant market position before
we are able to enter the market. The key competitive factors affecting the success of all of our programs are likely to be product safety,
efficacy, convenience, and treatment cost.

In the event we receive regulatory
approval for any of our product candidates, we will likely compete with other cost-effective and reimbursable treatments used to treat
cancer. The most common treatment modalities for patients with cancer are surgery, radiation, and drug therapy, including chemotherapy,
hormone therapy, biologic therapy, such as monoclonal and bispecific antibodies, immunotherapy, and cell-based therapy, used alone or
in combination to enhance efficacy. Our CER-T cell therapy candidates, if any are approved, may not be competitive with them. Some of
these drugs are branded and subject to patent protection, and others are available on a generic basis. Insurers and other third-party
payors may also encourage the use of generic products or specific branded products. As a result, obtaining market acceptance of any of
our CER-T cell therapies that we successfully introduce to the market may pose challenges.

Government Regulation

In the United States, biological
products are licensed by the FDA for marketing under the Public Health Service Act (“PHS Act”) and regulated under the Federal
Food, Drug, and Cosmetic Act (“FDCA”). Both the FDCA and the PHS Act and their corresponding regulations govern, among other
things, the testing, manufacturing, safety, purity, potency, efficacy, labeling, packaging, storage, recordkeeping, distribution, marketing,
sales, import, export, reporting, advertising, and other promotional practices involving biological products. FDA clearance of an IND
application must be obtained before commencing clinical testing of biological products. FDA licensure also must be obtained before marketing
of biological products. The process of obtaining regulatory approvals and the subsequent compliance with appropriate federal, state, local,
and foreign statutes and regulations require the expenditure of substantial time and financial resources.

U.S. Development Process

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

● completion
of nonclinical laboratory tests and animal studies according to Good Laboratory Practices (“GLPs”) and applicable requirements
for the humane use of laboratory animals or other applicable regulations;

● preparation
of clinical trial material in accordance with cGMPs;

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

● approval
by an institutional review board (“IRB”), reviewing each clinical site before each clinical trial may be initiated;

● performance
of adequate and well-controlled human clinical trials according to Good Clinical Practice (“GCP”) requirements and any additional
requirements for the protection of human research subjects and their health information, to establish the safety, purity, potency, and
efficacy, of the proposed biological product for its intended use;

● submission
to the FDA of a Biologics License Application (“BLA”) for marketing approval that includes substantive evidence of safety,
purity, potency, and efficacy from results of nonclinical testing and clinical trials;

● satisfactory
completion of an FDA inspection prior to BLA approval of the manufacturing facility or facilities where the biological product is produced
to assess compliance with cGMPs, to assure that the facilities, methods, and controls are adequate to preserve the biologic’s identity,
strength, quality, and purity;

● potential
FDA audit of the nonclinical and clinical study sites that generated the data in support of the BLA;

● potential
FDA advisory committee meeting to elicit expert input on critical issues and including a vote by external committee members;

● FDA
review and approval, or licensure, of the BLA, and payment of associated user fees, when applicable; and

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

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Before testing any biological
product candidate in humans, the product candidate enters the preclinical testing stage. Nonclinical tests include laboratory evaluations
of product chemistry, pharmacology, toxicity, and formulation, as well as animal studies to assess the potential safety and activity of
the product candidate. The conduct of the nonclinical tests must comply with federal regulations and requirements including GLPs.

The clinical study sponsor
must submit the results of the nonclinical tests, together with manufacturing information, analytical data, any available clinical data
or literature, and a proposed clinical protocol, to the FDA as part of the IND. Some nonclinical testing typically continues after the
IND is submitted. An IND is an exemption that allows an unapproved product to be shipped in interstate commerce for use in an investigational
clinical trial and a request for FDA authorization to administer an investigational product to humans. The IND automatically becomes effective
30 days after receipt by the FDA, unless the FDA requests certain changes to a protocol before the trial can begin, or the FDA places
the clinical trial on a clinical hold within that 30-day time period. In such a case, the IND sponsor and the FDA must resolve any outstanding
concerns before the clinical trial can begin. The FDA may also impose clinical holds on a biological product candidate at any time before
or during clinical trials due to safety concerns or non-compliance. If the FDA imposes a clinical hold, trials may not recommence without
FDA authorization and then only under terms authorized by the FDA.

Clinical trials may involve
the administration of the biological product candidate to healthy volunteers or subjects under the supervision of qualified investigators.
Clinical trials involving some products for certain diseases, including some rare diseases may begin with testing in patients with the
disease. 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, including stopping rules that assure
a clinical trial will be stopped if certain adverse events should occur. Each protocol and any amendments to the protocol must be submitted
to the FDA as part of the IND. Clinical trials must be conducted and monitored in accordance with the FDA’s regulations comprising
the GCP requirements, including the requirement that all research subjects or his or her legal representative provide informed consent.
Further, each clinical trial must be reviewed and approved by an independent 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 study 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 form and content of the informed consent that must be signed by each clinical trial subject or his or her legal
representative and must monitor the clinical trial until completed. Additionally, some trials are overseen by an independent group of
qualified experts organized by the trial sponsor, known as a data safety monitoring board or committee.

Human clinical trials are typically conducted
in three sequential phases that may overlap or be combined:

● Phase
1. The biological product is initially introduced into healthy human subjects and tested for safety. In the case of some products
for rare diseases, the initial human testing is often conducted in patients.

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

● Phase
3. Clinical trials are undertaken to further evaluate dosage, clinical efficacy, potency, and safety in an expanded patient population
at geographically dispersed clinical trial sites. These clinical trials are intended to establish the overall risk/benefit ratio of the
product and provide an adequate basis for product labeling. In biologics for rare diseases where patient populations are small and there
is an urgent need for treatment, Phase 3 trials might not be required if an adequate risk/benefit can be demonstrated by the Phase 2
trial.

Post-approval clinical trials,
sometimes referred to as Phase 4 clinical trials, may be conducted after initial marketing approval. These clinical trials are used to
gain additional experience from the treatment of patients in the intended therapeutic indication, particularly for long-term safety follow-up.

During all phases of clinical
development, the FDA requires extensive monitoring and auditing of all clinical activities, clinical data, and clinical trial investigators.
Annual progress reports detailing the results of the clinical trials must be submitted to the FDA. Written IND safety reports must be
promptly submitted to the FDA and the investigators for serious and unexpected adverse events, any findings from other studies, tests
in laboratory animals or in vitro testing that suggest a significant risk for human subjects, or any clinically important increase in
the rate of serious suspected adverse reactions over those listed in the protocol or investigator brochure. The sponsor must submit an
IND safety report within 15 calendar days after the sponsor determines that the information qualifies for such reporting. The sponsor
also must notify the FDA of any unexpected fatal or life-threatening suspected adverse reaction within 7 calendar days after the sponsor’s
initial receipt of the information. 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 biologic has been associated with unexpected serious harm to patients.

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Concurrent with clinical
trials, companies usually complete additional animal studies and must also develop additional information about the physical characteristics
of the biologic as well as finalize a process for manufacturing the product in commercial quantities in accordance with cGMP requirements.
To help reduce the risk of the introduction of adventitious agents with use of biologics, the PHS Act emphasizes the importance of manufacturing
control for products whose attributes cannot be precisely defined. The manufacturing process must be capable of consistently producing
quality batches of the product candidate and, among other things, the sponsor must develop methods for testing the identity, strength,
quality, potency, and purity of the final biological product. Additionally, appropriate packaging must be selected and tested and stability
studies must be conducted to demonstrate that the biological product candidate does not undergo unacceptable deterioration over its shelf
life.

There are also various laws
and regulations regarding laboratory practices, the experimental use of animals, and the use and disposal of hazardous or potentially
hazardous substances in connection with the research. In each of these areas, the FDA and other regulatory authorities have broad regulatory
and enforcement powers, including the ability to levy fines and civil penalties, suspend or delay issuance of approvals, seize or recall
products, and withdraw approvals.

Information about certain
clinical trials must be submitted within specific timeframes for public dissemination on the clinicaltrials.gov website. Sponsors or distributors
of investigational products for the diagnosis, monitoring, or treatment of one or more serious diseases or conditions must also have a
publicly available policy on evaluating and responding to requests for expanded access requests.

U.S. Review and Approval Processes

After the completion of clinical
trials of a biological product, FDA approval of a BLA must be obtained before commercial marketing of the product begins. The BLA must
include results of product development, laboratory, and animal studies, human studies, information on the manufacture and composition
of the product, proposed labeling, and other relevant information. The testing and approval processes require substantial time and effort
and there can be no assurance that the FDA will accept the BLA for filing and, even if filed, that any approval will be granted on a timely
basis, if at all.

Under the Prescription Drug
User Fee Act, as amended (“PDUFA”), each BLA may be accompanied by a significant user fee. Under federal law, the submission
of most applications is subject to an application user fee. The sponsor of an approved application is also subject to an annual program
fee. Fee waivers or reductions are available in certain circumstances, including a waiver of the application fee for the first application
filed by a small business. Additionally, no user fees are assessed on BLAs for product candidates designated as orphan drugs, unless the
product candidate also includes a non-orphan indication.

Within 60 days following
submission of the application, the FDA reviews a BLA submitted to determine if it is substantially complete before the agency accepts
it for filing. The FDA may refuse to file any BLA that it deems incomplete or not properly reviewable at the time of submission and may
request additional information. In this event, the BLA must be resubmitted with the additional information. The resubmitted application
is also subject to review before the FDA accepts it for filing. The application also needs to be published and submitted in an electronic
format that can be processed through the FDA’s electronic systems. If the electronic submission is not compatible with the FDA’s
systems, the BLA can be refused for filing. Once the submission is accepted for filing, the FDA begins an in-depth substantive review
of the BLA. The FDA reviews the BLA to determine, among other things, whether the proposed product is safe, potent, and effective, for
its intended use, and has an acceptable purity profile, and whether the product is being manufactured in accordance with cGMPs to assure
and preserve the product’s identity, safety, strength, quality, potency and purity. The FDA may refer applications for novel products
or products that 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 biological product approval process, the FDA also will determine whether a REMS is necessary to assure the safe use of the
biological product. If the FDA concludes a REMS is needed, the sponsor of the BLA must submit a proposed REMS; the FDA will not approve
the BLA without a REMS, if required.

Before approving a BLA, the
FDA may inspect the facilities at which the product is manufactured. 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 a BLA, the FDA will typically inspect one or more clinical trial sites
to assure that the clinical trials were conducted in compliance with IND study requirements and GCP requirements. To assure cGMP and GCP
compliance, an applicant must incur significant expenditure of time, money, and effort in the areas of training, record keeping, production
and quality control.

Notwithstanding the submission
of relevant data and information, the FDA may ultimately decide that the BLA does not satisfy its regulatory criteria for approval and
deny approval. Data obtained from clinical trials are not always conclusive and the FDA may interpret data differently than the sponsor
interprets the same data. If the agency decides not to approve the BLA in its present form, the FDA will issue a complete response letter
that describes all of the specific deficiencies in the BLA identified by the FDA. The deficiencies identified may be minor, such as requiring
labeling changes, or major, such as requiring additional clinical trials. Additionally, the complete response letter may 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 BLA, addressing all of the deficiencies identified in the letter, or withdraw the application.

If a product receives regulatory
approval, the approval may be significantly limited to specific diseases and dosages or the indications for use may otherwise be limited,
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. The FDA may impose restrictions and conditions on product distribution, prescribing, or dispensing
in the form of a risk management plan, or otherwise limit the scope of any approval. In addition, the FDA may require post-marketing clinical
trials, sometimes referred to as Phase 4 clinical trials, designed to further assess a biological product’s safety and effectiveness,
and testing and surveillance programs to monitor the safety of approved products that have been commercialized. As a condition for approval,
the FDA may also require additional nonclinical testing as a Phase 4 commitment.

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One of the performance goals
agreed to by the FDA under the PDUFA is to review standard BLAs in ten months from filing and priority BLAs in six months from filing,
whereupon a review decision is to be made. The FDA does not always meet its PDUFA goal dates for standard and priority BLAs and its review
goals are subject to change from time to time. The review process and the PDUFA goal date may be extended by three months if the FDA requests
or the BLA sponsor otherwise provides additional information or clarification regarding information already provided in the submission
within the last three months before the PDUFA goal date.

Post-Approval Requirements

Maintaining substantial compliance
with applicable federal, state, and local statutes and regulations requires the expenditure of substantial time and financial resources.
Rigorous and extensive FDA regulation of biological products continues after approval, particularly with respect to cGMP. We will rely,
and expect to continue to rely, on third parties for the production of clinical and commercial quantities of any products that we may
commercialize. Manufacturers of our products are required to comply with applicable requirements in the cGMP regulations, including quality
control and quality assurance and maintenance of records and documentation.

Following approval, the manufacturing
facilities are subject to inspections by the FDA, and such inspections may result in an issuance of FDA Form 483 deficiency observations,
untitled letter, or a warning letter, which can lead to plant shutdown and other more serious penalties and fines. Prior to the institution
of any manufacturing changes, a determination needs to be made regarding whether FDA approval is required in advance. If not done in accordance
with FDA expectations, the FDA may restrict supply and may take further action. Product reports are required to be submitted annually.
Other post-approval requirements applicable to biological products include reporting of cGMP deviations that may affect the identity,
potency, purity, and overall safety of a distributed product, recordkeeping requirements, reporting of adverse events, reporting updated
safety and efficacy information, and complying with electronic record and signature requirements.

After a BLA is approved,
the product also may be subject to official lot release. As part of the manufacturing process, the manufacturer is required to perform
certain tests on each lot of the product before it is released for distribution. If the product is subject to official release by the
FDA, the manufacturer submits samples of each lot of product to the FDA together with a release protocol showing a summary of the history
of manufacture of the lot and the results of all of the manufacturer’s tests performed on the lot. The FDA also may perform certain
confirmatory tests on lots of some products, such as viral vaccines, before releasing the lots for distribution by the manufacturer. In
addition, the FDA may conduct laboratory research related to the regulatory standards on the safety, purity, potency, and effectiveness
of biological products. Systems need to be put in place to record and evaluate adverse events reported by health care providers and patients
and to assess product complaints. An increase in severity or new adverse events can result in labeling changes or product recall. Defects
in manufacturing of commercial products can result in product recalls.

We also must comply with
the FDA’s advertising and promotion requirements, such as those related to direct-to-consumer advertising, the prohibition on promoting
products for uses or inpatient populations that are not described in the product’s approved labeling (known as “off-label
use”), industry-sponsored scientific and educational activities, and promotional activities involving the internet. Discovery of
previously unknown problems or the failure to comply with the applicable regulatory requirements may result in restrictions on the marketing
of a product or withdrawal of the product from the market as well as possible civil or criminal sanctions. Failure to comply with the
applicable U.S. requirements at any time during the product development process, approval process, or after approval may subject an applicant
or manufacturer to administrative or judicial civil or criminal sanctions and adverse publicity. FDA sanctions could include refusal to
approve pending applications, withdrawal of an approval or license revocation, clinical hold, warning or untitled letters, product recalls,
product seizures, total or partial suspension of production or distribution, injunctions, fines, refusals of government contracts, mandated
corrective advertising or communications with doctors, debarment, restitution, disgorgement of profits, or civil or criminal penalties.
Any agency or judicial enforcement action could have a material adverse effect.

Biological product manufacturers
and other entities involved in the manufacture and distribution of approved biological products are required to register their establishments
with the FDA and certain state agencies, and they are subject to periodic unannounced inspections by the FDA and certain state agencies
for compliance with cGMPs and other laws. Accordingly, manufacturers must continue to expend time, money, and effort in the areas of production
and quality control to maintain cGMP compliance. Manufacturers and other parties involved in the drug supply chain for prescription drug
products must also comply with product tracking and tracing requirements and for notifying the FDA of counterfeit, diverted, stolen and
intentionally adulterated products or products that are otherwise unfit for distribution in the United States. Discovery of problems with
a product after approval may result in restrictions on a product, manufacturer, or holder of an approved BLA, including withdrawal of
the product from the market. In addition, changes to the manufacturing process or facility generally require prior FDA approval before
being implemented, and other types of changes to the approved product, such as adding new indications and additional labeling claims,
are also subject to further FDA review and approval.

Orphan Drug Designation

Under the Orphan Drug Act,
the FDA may grant orphan drug designation (“ODD”), to a biological product intended to treat a rare disease or condition,
which is generally a disease or condition that affects fewer than 200,000 individuals in the United States, or more than 200,000 individuals
in the United States and for which there is no reasonable expectation that the cost of developing and making a biological product available
in the United States for this type of disease or condition will be recovered from sales of the product. ODD must be requested before submitting
a BLA. After the FDA grants ODD, the identity of the therapeutic agent and its potential orphan use are disclosed publicly by the FDA.
ODD does not convey any advantage in or shorten the duration of the regulatory review and approval process.

If a product that has ODD
receives the first FDA approval for the disease or condition for which it has such designation, the product is entitled to orphan product
exclusivity, which means that the FDA may not approve any other applications to market the same biological product for the same indication
for seven years, except in limited circumstances, such as not being able to supply the product for patients or showing clinical superiority
to the product with orphan exclusivity.

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Competitors, however, may
receive approval of different products for the indication for which the orphan product has exclusivity or obtain approval for the same
product but for a different indication for which the orphan product has exclusivity. Orphan product exclusivity also could block the approval
of one of our products for seven years if a competitor obtains approval of the same biological product as defined by the FDA or if our
product candidate is determined to be contained within the competitor’s product for the same indication or disease. If a biological
product designated as an orphan product receives marketing approval for an indication broader than what is designated, it may not be entitled
to orphan product exclusivity.

Expedited Review and Approval Programs

The FDA has various programs,
including fast track designation, priority review, accelerated approval, breakthrough therapy designation, and regenerative medicine advanced
therapy designation that are intended to expedite or simplify the process for the development and FDA review of biological products that
are intended for the treatment of serious or life-threatening diseases or conditions and demonstrate the potential to address unmet medical
needs. The purpose of these programs is to provide important new biological products to patients earlier than under standard FDA review
procedures.

To be eligible for a fast
track designation, the FDA must determine, based on the request of a sponsor, that a biological product is intended to treat a serious
or life-threatening disease or condition and demonstrates the potential to address an unmet medical need. The FDA will determine that
a product will fill an unmet medical need if it will provide a therapy where none exists or provide a therapy that may be potentially
superior to existing therapy based on efficacy or safety factors. In addition to other benefits, such as the ability to have greater interactions
with the FDA, the FDA may initiate review of sections of a fast track BLA before the application is complete, a process known as rolling
review.

The FDA may give a priority
review designation to biological products that treat a serious condition and, if approved, would provide a significant improvement in
safety or effectiveness. A priority review means that the goal for the FDA to review an application is six months, rather than the standard
review of ten months under current PDUFA guidelines. Most products that are eligible for fast track designation may also be considered
appropriate to receive a priority review. In addition, 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
and may be approved on the basis of adequate and well-controlled clinical trials establishing that the biological product has an effect
on a surrogate endpoint that is reasonably likely to predict clinical benefit, or on a clinical endpoint that can be measured earlier
than irreversible morbidity or mortality, that is reasonably likely to predict an effect on irreversible morbidity or mortality or other
clinical benefit, taking into account the severity, rarity, or prevalence of the condition and the availability or lack of alternative
treatments. As a condition of approval, the FDA may require a sponsor of a biological product receiving accelerated approval to perform
adequate and well-controlled post-marketing studies to verify and describe the predicted effect on irreversible morbidity or mortality
or other clinical endpoint. Under the Food and Drug Omnibus Reform Act of 2022 (“FDORA”), the FDA may require, as appropriate,
that such trials be underway prior to approval or within a specific time period after the date of approval for a product granted accelerated
approval.

Under FDORA, the FDA has
increased authority for expedited procedures to withdraw approval of a drug or indication approved under accelerated approval if, for
example, the confirmatory trial fails to verify the predicted clinical benefit of the product. In addition, for products being considered
for accelerated approval, the FDA generally requires, unless otherwise informed by the agency, that all advertising and promotional materials
intended for dissemination or publication within 120 days of marketing approval be submitted to the agency for review during the pre-approval
review period.

Moreover, a sponsor can request
designation of a product candidate as a “breakthrough therapy.” A breakthrough therapy is defined as a drug or biological
product that is intended, alone or in combination with one or more other drugs or biologics, to treat a serious or life-threatening disease
or condition, and preliminary clinical evidence indicates that the drug or biological product may demonstrate substantial improvement
over existing therapies on one or more clinically significant endpoints, such as substantial treatment effects observed early in clinical
development. Drug and biological products designated as breakthrough therapies are also eligible for accelerated approval. The FDA must
take certain actions, such as holding timely meetings and providing advice, intended to expedite the development and review of an application
for approval of a breakthrough therapy.

Finally, the FDA can accelerate
review and approval of products designated as regenerative medicine advanced therapies. A product is eligible for this designation if
it is a regenerative medicine therapy that is intended to treat, modify, reverse or cure a serious or life-threatening disease or condition
and preliminary clinical evidence indicates that the product has the potential to address unmet medical needs for such disease or condition.
The benefits of a regenerative medicine advanced therapy designation include early interactions with FDA to expedite development and review,
benefits available to breakthrough therapies, potential eligibility for priority review and accelerated approval based on surrogate or
intermediate endpoints.

Even if a product qualifies
for one or more of these programs, the FDA may later decide that the product no longer meets the conditions for qualification or decides
that the time period for FDA review or approval will not be shortened. Furthermore, fast-track designation, priority review, accelerated
approval, and breakthrough therapy designation do not change the standards for approval and may not ultimately expedite the development
or approval process.

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Biologics Price Competition and Innovation
Act

The Biologics Price Competition
and Innovation Act of 2009 (“BPCIA”), which was enacted as part of the Patient Protection and Affordable Care Act, as amended
by the Health Care and Education Reconciliation Act of 2010 (collectively, the “Affordable Care Act”), created an abbreviated
approval pathway for biological products that are demonstrated to be “biosimilar” or “interchangeable” with an
FDA-licensed reference biological product via an approved BLA. Biosimilarity to an approved reference product requires that there be no
differences in conditions of use, route of administration, dosage form, and strength, and no clinically meaningful differences between
the biological product and the reference product in terms of safety, purity, and potency. Biosimilarity is demonstrated in steps beginning
with rigorous analytical studies or “fingerprinting”, in vitro studies, in vivo animal studies, and generally at least one
clinical study. If at any point in the stepwise biosimilarity process a significant difference is observed, then the products are not
biosimilar, and the development of a standalone BLA is necessary. In order to meet the higher hurdle of interchangeability, a sponsor
must demonstrate that the biosimilar product can be expected to produce the same clinical result as the reference product, and for a product
that is administered more than once, that the risk of switching between the reference product and biosimilar product is not greater than
the risk of maintaining the patient on the reference product. Complexities associated with the larger, and often more complex, structures
of biological products, as well as the process by which such products are manufactured, pose significant hurdles to implementation that
are still being evaluated by the FDA. Under the BPCIA, a reference biologic is granted 12 years of exclusivity from the time of first
licensure of the reference product.

Regulation Outside of the United States

In addition to regulations
in the United States, we are subject to a variety of regulations in other jurisdictions governing clinical studies, commercial sales,
and distribution of our products. Most countries outside of the United States require that clinical trial authorization applications be
submitted to and approved by the local regulatory authority for each clinical study. In the European Union, for example, an application
must be submitted to the national competent authority and an independent ethics committee in each country in which we intend to conduct
clinical trials, much like the FDA and IRB, respectively. Under the Clinical Trials Regulation (EU) No 536/2014, which replaced the Clinical
Trials Directive 2001/20/EC on January 31, 2022, a single application is now made through the Clinical Trials Information System for clinical
trial authorization in up to 30 EU/EEA countries at the same time and with a single set of documentation.

The assessment of applications
for clinical trials is divided into two parts (Part I contains scientific and medicinal product documentation and Part II contains the
national and patient-level documentation). Part I is assessed by a coordinated review by the competent authorities of all European Union
member states in which an application for authorization of a clinical trial has been submitted (Member States concerned) of a draft report
prepared by a reference Member State. Part II is assessed separately by each Member State concerned. The role of the relevant ethics committees
in the assessment procedure continues to be governed by the national law of the Member State concerned, however overall related timelines
are defined by the Clinical Trials Regulation. The Clinical Trials Regulation also provides for simplified reporting procedures for clinical
trial sponsors.

In addition, whether or not
we obtain FDA approval for a product, we must obtain approval of a product by the comparable regulatory authorities of countries outside
the United States before we can commence marketing of the product in those countries. The approval process and requirements vary from
country to country, so the number and type of nonclinical, clinical, and manufacturing studies needed may differ, and the time may be
longer or shorter than that required for FDA approval.

To obtain regulatory approval
of our medicinal products under the European Union regulatory system, we are required to submit a marketing authorization application
(“MAA”), to be assessed in the centralized procedure. The centralized procedure allows applicants to obtain a marketing authorization
(“MA”) that is valid throughout the European Union, and the additional countries of the European Economic Area (Iceland, Liechtenstein
and Norway) (“EEA”). It is compulsory for medicinal products manufactured using biotechnological processes, orphan medicinal
products, advanced therapy medicinal products (gene-therapy, somatic cell-therapy or tissue-engineered medicines) and medicinal products
containing a new active substance which is not authorized in the European Union and which is intended for the treatment of HIV, AIDS,
cancer, neurodegenerative disorders, auto-immune and other immune dysfunctions, viral diseases or diabetes. The centralized procedure
is optional for any other products containing new active substances not authorized in the European Union or for products which constitute
a significant therapeutic, scientific, or technical innovation or for which a centralized authorization is in the interests of public
health at European Union level. When a company wishes to place on the market a medicinal product that is eligible for the centralized
procedure, it sends an application directly to the EMA, to be assessed by the Committee for Medicinal Products for Human Use (“CHMP”).
The CHMP is responsible for conducting the assessment of whether a medicine meets the required quality, safety, and efficacy requirements,
and whether the product has a positive risk/benefit profile. The time limit for the evaluation procedure is 210 days (excluding clock
stops, when additional written or oral information is to be provided by the applicant in response to questions asked by the CHMP). The
CHMP opinion is forwarded to the European Commission, which will make a binding decision on the grant of an MA within the statutory timeframes
(generally within 67 days of receipt of the CHMP opinion).

National marketing authorizations,
which are issued by the competent authorities of the Member States of the European Union and only cover their respective territory, are
available for products not falling within the mandatory scope of the centralized procedure. Where a product has already been authorized
for marketing in a Member State of the European Union, this national authorization can be recognized in other Member States through the
mutual recognition procedure. If the product has not received a national authorization in any Member State at the time of application,
it can be approved simultaneously in various Member States through the decentralized procedure.

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In the European Union, new
active substances (including both small molecules and biological medicinal products) approved on the basis of a complete and independent
data package qualify for eight years of data exclusivity from the date of first marketing authorization in the European Union and an additional
two years of market exclusivity. Data exclusivity prevents generic or biosimilar applicants from referencing the innovator’s preclinical
and clinical trial data contained in the dossier of the reference product when applying for a generic or biosimilar MA, for a period of
eight years from the date on which the reference product was first authorized in the European Union. During the additional two-year period
of market exclusivity, a generic or biosimilar MAA can be submitted, and the innovator’s data may be referenced, but no generic
or biosimilar medicinal product can be marketed until the expiration of the market exclusivity. The overall ten-year period will be extended
to a maximum of eleven years if, during the first eight years of those ten years, the MA holder obtains an authorization for one or more
new therapeutic indications which, during the scientific evaluation prior to authorization, is held to bring a significant clinical benefit
in comparison with currently approved therapies. There is no guarantee that a product will be considered by the EMA to be a new active
substance, and products may not qualify for data exclusivity. Even if the innovator gains the prescribed period of data exclusivity, another
company could nevertheless also market another version of the product if such company obtained an MA based on an MAA with a complete and
independent data package of pharmaceutical tests, preclinical tests and clinical trials.

The criteria for designating
an “orphan medicinal product” in the European Union are similar in principle to those in the United States. Under Article
3 of Regulation (EC) 141/2000, a medicinal product may be designated as an orphan medicinal product if it is intended for the diagnosis,
prevention, or treatment of a life-threatening or chronically debilitating condition that affects no more than five in 10,000 persons
in the European Union when the application is made. In addition, orphan designation can be granted if the product is intended for a life
threatening, seriously debilitating, or serious and chronic condition in the European Union and, without incentives, it is unlikely that
sales of the product in the European Union would be sufficient to justify the necessary investment in its development. Orphan designation
is only available if there is no other satisfactory method approved in the European Union of diagnosing, preventing, or treating the applicable
orphan condition, or if such a method exists, the proposed orphan medicinal product will be of significant benefit to patients affected
by such condition, as defined in Regulation (EC) 847/2000.

Orphan designation provides
opportunities for fee reductions, protocol assistance, and access to the centralized procedure. Fee reductions are available in accordance
with applicable EMA rules, including for small and medium enterprises. In addition, if a product which has an orphan designation subsequently
receives a centralized MA for the indication for which it has such designation, the product is entitled to orphan market exclusivity,
which means the EMA may not approve any other application for a marketing authorization for a similar medicinal product for the same indication
as the authorized orphan product for a period of ten years. A “similar medicinal product” is defined as a medicinal product
containing a similar active substance or substances as contained in an authorized orphan medicinal product, and which is intended for
the same therapeutic indication. The exclusivity period may be reduced to six years if, at the end of the fifth year, it is shown that
the designation criteria are no longer met, including where it is shown that the product is sufficiently profitable not to justify maintenance
of market exclusivity. Additionally, an MA may be granted to a similar medicinal product for the same indication as an authorized orphan
product at any time if:

● the
second applicant can establish that its product, although similar to the authorized orphan product, is safer, more effective or otherwise
clinically superior;

● the
MA holder of the authorized orphan product consents to a second medicinal product application; or

● the
MA holder of the authorized product cannot supply enough orphan medicinal product.

A pediatric investigation
plan (“PIP”) in the European Union is aimed at ensuring that the necessary data are obtained to support the authorization
of a medicine for children, through studies in children. All applications for MAs for new medicines have to include the results of studies
as described in an agreed PIP, unless the medicine is exempt because of a deferral or waiver. This requirement also applies when an MA
holder wants to add a new indication, pharmaceutical form, or route of administration for a medicine that is already authorized and covered
by intellectual property rights. Several rewards and incentives for the development of pediatric medicines for children are available
in the European Union. Medicines authorized across the European Union with the results of studies from a PIP included in the product information
are eligible for an extension of their supplementary protection certificate (“SPC”) by six months (provided an application
for such extension is made at the same time as filing the SPC application for the product, or at any point up to two years before the
SPC expires). This is the case even when the studies’ results are negative. For orphan medicinal products, the incentive is an additional
two years of market exclusivity. Scientific advice and protocol assistance at the EMA are free of charge for questions relating to the
development of pediatric medicines. Medicines developed specifically for children that are already authorized but are not protected by
a patent or supplementary protection certificate are eligible for a pediatric-use MA (“PUMA”). If a PUMA is granted, the product
will benefit from ten years of market protection as an incentive.

In March 2016, the EMA launched
an initiative, the PRIority MEdicines (“PRIME”) scheme, to facilitate development of product candidates in indications, often
rare, for which few or no therapies currently exist. The PRIME scheme is intended to encourage development of products in areas of unmet
medical need and may provide eligibility for accelerated assessment of products representing substantial innovation reviewed under the
centralized procedure. Products from small- and medium-sized enterprises may qualify for earlier entry into the PRIME scheme than larger
companies on the basis of compelling non-clinical data and tolerability data from initial clinical trials. Many benefits accrue to sponsors
of product candidates with PRIME designation, including but not limited to, early and proactive regulatory dialogue with the EMA, frequent
discussions on clinical trial designs and other development program elements, and potentially accelerated MAA assessment once a dossier
has been submitted. Importantly, once a candidate medicine has been selected for the PRIME scheme, a dedicated contact and rapporteur
from the CHMP or from the Committee for Advanced Therapies (“CAT”) are appointed early in the PRIME scheme facilitating increased
understanding of the product at the EMA’s committee level. An initial meeting with the CHMP/CAT rapporteur initiates these relationships
and includes a team of multidisciplinary experts at the EMA to provide guidance on the overall development and regulatory strategies.
PRIME eligibility does not change the standards for product approval, and there is no assurance that any such designation or eligibility
will result in expedited review or approval.

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The aforementioned European
Union rules are generally applicable in the EEA.

The European Commission introduced
legislative proposals in April 2023 that, if implemented, will replace the current regulatory framework in the European Union for all
medicines (including those for rare diseases and for children). In April 2024, the European Parliament adopted its position on the legislative
proposals and, in June 2025, the Council of the European Union adopted its position. A common position on the text was agreed upon on
December 11, 2025, in the context of subsequent inter-institutional trilogue negotiations. The proposed revisions remain to be adopted,
and are not expected to become applicable before 2028.

Following the end of the
Brexit transition period on January 1, 2021 and the implementation of the Windsor Framework on January 1, 2025, the United Kingdom is
not generally subject to EU laws in respect of medicines. The EU laws that have been transposed into UK law through secondary legislation
remain applicable in the UK, however, new legislation such as the Clinical Trials Regulation (EU) No 536/2014 is not applicable in the
UK. As of January 1, 2021, the Medicines and Healthcare products Regulatory Agency (“MHRA”) is the UK’s standalone medicines
and medical devices regulator. As a result of the Northern Ireland Protocol, different rules applied in Northern Ireland than in England,
Wales, and Scotland (together, “Great Britain”), as Northern Ireland continued to follow the EU regulatory regime for a period
of time after Brexit. However, on January 1, 2025 a new arrangement called the “Windsor Framework” came into effect and reintegrated
Northern Ireland under the regulatory authority of the MHRA with respect to medicinal products. The Windsor Framework removes EU licensing
processes and EU labeling and serialization requirements in relation to Northern Ireland and introduces a UK-wide licensing process for
medicines. In particular, the MHRA is now responsible for approving medicinal products placed on the UK market (i.e., Great Britain and
Northern Ireland), and the EMA no longer has a role in UK marketing authorizations. A single UK-wide MA will be granted by the MHRA for
medicinal products to be sold in the UK, enabling products to be sold in a single pack and under a single authorization throughout the
UK. In addition, the new arrangements require, for packs placed on the UK market on or after January 1, 2025, a “UK Only”
label, indicating they are not for sale in the EU.

The MHRA has introduced changes
to national licensing procedures, including procedures to prioritize access to new medicines that will benefit patients, an accelerated
assessment procedure and new routes of evaluation for novel products and biotechnological products. Although separate authorization is
now required to market medicinal products in the UK, since January 1, 2024, the MHRA may rely on the International Recognition Procedure
when reviewing certain types of MAAs, under which the MHRA will take into account the expertise and decision-making of trusted regulatory
partners including the medicines regulatory authorities in Australia, Canada, Switzerland, Singapore, Japan, the United States and the
EMA in the EU.

There is no pre-MA orphan
designation in the UK. Instead, the MHRA reviews applications for orphan designation alongside the corresponding MAA. The criteria are
essentially the same, but have been tailored for the UK market, i.e., the prevalence of the condition in UK (rather than the European
Union) must not be more than five in 10,000. Should an orphan designation be granted, the period of market exclusivity is set from the
date of first approval of the product in the UK.

Healthcare Laws and Regulations

Sales of our product candidate,
if approved, or any other future product candidate, will be subject to healthcare regulation and enforcement by the federal government
and the states and foreign governments in which we might conduct our business. The healthcare laws and regulations that may affect our
ability to operate include the following:

● The
federal Anti-Kickback Statute makes it illegal for any person or entity to knowingly and willfully, directly or indirectly, solicit,
receive, offer, or pay any remuneration that is in exchange for or to induce the referral of business, including the purchase, order,
lease of any good, facility, item or service for which payment may be made under a federal healthcare program, such as Medicare or Medicaid.
The term “remuneration” has been broadly interpreted to include anything of value;

● Federal
false claims, and false statement laws, including the federal civil False Claims Act, and Civil Monetary Penalties Law, prohibits, among
other things, any person or entity from knowingly presenting, or causing to be presented, for payment to, or approval by, federal programs,
including Medicare and Medicaid, claims for items or services, including drugs and biologics, that are false or fraudulent;

● Health
Insurance Portability and Accountability Act of 1996 (“HIPAA”) created additional federal criminal statutes 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 or making any false, fictitious or fraudulent statement in connection with the delivery of or payment
for healthcare benefits, items or services;

● HIPAA,
as amended by the Health Information Technology for Economic and Clinical Health Act of 2009 and their implementing regulations, imposes
obligations on certain covered healthcare providers, health plans, and healthcare clearinghouses and their respective business associates
and covered subcontractors types of individuals and entities regarding the electronic exchange of information in common healthcare transactions,
as well as standards relating to the privacy and security of individually identifiable health information;

● The
federal Physician Payments Sunshine Act requires certain manufacturers of drugs, devices, biologics and medical supplies for which payment
is available under Medicare, Medicaid or the Children’s Health Insurance Program, with specific exceptions, to report annually
to the Centers for Medicare and Medicaid Services (“CMS”), information related to payments or other transfers of value made
to physicians (defined to include doctors, dentists, optometrists, podiatrists and chiropractors), physician assistants, nurse practitioners,
clinical nurse specialists, anesthesiologist assistants, certified nurse anesthetists and certified nurse-midwives and teaching hospitals,
as well as ownership and investment interests held by physicians and their immediate family members.;

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● Federal
and state laws that require pharmaceutical manufacturers to report product pricing information; and

● The
Foreign Corrupt Practices Act prohibits U.S. businesses and their representatives from offering to pay, paying, promising to pay or authorizing
the payment of money or anything of value to a foreign official in order to influence any act or decision of the foreign official in
his or her official capacity or to secure any other improper advantage in order to obtain or retain business.

Many states have similar
laws and regulations, such as anti-kickback and false claims laws, that may be broader in scope and may apply regardless of payor, in
addition to items and services reimbursed under Medicaid and other state programs. Additionally, we may be subject to state laws that
require pharmaceutical companies to comply with the federal government’s and/or pharmaceutical industry’s voluntary compliance
guidelines, state laws that require drug and biologics manufacturers to report information related to payments and other transfers of
value to physicians and other healthcare providers or marketing expenditures, as well as state and foreign laws governing the privacy
and security of health information, many of which differ from each other in significant ways and often are not preempted by HIPAA. Additionally,
to the extent that our product is sold in a foreign country, we may be subject to similar foreign laws.

Pharmaceutical Coverage, Pricing and Reimbursement

Significant uncertainty exists
as to the coverage and reimbursement status of any product candidates for which we obtain regulatory approval. In the United States and
markets in other countries, sales of any products for which we receive regulatory approval for commercial sale will depend, in part, on
the extent to which third-party payors provide coverage, and establish adequate reimbursement levels for such drug products. In the United
States, third-party payors include federal and state healthcare programs, government authorities, private managed care providers, private
health insurers and other organizations.

Third-party payors are increasingly
challenging the price, examining the medical necessity and reviewing the cost-effectiveness of medical drug products and medical services,
in addition to questioning their safety and efficacy. Such payors may limit coverage to specific drug products on an approved list, also
known as a formulary, which might not include all of the FDA-approved drugs for a particular indication. We may need to conduct expensive
pharmaco-economic studies in order to demonstrate the medical necessity and cost-effectiveness of our products, in addition to the costs
required to obtain the FDA approvals. Nonetheless, our product candidates may not be considered medically necessary or cost-effective.
Moreover, the process for determining whether a third-party payor will provide coverage for a drug product may be separate from the process
for setting the price of a drug product or for establishing the reimbursement rate that such a payor will pay for the drug product. A
payor’s decision to provide coverage for a drug product does not imply that an adequate reimbursement rate will be approved. Further,
one payor’s determination to provide coverage for a drug product does not assure that other payors will also provide coverage for
the drug product. Adequate third-party reimbursement may not be available to enable us to maintain price levels sufficient to realize
an appropriate return on our investment in product development.

The marketability of any
product candidates for which we receive regulatory approval for commercial sale may suffer if the government and third-party payors fail
to provide adequate coverage and reimbursement. In addition, emphasis on managed care in the United States has increased and could increase
the pressure on pharmaceutical pricing. Coverage policies and third-party reimbursement rates may change at any time. Even if favorable
coverage and reimbursement status is attained for one or more products for which we receive regulatory approval, less favorable coverage
policies and reimbursement rates may be implemented in the future.

Healthcare Reform

The United States and many foreign jurisdictions have enacted or proposed
legislative and regulatory changes affecting the healthcare system. The United States government, state legislatures and foreign governments
also have shown significant interest in implementing cost-containment programs to limit the growth of government-paid healthcare costs,
including price controls, restrictions on reimbursement, and requirements for substitution of generic products for branded prescription
drugs and biologics. In recent years, Congress has considered reductions in Medicare reimbursement levels for drugs and biologics administered
by physicians. CMS, the agency that administers the Medicare and Medicaid programs, also has authority to revise reimbursement rates and
to implement coverage restrictions for some drugs and biologics. Cost reduction initiatives and changes in coverage implemented through
legislation or regulation could decrease utilization of and reimbursement for any approved products. While Medicare regulations apply
only to drug benefits for Medicare beneficiaries, private payors often follow Medicare coverage policy and payment limitations in setting
their own reimbursement rates. Therefore, any reduction in reimbursement that results from federal legislation or regulation may result
in a similar reduction in payments from private payors.

The Affordable Care Act substantially
changed the way healthcare is financed by both governmental and private insurers, and significantly impacts the pharmaceutical industry.
The Affordable Care Act is intended to broaden access to health insurance, reduce or constrain the growth of healthcare spending, enhance
remedies against healthcare fraud and abuse, add new transparency requirements for healthcare and health insurance industries, impose
new taxes and fees on pharmaceutical and medical device manufacturers, and impose additional health policy reforms. Among other things,
the Affordable Care Act expanded manufacturers’ rebate liability under the Medicaid Drug Rebate Program by increasing the minimum
Medicaid rebate for both branded and generic drugs and biologics, expanded the 340B program, and revised the definition of average manufacturer
price (“AMP”), which could increase the amount of Medicaid drug rebates manufacturers are required to pay to states. The legislation
also extended Medicaid drug rebates, previously due only on fee-for-service Medicaid utilization, to include the utilization of Medicaid
managed care organizations as well and created an alternative rebate formula for certain new formulations of certain existing products
that is intended to increase the amount of rebates due on those drugs.

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Other legislative changes
have been proposed and adopted since passage of the Affordable Care Act. The Budget Control Act of 2011, among other things, included
automatic reductions to several government programs, including aggregate reductions to Medicare payments to healthcare providers of up
to 2.0% per fiscal year, which remain in effect through 2031. The American Taxpayer Relief Act of 2012, among other things, reduced Medicare
payments to several types of providers, including hospitals, imaging centers and cancer treatment centers, and increased the statute of
limitations period for the government to recover overpayments to providers from three to five years.

Further legislative and regulatory
changes under the Affordable Care Act remain possible, and it is unknown what form any such changes or any law would take, and how or
whether it may affect our business in the future. We expect that changes or additions to the Affordable Care Act, the Medicare and Medicaid
programs, changes allowing the federal government to directly negotiate drug prices, and changes stemming from other healthcare reform
measures, especially with regard to healthcare access, financing or other legislation in individual states, could have a material adverse
effect on the healthcare industry.

The Affordable Care Act requires
pharmaceutical manufacturers to provide a 50% discount (increased by subsequent legislation to a 70% discount) off the negotiated price
of prescriptions filled by beneficiaries in the Medicare Part D coverage gap, referred to as the “donut hole.” The Inflation
Reduction Act of 2022 (“IRA”) includes provisions that reduce the out-of-pocket spending cap for Medicare Part D beneficiaries
from $7,050 to $2,000 starting in 2025, thereby effectively eliminating the donut hole. The IRA also requires pharmaceutical manufacturers
to provide a 10% discount of all biosimilar and brand name prescription drugs covered under the Medicare Part D plan benefit during the
initial coverage period before the beneficiary reaches the $2,000 out-of-pocket spending cap. Once the patient reaches the out-of-pocket
spending cap, they enter catastrophic coverage and drug manufacturer liability for biosimilar and brand name drugs increases to 20%. Furthermore,
the IRA allows the U.S. government to negotiate Medicare Part B and Part D price caps for certain high-cost drugs and biologics without
generic or biosimilar competition; requires companies to pay rebates to Medicare for certain drug prices that increase faster than inflation;
and delays until January 1, 2032 the implementation of a U.S. Department of Health and Human Service (“HHS”) rebate rule that
would have limited the fees that pharmacy benefit managers can charge.

The Affordable Care Act also
expanded the Public Health Service’s 340B drug pricing program, which requires participating manufacturers to agree to charge statutorily
defined covered entities no more than the 340B “ceiling price” for the manufacturer’s covered outpatient drugs. The
Affordable Care Act expanded the 340B program to include additional types of covered entities: certain freestanding cancer hospitals,
critical access hospitals, rural referral centers, and sole community hospitals, each as defined by the Affordable Care Act. Because the
340B ceiling price is determined based on AMP and Medicaid drug rebate data, revisions to the Medicaid rebate formula and AMP definition
could cause the required 340B discounts to increase.

Other legislative changes
have been proposed and adopted since passage of the ACA, including the Budget Control Act of 2011 and subsequent legislation, which among
other things, resulted in reductions in Medicare payments to healthcare providers of up to 2.0% per fiscal year through 2031. Further,
the American Taxpayer Relief Act of 2012, among other things, reduced Medicare payments to several types of providers, including hospitals,
imaging centers and cancer treatment centers, and increased the statute of limitations period for the government to recover overpayments
to providers from three to five years. The American Rescue Plan Act of 2021 eliminated the statutory Medicaid drug rebate cap, previously
set at 100% of a drug’s AMP, for single source and innovator multiple source drugs, beginning January 1, 2024. In addition, the
One Big Beautiful Bill Act of 2025 imposed significant reductions in Medicaid funding, additional work requirements for certain Medicaid
beneficiaries and more frequent eligibility redeterminations. These changes are expected to place increased pressure on state Medicaid
budgets and could reduce enrollment, utilization and reimbursement levels for prescription drugs, including our products, which could
adversely affect our business.

Further legislative and regulatory
changes under the Affordable Care Act remain possible. It is unknown what form any such changes or any law would take, and how or whether
it may affect our business in the future. We expect that changes or additions to the Affordable Care Act, the Medicare and Medicaid programs,
allowing the federal government to directly negotiate drug prices and changes stemming from other healthcare reform measures, especially
with regard to healthcare access, financing or other legislation in individual states, could have a material adverse effect on the healthcare
industry. Payment methodologies may be subject to changes in healthcare legislation and regulatory initiatives as well. For example,
CMS may develop new payment and delivery models, such as bundled payment models.

The costs of drugs have also
been the subject of considerable discussion in the United States. To date, there have been several recent U.S. congressional inquiries,
as well as proposed and enacted federal and state legislation designed to, among other things, bring more transparency to drug pricing,
review the relationship between pricing and manufacturer patient programs, reduce the costs of drugs under Medicare and reform government
program reimbursement methodologies for drug products. The Trump Administration has issued executive orders and supported proposed regulatory
initiatives in 2025 that could have a significant impact on the prices that we, or any collaborators, may receive for any approved products.

On May 12, 2025, President
Trump signed an executive order directing the Secretary of HHS to set and communicate most-favored-nation (“MFN”) price targets
to manufacturers and propose a rulemaking plan to impose MFN pricing if “significant progress” is not made, and also directing
the federal government to support regulatory paths to allow direct-to-patient sales for companies that meet these targets. The executive
order further states that the Administration will take additional action (for example, examining whether marketing approvals should be
modified or rescinded or considering individual drug importation waiver authorities) should manufacturers fail to offer American consumers
the MFN lowest price. In July 2025, President Trump sent letters to certain pharmaceutical companies demanding that these companies extend
MFN pricing to Medicaid and newly launched drugs as well as move to direct-to-consumer models priced at MFN pricing, and soliciting binding
commitments by September 29, 2025. Since this time, multiple drug manufacturers have announced plans to, for certain of their drugs, lower
prices to reflect similar pricing around the world, and to sell these reduced-price drugs on a direct-to-consumer purchasing platform
developed by the federal government; however, it is not known what results will occur to the extent the recipients of these letters do
not reduce their U.S. prices.

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On December 19, 2025, CMS
released two proposed rules that would incorporate MFN pricing principles into federal reimbursement for prescription drugs. The first
proposal, the Global Benchmark for Efficient Drug Pricing Model (“GLOBE”) for Medicare Part B, would require manufacturers
of specified single source drugs and sole source biologics to pay incremental rebates based on international benchmark prices, with participation
triggered for products meeting CMS’s spending and eligibility criteria. The second proposal, the Guarding U.S. Medicare Against
Rising Drug Costs (“GUARD”) model for Medicare Part D, would similarly mandate manufacturer rebates for qualifying sole source
drugs where the Medicare net price exceeds an MFN benchmark derived from international reference pricing methodologies. As proposed, GLOBE
would begin a five year performance period on October 1, 2026 and GUARD would begin its performance period in 2027. These proposals will
likely be subject to legal challenges that could delay their implementation or modify their impact on manufacturer pricing and revenue.
Additionally, in November 2025, CMS introduced the GENErating cost Reductions fOr U.S. Medicaid (“GENEROUS”) Model, a voluntary
MFN framework for manufacturers participating in the Medicaid Drug Rebate Program. Although it is voluntary, the GENEROUS Model could
also impact the drug pricing landscape for manufacturers.

At the state level, legislatures
have 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 expect that additional
federal, state, and foreign healthcare reform measures will be adopted in the future, any of which could limit the amounts that federal
and state governments will pay for healthcare products and services, which could result in limited coverage and reimbursement and reduced
demand for our products, once approved, or additional pricing pressures.

Employees and Human Capital Resources

As of December 31, 2025,
we had eight full-time employees, including two executive officers and six employees conducting Research and Development. Our employees
are not represented by labor unions or covered by collective bargaining agreements and we consider our relationship with our employees
to be good.

Compensation and Benefits

Our employee-related objectives
include, as applicable, identifying, recruiting, retaining, and incentivizing our management team and our clinical, scientific and other
employees and consultants. The principal purposes of our equity and cash incentive plans are to attract, retain and motivate personnel
through the granting of stock-based and cash-based compensation awards, in order to align our interests and the interests of our stockholders
with those of our employees and consultants. In addition, all of our employees are eligible for health insurance, paid and unpaid leaves
including paid parental leave, a retirement plan, life and disability/accident coverage, and parking or commuter assistance and employee
assistance.

Corporate Information

We were incorporated under
the laws of the state of Delaware on October 2, 2020 under the name Phoenix Biotech Acquisition Corporation. Legacy CERo was incorporated
under the laws of the state of Delaware on September 23, 2016. On February 14, 2024, we consummated a merger with Legacy CERo and subsequently
changed our name to “CERo Therapeutics Holdings, Inc.” Our corporate headquarters are currently located at 210 Haskins Way,
Suite 230, South San Francisco, California 94080, and our telephone number is (650) 407-2376. Our website is www.cero.bio. The
information on our website is not incorporated by reference in this filing or in any other filings we make with the SEC.

Available Information

Our internet address is www.cero.bio.
Our investor relations website is located at www.cero.bio/investors. We make available free of charge on our investor relations
website under “SEC Filings” our annual reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K,
our directors’ and officers’ Section 16 reports and any amendments to those reports as soon as reasonably practicable after
filing or furnishing such materials to the SEC. They are also available for free on the SEC’s website at www.sec.gov.

We use our investor relations
website as a means of disclosing material non-public information and for complying with our disclosure obligations under Regulation FD.
Investors should monitor such website, in addition to following our press releases, SEC filings and public conference calls and webcasts.
Information relating to our corporate governance is also included on our investor relations website. The information in or accessible
through the SEC and our website are not incorporated into, and are not considered part of, this filing.

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