NASDAQ: LIMN

CD47 immune checkpoint inhibitors are expected to penetrate the market primarily through combination therapy with already established PD-1/PD-L1 blockades rather than as standalone treatments. The global market for PD-1/PD-L1 blockades was estimated at $49.5 billion in 2023 and is projected to reach $123.3 billion by 2033. If CD47 immune checkpoint inhibitors are successfully brought to market, they are expected to grow alongside the PD-1/PD-L1 blockade market, potentially starting at 10-20% of the PD-1/PD-L1 market size by 2030 and rapidly expanding to reach the same market scale.

Global Market Size Projections for PD-1/PD-L1 Blockades (adapted from Future Market Insights)

Our asset targets patients with significant unmet need. Our vision is to develop a broad array of transformative therapies for cancer patients as a leading global biopharmaceutical company. We intend to do this through establishing a leadership position in immune-oncology and by strengthening the differentiation of the next generation anti-CD47 monoclonal antibody from IND enabling studies through to clinical development and broadening the portfolio through in-licensing highly promising and differentiated therapeutic assets.

Overview

Liminatus is a pre-clinical stage biopharmaceutical company developing novel cancer therapies. Our product candidate is exploiting CD47 antibodies to target cancer cells. Our product candidate has the potential to become cornerstones of treatment for solid cancers.

We are developing a next generation CD47 immune checkpoint inhibitor. CD47 is a potent ‘do not eat me’ signal that enables cancer cells to evade detection by the immune system. CD47 blockade promotes uptake of tumor antigens and tumor cells by macrophages. Anti-CD47 monoclonal antibodies (mAb) generally induce anemia and thrombocytopenia due to their binding to red blood cells and platelets. The Liminatus CD47 mAb has shown to preferentially bind to immune cells, but not to red blood cells and platelets and does not induce hemolysis. Our clinical candidate is currently in the late preclinical stage, with most of the necessary research completed.

The next steps in the clinical process will include preparing the IND package required for the submission of a Phase 1 clinical trial approval application.

InnoBation (licensor to Liminatus) has actively invested in the CD47 asset following its licensing to Liminatus. Funds were allocated towards critical preclinical work, including CMC development and the monkey toxicity study, which were essential steps in advancing the CD47 asset. These studies were completed in collaboration with GenScript ProBio and Charles River Laboratories.

In addition to these developments, InnoBation conducted its own independent animal studies to explore the effects of long-term administration of the CD47 asset. During these studies, we discovered that the CD47 asset, in addition to its potential as an anti-cancer therapeutic, also shows promise in reducing chronic inflammation and inducing weight loss. This is likely due to the asset’s ability to enhance macrophage proliferation and differentiation, which improves the scavenging of apoptotic cells. This effect not only aids in cancer treatment by enhancing the immune response but also suggests potential applications in preventing or mitigating age-related diseases such as cardiovascular disease and obesity, which are often driven by chronic low-grade inflammation due to accumulated senescent cells.

InnoBation’s ongoing research into the CD47 asset has uncovered these potential new therapeutic applications, expanding the scope of its utility.

The following overview shows our clinical plan after closing the business combination:

Candidate

​ ​ ​

Indication

​ ​ ​

Clinical trial

​ ​ ​

Notes

IBA101 Mono

Advanced solid cancers

Phase 1 clinical trial is scheduled solely for safety confirmation. A global Phase 1 clinical trial in South Korea will focus on lung cancer patients.

IBA101 + Durvalumab or pembrolizumab

≥ stage III NSCLC

Both PD-L1High and PD-L1Low patients. A global Phase 1 clinical trial in South Korea will focus on lung cancer patients.

Corporate History and Our Team

Liminatus was founded in 2018, having obtained an exclusive license for GCC CAR-T-related patents and know-how from Targeted Diagnostics & Therapeutics, Inc. (TDT), which licensed the GCC CAR-T intellectual property from Thomas Jefferson University, and assignment of a sub-license from Viral Gene for the GCC vaccine diagnostics. Subsequently, the Company was assigned the license to the CD47 immune checkpoint inhibitor from InnoBation Bio Co. Ltd. and Valetudo Therapeutics LLC. The TDT licenses have been terminated as of August 2024.

We believe that our leadership team’s extensive global experience within the biopharma industry, which spans all stages of development, commercialization and financing of pharmaceutical products, is a key competitive advantage for Liminatus in maximizing the full potential value of its pipeline. Members of our team have also been heavily involved in business development, capital formation and investor engagement across a range of industries. For further information and biographies of our management team, see “Management.”

Our Vision and Our Strategy

Our vision is to develop transformative therapies for cancer patients as a global biopharmaceutical company offering advanced, differentiated, best-in-class therapies that induce powerful and durable responses in patients resulting in quality survival and a chance for cure. To accomplish this goal, we plan to execute on the following:

● Strengthen the differentiation of our anti-CD47 monoclonal antibody from IND enabling studies through to clinical development.

● Maximize the value of our product candidate by selectively entering into strategic collaborations with world leading academic and industrial partners.

● Build a leading immuno-oncology company while maintaining a strong culture of innovation, valuing diversity, and putting patients at the center of everything we do.

● Maintain, deepen, and protect our intellectual property portfolio. We intend to continue extending our global intellectual property portfolio to protect our assets.

● Pursue business development and strategic partnerships. We may seek to form strategic alliances, enter into licensing agreements, or collaborate with third parties with the aim of strengthening and aiding our research, development, and commercialization of our assets more broadly.

● Broaden our portfolio. We are actively engaged in evaluating additional assets for in-licensing or partnership and may execute additional transactions to add to our pipeline. We believe that our leadership team has a proven track record for identifying and transacting upon de-risked clinical stage assets.

Our Approach to Cancer Immunotherapy

Our product candidate exploits the body’s immune system to recognize and attack cancer cells. Our product candidate has the potential to become a significant treatment option for cancer patients.

Checkpoint Inhibitor CD47

A critical feature of the immune system is its ability to distinguish between normal cells in the body and those deemed as “foreign” (such as germs and cancer cells). This allows the immune system to attack the foreign cells while leaving normal cells unharmed. The immune system does this, in part, by using “checkpoint” proteins on immune cells. The checkpoints act like switches that need to be turned on or off to start an immune response. But tumors can find ways to manipulate these on/off immune checkpoints to avoid being attacked by the immune system. Monoclonal antibodies targeting immune checkpoints are designed as therapies to forcefully activate the “on” switch of the immune response, allowing the immune system to mount an effective anti-tumor attack. These medicines, known as immune checkpoint inhibitors, work by targeting checkpoint proteins to block the tumor’s ability to shut down the immune response and thereby induce a potent anti-cancer effect. Rather than killing cancer cells directly, they aid the immune system to detect and mount an attack on cancer cells. Several therapeutics that target different checkpoint proteins have been approved to treat some types of cancer including PD-1 (Pembrolizumab, Merck & Co; Novolumab, BMS; Cemiplimab, Regeneron), PD-L1(Atezolizumab, Genentech; Avelumab EMD Serono & Pfizer; Durvalumab, AstraZeneca), CTLA-4 (Ipilumab, BMS; tremelimumab, AstraZeneca), and LAG-3 (Opdulag, BMS) inhibitors.

Although such therapies have revolutionized cancer treatment showing to be remarkably effective in certain subsets of patients with specific types of tumors, there are a significant number of cancer patients for whom these therapies are not effective. Another novel, yet well-established immune checkpoint is CD47 which plays a broad role in cancer immune evasion across multiple cancers. CD47 is a transmembrane protein, an integral membrane protein that spans the entirety of the cell membrane, and upon its interaction with SIRPα, which is expressed on macrophages, a “don’t eat me” signal is sent to the macrophages. This helps tumors achieve immune escape by stopping macrophages from acting on these tumor cells to undergo phagocytosis. Blockade of the interaction between CD47 and SIRPα could restore phagocytic activity and eliminate tumor cells. However, the first generation of anti-CD47 monoclonal antibodies have induced anemia and thrombocytopenia due to their binding to red blood cells and platelets. Our CD47 therapeutic candidate is a next generation anti-CD47 monoclonal antibody and has shown to preferentially bind to immune cells, but not to red blood cells and platelets and does not induce hemolysis (destruction of red blood cells). Furthermore, the CD47 mAb has been shown to synergistically enhance anti-tumor responses in combination with other immune-oncology therapies. The CD47 mAb has completed key preclinical studies and is now preparing for the IND application.

CD47 Immune Checkpoint Inhibitor Program

Overview

The CD47 therapeutic candidate is a high affinity humanized anti CD47 antibody that has the potential to translate into clinic for CD47 SIRPα blocking and restoring the anti-tumor function of innate immune cells without inducing hemagglutination or hemolysis.

Benefits

● K D (equilibrium dissociation constant) value of 0.48 nM for human CD47 protein and effectively blocked the interaction of CD47 on cancer cells and soluble SIRPα protein, in vitro.

● Did not bind to red blood cells and platelets and did not cause hemolysis.

● In an animal tumor model, where MC38 murine colon adenocarcinoma cells expressing human CD47 were implanted in immune competent mice, the CD47 mAb (Hu3A5) completely suppressed the tumor in combination with an anti PD1 antibody.

● CD47 mAb (Hu3A5) showed the expected moderate tumor suppression in the hCD47/hSIRPα knock-in mice model expressing human CD47 and human SIRPalpha, using MC38 cells expressing hCD47.

Pre-Clinical Development to Date

● The anti-CD47 monoclonal antibody has been generated by immunizing mice with the extracellular domain of human CD47 protein. This antibody has been further humanized by CDR grafting and selecting the clone 3A5-V10 (Hu3A5) for further screening. Hu3A5 has a KD (equilibrium dissociation constant) value of 0.48 nM for human CD47 protein and has shown to effectively block the interaction of CD47 on cancer cells and soluble SIRPα protein, in vitro.

● In vitro assay, Hu3A5 did not bind to red blood cells and platelets and did not cause hemolysis (destruction of red blood cells) in vitro.

● In an animal tumor model, where MC38 murine colon adenocarcinoma cells expressing human CD47 — the only commercially available cancer cell line used in immune-competent animal models for human CD47 research — were implanted in immune-competent mice, the CD47 mAb (Hu3A5) completely suppressed the tumor in combination with an anti-PD1 antibody. Additionally, the Hu3A5 antibody demonstrated moderate tumor suppression in a mouse model that was engineered to express human CD47 and SIRPα, after being implanted with MC38 tumor cells. However, when combined with other treatments like anti-PD-1, anti-TIGIT blocking antibodies, or an agonistic anti-4-1BB antibody, the Hu3A5 antibody completely suppressed tumor growth. This result shows that Hu3A5 can work synergistically with various immune checkpoint inhibitors, highlighting its versatility as a potential cancer therapy. In addition, DSC analysis has shown good thermostability.

● Further IND-enabling studies are underway in preparation for early-stage clinical testing. Based on the prepared data, a pre-IND meeting will be prioritized with the FDA. Since the primary indication for CD47 mAb (Hu3A5) is lung cancer, additional preclinical animal studies utilizing mouse lung cancer cell lines, such as LL/2, will be conducted if requested to evaluate efficacy in lung cancer models by the FDA. For this purpose, LL/2 expressing human CD47 has been prepared.

Toxicity-related experiments

● CD47 mAb preferentially binds to CD47 on tumor and immune cells, but not to RBCs and platelets.

● Murine 3A5, humanized 3A5 with human IgG1 Fc (Hu3A5-V10), and humanized 3A5 with human IgG4 (Hu3A5-G4) strongly bind to CD47-positive MCF-7 human cancer cells and most of immune cells including T/B lymphocytes and phagocytic cells, but not to human RBCs and platelets.

● CD47 mAb does not induce hemolysis of RBCs in vitro.

● Anti-CD47 blocking mAb (Hu3A5) typically induce hemolysis of RBCs and thus developing anemia.

● However, Hu3A5 does not induce hemolysis of RBCs (perhaps due to the inability of binding to CD47 on RBCs).

● CD47 mAb does not induce severe hematologic disorder.

● Animal in vivo experiments using C57BL/6-hCD47/hSIRPα mice showed that although Hu3A5-G4 was binding to human CD47 over-expressed on mouse RBCs of C57BL/6-hCD47/hSIRPα mice, it did not induce hemolysis of mouse RBCs.

● C57BL/6-hCD47/hSIRPα mice were repeatedly injected with Hu3A5-G4 mAb even in combination with anti-mPD-1 mAb, but they survived over the experimental period and their body weight barely changed compared with that of rat IgG-treated mice.

● Anti-human CD47 mAb induces no/minimal inflammation in organs.

● C57BL/6-hCD47/hSIRPα mice were subcutaneously engrafted with MC38-hCD47 tumor cells and were repeatedly injected with Hu3A5-G4 mAb and/or anti-mPD-1 mAb.

● Lung, liver and kidney from each group of mice were collected 4th injection of Abs. H&E staining of organs showed that there was minimal or no inflammation in those organs.

A 4-week Toxicity Study in Cynomolgus Monkeys Followed by a 4-Week Recovery Period

● Objective of monkey toxicity study

● The objective of this study was to determine the potential toxicity of IBA101(Anti-CD47 mAb), a monoclonal antibody conjugated with IgG4 Fc, when administered as an intravenous bolus injection once weekly (Days 1, 8, 15, 22, and 29) to non-human primates and to evaluate the potential reversibility of any findings following a 4-Week recovery period. In addition, the toxicokinetic characteristics of IBA101(Anti-CD47 mAb) were determined. The study design was as follows:

Dose

Main Study

Recovery Study

​ ​ ​

​ ​ ​

Dose Level

​ ​ ​

Dose Volume(a)

​ ​ ​

Concentration

​ ​ ​

No. of

​ ​ ​

No. of

​ ​ ​

No. of

​ ​ ​

No. of

Group No.

Test Article

(mg/kg/dose)

(mL/kg)

(mg/mL)

Males

Females

Males

Females

1

Vehicle Control

3

3

2

2

2

5

3

3

—

—

3

IBA101

3

3

—

—

3

3

2

● Study design and standards

● The 4-week toxicity study of IBA101 in Cynomolgus monkeys, conducted by Charles River Laboratories, was designed and analyzed according to GLP (Good Laboratory Practice) standards. This ensured the reliability and reproducibility of the data, adhering to rigorous quality standards throughout the study.

● Parameters and endpoints of evaluation

Based on the most recent body weight measurement, the following parameters and endpoints were evaluated:

● Mortality, clinical signs, body weight, ophthalmology, electrocardiographic examinations

● Clinical pathology parameters (hematology, coagulation, clinical chemistry, and urinalysis)

● Anti-drug antibody analysis, toxicokinetic parameters, organ weights, and macroscopic and microscopic examinations.

● Conclusion: Toxicokinetic Analysis

Following once-weekly (Days 1, 8, 15, 22, and 29) intravenous dosing of IBA101 to Cynomolgus monkeys at 0, 10, 30, or 100 mg/kg/dose:

● No significant IBA101-related effects were noted at any dose level, indicating that 100 mg/kg/dose was well-tolerated.

● All study parameters, including body weight, clinical pathology results, and toxicokinetic measurements, were analyzed for statistical significance using standard statistical methods. At the highest dose tested (100 mg/kg), no statistically significant differences were observed in any parameter compared to the vehicle control group, supporting the determination of the No Observed Adverse Effect Level (NOAEL) at 100 mg/kg/ dose. Anti-drug antibody analysis, toxicokinetic parameters, organ weights, and macroscopic and microscopic examinations.

On Day 22, the combined sex mean C0, Cmax, and AUC0-168hr values of IBA101 at the NOAEL were:

● No C0 (Initial Plasma Concentration): 4,310,000 ng/mL

● Cmax (Maximum Plasma Concentration): 4,080,000 ng/mL

● AUC0-168hr (Area Under the Concentration-Time Curve): 359,000,000 hr*ng/mL.

● These toxicokinetic results suggest a good safety profile of IBA101 under the tested conditions and provide statistical evidence for its tolerability.

Efficacy-related studies

● CD47 antibody blocks interaction of CD47 and SIRPα

● A competitive ELISA assay demonstrated that the interaction between recombinant CD47 and recombinant SIRPα proteins was blocked by Hu3A5 in vitro.

● CD47 antibody promotes phagocytosis of live tumor cells by human macrophages.

● In vitro phagocytosis assay demonstrated that human macrophages promoted the uptake of live tumor cells in the presence of as low as > 0.1 micro grams/ml of CD47 mAb.

● Exclusive blockade of human CD47 on tumor cells with Hu3A5 in combination with check-point inhibitors induces a limited synergistic suppression of tumor growth.

● To assess how effectively CD47 blockade enhances anti-tumor responses, hCD47-expressing MC38 tumor cells were subcutaneously engrafted into normal C57BL/6 mice, and anti-human CD47 monoclonal antibodies were injected to specifically block the function of the hCD47 protein on tumor cells, allowing evaluation of the resulting increase in anti-tumor effects.

● This induced moderate delayed tumor growth.

● However, in combination with anti-PD-L1 and anti-TIGIT check-point inhibitors significant synergistic activity was observed where tumor growth was regressed and most of the mice became tumor-free.

● Global blockade of human CD47 on tumor and immune cells induces significant reduction of tumor growth.

● Investigated whether global effects of CD47 blockade would be beneficial if all cells including immune cells were expressing human CD47.

● Instillation of Hu3A5 alone to C57BL/6-hCD47/hSIRPα knock-in mice engrafted with MC38- hCD47 tumor cells suppressed tumor growth.

● When Hu3A5 treatment was combined with anti-mPD-1 mAb, tumor-free mice were generated.

New Aspects of the CD47 Asset and Expanded Indications

● Chronic Inflammation: Hu3A5, an anti-CD47 antibody, plays a unique role in helping immune cells called macrophages develop and survive in the body. These cells are critical in fighting disease. IBA101 not only promotes the formation of these macrophages but also increases the number of a special type, called M1 macrophages, that actively destroy harmful cells.

● Reducing Chronic Inflammation: As we age, our body becomes less effective at clearing out dead cells, leading to a buildup that contributes to chronic inflammation and diseases such as atherosclerosis (narrowing of arteries), obesity, and dementia. By

enhancing the activity of macrophages, Hu3A5 could help reduce this buildup and, in turn, lower the risk of these inflammation-related diseases.

● Animal Study: To explore this possibility, we conducted an experiment on mice fed a high-fat diet. These mice were given Hu3A5 — CD47 blockade to see if it could help reduce obesity and improve overall health. The early results were promising: mice treated with Hu3A5 showed significant reductions in obesity, along with improvements in fat tissue health.

● Industry Context: Dr. Irving Weissman, a pioneer in CD47 research, founded a company called Forty Seven Inc. to develop CD47-targeted therapies for cancer. Though Gilead Sciences acquired the company for $4.9 billion in 2020, some of the clinical trials were stopped due to serious side effects. However, Dr. Weissman didn’t give up on CD47 research. He later founded Bitterroot in 2023, aiming to use CD47 blockers for cardiovascular diseases. This shift aligns with our own findings, suggesting that Hu3A5 could have broader applications, not only in cancer but also in reducing chronic inflammation and potentially treating diseases like obesity, heart disease, and dementia.

Manufacturing

We will rely upon established, large scale, GMP compliant, third-party manufacturers for our current and future manufacturing needs for both bulk drug substance and finished drug product. There are no current plans to build our own manufacturing capabilities.

Intellectual property

Our commercial success depends in large part on our ability to obtain and maintain patent protection for our assets, their uses, components, formulations, methods of manufacturing and methods of treatment in the U.S. and other countries; to operate without infringing valid and enforceable patents and proprietary rights of others; and to prevent others from infringing on our proprietary or intellectual property rights.

Our intellectual property strategy is, where appropriate, to file new patent applications in the U.S. and certain other regions/countries (including the EU) on inventions, including improvements to existing products/ candidate(s) and formulations, methods of treatment and processes to improve our competitive edge or to improve business opportunities. We continually assess and refine our intellectual property strategy to ensure appropriate protection and rights are obtained.

We rely on trade secrets and know-how to protect aspects of our business that are not amenable to, or that we do not consider appropriate for, patent protection, and which are difficult to reverse engineer. We intend to take advantage of regulatory protection afforded through data exclusivity, market exclusivity and patent term extensions, where available.

Our asset is in-licensed. CD-47 originates with a Korean company, InnoBation Bio Co. Ltd. The Anti-CD47 antibody is covered by three early-stage applications. Additional work is being done to characterize the mechanisms and properties that differentiate the antibody. One is a published application directed to CDRs, which essentially define the target and specificity of the antibody. There is also an unpublished application to the humanized antibody, i.e., the therapeutic entity Hu3A5. There is also a separate application covering back-ups. If granted, the cases have a long duration of with a normal expiry of 2040 and 2041.

Liminatus will, where appropriate, seek to file on future IP opportunities that may arise, such as commercial formulations, dosing regimens, combination therapies, manufacturing methods, biomarkers, and new patient populations. The strategy going forward will be to file an International PCT application claiming priority from the U.S. or other provisional applications, with a view to ultimately entering the national/ regional phase in core pharmaceutical markets (such as US, Europe, Japan, China, etc.).

The life of a patent and the protection it affords is limited. For example, in the United States, the natural expiration of a patent is generally 20 years from its earliest U.S. non-provisional filing date. In Europe the expiration of an invention patent is 20 years from its filing date.

In addition to patent protection there is regulatory protection for licensed products. Biologicals currently receive 12 years regulatory protection in the U.S. In Europe there is 8 years data exclusivity followed by 2 years market exclusivity, plus 1 year for further significant indications. This means that during the first 8 years from the grant of the first marketing authorization in the E.U., data exclusivity applies. After the initial 8 year period has expired, a generic company can make use of the pre-clinical and clinical trial data of the originator in their regulatory application in an application for regulatory approval, but they still cannot market their drug during the two year period of market exclusivity. This therefore provides a total 10-year period of exclusivity.

Liminatus is not currently aware of any third-party patent property that presents a barrier to the proposed commercialization of our therapeutic asset.

License Agreements

The InnoBation License

In December 2022, the Company entered into a Subscription Agreement In Kind (the “Metavagen License”) with Metavagen LLC, owned by Chris Kim (“Metavagen”), whereby the Company received the license rights initially granted from InnoBation Bio Co., Ltd., a Korean company (“InnoBation”) to Metavagen to develop, market and sell YN1203, InnoBation Bio CAR NK biomarkers, including devices, compounds and products used to detect analyte in body or tissue, in exchange for 40,000,000 shares of Class A membership interest in the Company. The Metavagen License transaction was consummated as the Company had the right to use the license, but the license was not transferred. In March 2023, the Metavagen License was cancelled, and the Company membership interest was returned.

On October 1, 2022, Metavagen was assigned the License and Development Agreement dated as of March 30, 2022, by and between InnoBation Bio Co. Ltd. and Valetudo Therapeutics LLC, as may have been amended (the “InnoBation License”), granting exclusive worldwide rights to Develop and Commercialize the CD47 Product in the Field and exclusive worldwide rights to Develop and Commercialize the Companion Diagnostics to the CD47 Products in the Field (such italicized items bearing the meanings ascribed to them in the InnoBation License). Under the InnoBation License, the licensee is responsible for all of the developmental costs for the CD47 Products after the upfront payment of $8.2 million, which was paid by Viral Gene to InnoBation. The Company will also pay license fees and management fees to be mutually agreed with InnoBation from time to time.

The term of the InnoBation License expires on a licensed product-by-licensed product and country-by- country basis until the expiration of all royalty terms. “Royalty Term” means, on a royalty bearing CD47 product-by-royalty bearing CD47 Product and country-by-country basis, the period beginning upon commencement of the Patent Royalty Term in the applicable country and ending upon the expiration of Know-How Royalty Term in the applicable country. The License Agreement can be terminated (i) by either party if the other party remains in material breach of the license agreement following a cure period to remedy the breach, (ii) by us at will, or (iii) by either party, in its entirety, upon the other party’s bankruptcy or insolvency.

U.S. patent term restoration and marketing exclusivity

Depending upon the timing, duration and specifics of the FDA approval of a biological product, some of a sponsor’s U.S. patents may be eligible for limited patent term extension under the Hatch-Waxman Amendments. The Hatch-Waxman Amendments permit a patent restoration term of up to five years as compensation for patent term lost during product development and the FDA regulatory review process. However, patent term restoration cannot extend the remaining term of a patent for more than five years, or beyond a total of 14 years from the product’s approval date. The patent term restoration period is composed of a “testing phase” and a “review phase” (also referred to as an “approval phase”).

The testing phase begins on the effective date of an IND and ends on the date a BLA or a New Drug Application (“NDA”) is initially submitted to FDA. The review phase is the period between the initial submission of the BLA or NDA and approval. The term of a patent may be extended for a period that is the sum of one-half of the time in the testing phase, plus all the time in the review phase, and minus any of the regulatory review period that occurs prior to the patent grant or where the sponsor did not act with due diligence. Only one patent applicable to an approved biological product is eligible for the extension and the application for the extension must be submitted prior to the expiration of the patent. In addition, a patent can only be extended once and only for a single product. The USPTO, in consultation with the FDA, reviews and approves the application for any patent term extension or restoration.

Similar provisions for supplementary protection to compensate applicants for regulatory delays also exist in a number of territories, including Europe and Japan. Where possible we intend to apply for supplementary protection for our therapeutic assets.

Data and market exclusivity

The Patient Protection and Affordable Care Act, as amended by the Health Care and Education Reconciliation Act, or collectively the ACA, includes a subtitle called the Biologics Price Competition and Innovation Act of 2009, or BPCIA, which created an abbreviated approval pathway for biological products shown to be biosimilar to, or interchangeable with, an FDA-licensed reference biological product.

This amendment to the PHS Act attempts to minimize duplicative testing. Biosimilarity, which requires that there be no clinically meaningful differences between the biological product and the reference product in terms of safety, purity, and potency, can be shown through analytical studies, animal studies, and a clinical trial or trials. Interchangeability requires that a product is biosimilar to the reference product and the product must demonstrate that it can be expected to produce the same clinical results as the reference product and, for products administered multiple times, the biologic and the reference biologic may be switched after one has been previously administered without increasing safety risks or risks of diminished efficacy relative to exclusive use of the reference biologic. However, complexities associated with the large, and often complex, structure of biological products, as well as the process by which such products are manufactured, may pose significant hurdles to implementation.

At the present time, the FDA will not accept an application for a biosimilar or interchangeable product based on the reference biological product until four years after the date of first licensure of the reference product, and FDA will not approve an application for a biosimilar or interchangeable product based on the reference biological product until 12 years after the date of first licensure of the reference product.

“First licensure” typically means the initial date the particular product at issue was licensed in the U.S. Date of first licensure does not include the date of licensure of (and a new period of exclusivity is not available for) a biological product if the licensure is for a supplement for the biological product or for a subsequent application by the same sponsor or manufacturer of the biological product (or licensor, predecessor in interest, or other related entity) for a change (not including a modification to the structure of the biological product) that results in a new indication, route of administration, dosing schedule, dosage form, delivery system, delivery device or strength, or for a modification to the structure of the biological product that does not result in a change in safety, purity, or potency.

The BPCIA is complex and continues to be interpreted and implemented by the FDA. In addition, government proposals have sought to reduce the 12-year reference product exclusivity period. Other aspects of the BPCIA, some of which may impact the BPCIA exclusivity provisions, have also been the subject of recent litigation. As a result, the ultimate implementation and impact of the BPCIA is subject to significant uncertainty.

In Europe (EEA), upon receiving marketing authorization, innovative medicinal products generally receive eight years of data exclusivity and an additional two years of market exclusivity. If granted, data exclusivity prevents generic or biosimilar applicants from referencing the innovator’s pre-clinical and clinical trial data contained in the dossier of the reference product when applying for a generic or biosimilar marketing authorization in the EEA, during a period of eight years from the date on which the reference product was first authorized in the EEA. During the additional two-year period of market exclusivity, a generic or biosimilar marketing authorization application can be submitted, and the innovator’s data may be referenced, but no generic or biosimilar 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 marketing authorization 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 existing therapies. There is no guarantee that a product will be considered by the EMA to be an innovative medicinal product, and products may not qualify for data exclusivity.

Another company may market another version of the product if such company obtained a marketing authorization based on a completely independent data package of pharmaceutical tests, preclinical tests and clinical trials.

Pediatric Development

A biological product can obtain pediatric market exclusivity in the U.S. Pediatric exclusivity, if granted, adds six months to existing exclusivity periods, including some regulatory exclusivity periods. This six-month exclusivity, which runs from the end of other exclusivity protection or patent term, may be granted based on the voluntary completion of a pediatric study in accordance with an FDA-issued “Written Request” for such a study. Similar provisions are also available in other territories, such as Europe.

In the EEA, companies developing a new medicinal product must agree upon a Pediatric Investigation Plan, or PIP, with the EMA’s pediatric committee, or PDCO. Products that are granted a marketing authorization with the results of the pediatric clinical trials conducted in accordance with the PIP are eligible for a six month extension of exclusivity.

Competition

We face competition with respect to our current product candidate and will face competition with respect to future product candidates from segments of the pharmaceutical, biotechnology and other related markets that pursue immune-oncology treatments. Specifically,

there are many companies that commercialize or are developing immuno-oncology treatments for cancer including large pharmaceutical and biotechnology companies such as Amgen, AstraZeneca, BMS, Merck, Novartis, Pfizer, Roche, and its subsidiary Genentech. Some of these competitors and competitor assets could also be opportunities for combination opportunities which is an established method that all these pharma companies have employed and are constantly searching for highly promising Liminatus type assets for such opportunities.

CD47

There are currently several CD47-targeting drug candidates in development for various cancer treatments. Magrolimab, developed by Forty Seven (acquired by Gilead Sciences), has been one of the most advanced CD47/ SIRPα axis-targeting drug candidates in development for cancer treatment. Initially seen as a frontrunner, it was under investigation in Phase 3 clinical trials for indications such as acute myeloid leukemia (AML) and high-risk myelodysplastic syndromes (MDS), often in combination with Azacitidine. However, the program has faced substantial setbacks due to efficacy concerns and safety risks. Below is an update on Magrolimab’s current status:

● Investigated ENHANCE-3 (AML): This trial evaluated a combination therapy of Magrolimab, Azacitidine, and Venetoclax. A futility analysis revealed a lack of therapeutic benefit and an increased risk of mortality, leading to the trial’s termination.

● ENHANCE (High-Risk MDS): The Phase 3 ENHANCE trial compared Magrolimab plus Azacitidine versus placebo plus Azacitidine. On July 25, 2023, the trial was discontinued due to insufficient efficacy.

● ENHANCE-2 (TP53-Mutated AML): This trial tested Magrolimab and Azacitidine against Venetoclax plus Azacitidine and other standard-of-care regimens in patients with TP53-mutated AML. It was terminated on September 26, 2023, again due to futility concerns.

● Solid Tumor Studies (ELEVATE Program): Gilead placed a partial clinical hold on Magrolimab’s solid tumor studies, including Phase 2 trials for head and neck squamous cell carcinoma (NCT04854499), solid tumors (NCT04827576), triple-negative breast cancer (NCT04958785), and colorectal cancer (NCT05330429). Although enrollment is paused, patients already enrolled and deriving clinical benefit may continue treatment after re-consenting.

Despite its potential, Magrolimab’s clinical development has been significantly hampered by challenges such as anemia caused by red blood cell binding, which remains a major safety concern. These setbacks highlight the need for improved CD47-targeting strategies, emphasizing the importance of addressing both efficacy and safety issues to realize the therapeutic promise of this target.

In contrast, our CD47 program has been designed specifically to avoid RBC binding and prevent anemia, a common side effect seen with first-generation CD47 inhibitors. This key advantage has been initially demonstrated through in vitro experiments using human blood and in vivo toxicity studies in monkeys, further supporting its safety profile. In addition, the strong results from our preclinical in vivo studies show that when our CD47 antibody is combined not only with already marketed PD-1/PD-L1 blockades but also with T cell boosters like LAG-3, TIGIT, TIM-3, and ICOS blockades, which are currently in active clinical development, it demonstrates a powerful synergistic effect. This versatility suggests significant market expansion potential as it could enhance the efficacy of various immune checkpoint inhibitors across multiple indications.

Figure 4: Second generation anti-CD47 monoclonal antibodies leading immuno-oncology drug development targeting innate immunity

Properties

On July 17, 2025, the Company entered into a sublease in Cerritos, CA for office space of approximately 1,320 sq. ft. commencing September 1, 2025 and ending June 30, 2026. The monthly rent is $2,784 per month.

We believe the property has been adequately maintained, is generally in good condition, and is suitable and adequate for our business.

Employees

As of December 31, 2025, Liminatus had one full-time employee, its Chief Executive Officer, Chris Kim. Liminatus also engaged advisors, including its Chief Financial Officer, Scott Dam, and several third-party contractors, who were engaged in research and development activities. In order to successfully implement its development and commercialization plans and strategies, and as the Company continues operating as a public company, the Company expects to need additional managerial, operational, sales, marketing, financial, and other personnel.

Insurance

Our insurance policies currently include policies that cover product liability and property, casualty and general liability risks, protecting us against certain risks of loss consistent with the exposures associated with the nature and scope of our operations. Our policies are generally subject to certain deductibles, limits and policy terms and conditions.

Legal Proceedings

From time to time, we may become involved in actions, claims, litigation, and other legal proceedings occurring in the ordinary course of its business from time to time, including assertions by third parties relating to intellectual property infringement, contract breaches, or employment-related matters. Except as described below, we are not currently a party to any actions, claims, suits, or other legal procedures whose conclusion, if not determined in our favor, would have a major adverse effect on our business, financial condition, or results of operations, either individually or in the aggregate.

On August 4, 2025, Dr. Someit Sidhu (“Dr. Sidhu”) filed a complaint against the Company (collectively, the “Sidhu Matter”) for breach of contract in the New York State Supreme Court, County of New York. Dr. Sidhu alleges the Company breached a certain Letter Agreement for Consulting Services, dated December 8, 2022 (the “Consulting Agreement”) entered into by Dr. Sidhu and Iris prior to the Business Combination by failing to pay Dr. Sidhu an advisory fee of $25,000 (“Advisory Fee”) upon the execution of the Business Combination Agreement, and a $1,400,000 despac success fee (“Despac Fee” together with the Advisory Fee, the “Fees”) upon consummation of the Business Combination. Dr. Sidhu also alleges claims of unjust enrichment and quantum meruit, which likewise arise out of the Company’s alleged failure to pay Dr. Sidhu the Fees. On December 10, 2025, the Company filed a motion to dismiss Dr. Sidhu’s complaint with prejudice, which motion remains pending.

On February 6, 2026, the Company entered into a settlement and release agreement (the “Settlement Agreement”) with Clear Street LLC (the “Holder”), pursuant to which the Company agreed to issue 4,000,000 shares of its common stock, to the Holder in exchange for the surrender and cancellation of 805,377 warrants to purchase shares of common stock held by the Holder. No commission or other remuneration was paid or given, directly or indirectly, in connection with the exchange of the warrants for the shares. Pursuant to the Settlement Agreement, the Company and the Holder agreed to dismiss (a) an action pending in the United States District Court for the Central District of California and (b) an action pending in the United States District Court for the Southern District of New York, in which previously the Court entered a default judgment against the Company in the amount of $7,500,000 plus approximately $515,000 in interest, which judgment was registered in the Central District of California in the fourth quarter of 2025.

Recent Developments

Nasdaq Notices

On November 19, 2025, we received notices from Nasdaq indicating that we were no longer in compliance with (i) Nasdaq Listing Rule 5450(b)(2)(A) due to our failure to maintain a minimum Market Value of Listed Securities (MVLS) of $50,000,000 (the “MVLS Rule”), based upon a review of our MVLS for the last 30 consecutive business days and (ii) Nasdaq Listing Rule 5450(b)(2)(C) due to our failure to maintain a minimum Market Value of Publicly Held Shares (MVPHS) of $15,000,000 (the “MVPHS Rule”), based upon a review of our MVPHS for the last 30 consecutive business days.

Under the Nasdaq rules, we have been provided a compliance period of 180 calendar days, or until May 18, 2026, in which to regain compliance with the MVLS Rule. If at any time during this compliance period our MVLS closes at $50,000,000 or more for a minimum of ten consecutive business days, Nasdaq will provide us written confirmation of compliance and this matter will be closed. In the event we do not regain compliance with the MVLS Rule prior to the expiration of the compliance period, we will receive written notification that our securities are subject to delisting. At that time, we may appeal the delisting determination to a Nasdaq Hearings Panel. Alternatively, we may consider applying for a transfer to the Capital Market tier of Nasdaq, provided we meet such tier’s continued listing requirements.

Under the Nasdaq rules, we have been provided a compliance period of 180 calendar days, or until May 18, 2026, in which to regain compliance with the MVPHS Rule. If at any time during this compliance period our MVPHS closes at $15,000,000 or more for a minimum of ten consecutive business days, Nasdaq will provide us written confirmation of compliance and this matter will be closed. In the event we do not regain compliance with the MVPHS Rule prior to the expiration of the compliance period, we will receive written notification that our securities are subject to delisting. At that time, we may appeal the delisting determination to a Nasdaq Hearings Panel. Alternatively, we may consider applying for a transfer to the Capital Market tier of Nasdaq, provided we meet such tier’s continued listing requirements.

On January 15, 2026, we received a notice from the Nasdaq Listing Qualifications Department of Nasdaq indicating that, based upon the closing bid price for the last 30 consecutive business days, we were no longer in compliance with Nasdaq Listing Rule 5450 (a) (1) (the “Bid Price Rule”) which requires listed securities to maintain a minimum bid price of $1 per share.

Under the Nasdaq rules, we have been provided a compliance period of 180 calendar days, or until July 14, 2026, in which to regain compliance with the Bid Price Rule. If at any time during this 180 day period the closing bid price of our common stock is at least $1 for a minimum of ten consecutive business days, Nasdaq will provide us written confirmation of compliance and this matter will be closed. If we choose to implement a reverse stock split, it must complete the split no later than ten business days prior to the expiration date of the compliance period, in order to regain compliance. In the event the Company does not regain compliance during the initial compliance period, the Company may be eligible for additional time to regain compliance with the Bid Price Rule.

We are working diligently to regain compliance with Nasdaq’s listing rules. However, there can be no assurance that we will be able to regain compliance within the prescribed time period.

February 2026 Public Offering

On February 18, 2026, we closed a best efforts public offering for the sale of (i) 8,270,000 shares of our common stock, (ii) 5,543,000 pre-funded warrants to purchase up to 5,543,000 shares of our common stock and (iii) 13,813,000 common stock purchase warrants to purchase up to 20,719,500 shares of common stock, at a combined public offering price of $0.29 per share (or $0.2899 per pre-funded warrant) and accompanying warrant (the “Offering”), for aggregate net proceeds of approximately $3.46 million after deducting the estimated offering expenses, including the placement agent fees. Each pre-funded warrant has an exercise price of $0.0001 per share upon issuance for one share of common stock and will not expire prior to exercise. Each warrant has an exercise price of $0.29 per share, is exercisable upon issuance for one and a half shares of common stock, and will expire five years following the date of issuance. The exercise price and number of shares of common stock issuable upon exercise is subject to appropriate adjustment in the event of stock dividends, stock splits, reorganizations or similar events affecting the common stock and the exercise price. Maxim Group LLC acted as the placement agent in connection with the Offering.

In connection with the Offering, on February 17, 2026, we entered into a securities purchase agreement (the “Purchase Agreement”) with certain purchasers party thereto. Pursuant to the Purchase Agreement, we agreed not to issue, enter into any agreement to issue or announce the issuance or proposed issuance of any shares of common stock or any securities convertible into or exercisable or exchangeable for shares of common stock or file any registration statement or prospectus, or any amendment or supplement thereto for 180 days after the closing date of the Offering, subject to certain exceptions. We also agreed not to effect or enter into an agreement to effect any issuance of common stock or any securities convertible into or exercisable or exchangeable for shares of common stock involving a Variable Rate Transaction (as defined in the Purchase Agreement) until 180 days after the closing date of the Offering, subject to certain exceptions.

In connection with the Offering, on February 17, 2026, we entered into a placement agency agreement with Maxim Group LLC, as placement agent in connection with the Offering (the “Placement Agent”). We paid the Placement Agent a cash fee of 8.0% of the aggregate gross proceeds raised in the Offering. We also agreed to reimburse the Placement Agent for all reasonable out-of-pocket costs and expenses incurred in connection with the Offering in an aggregate amount up to $100,000. In addition, we issued to the Placement Agent warrants (the “Placement Agent Warrants”) to purchase 690,650 shares of common stock (representing 5.0% of the number of shares of common stock sold in the Offering). The Placement Agent Warrants are immediately exercisable at an exercise price of $0.319 (or 110% of the public offering price for the shares of common stock and common warrants offered in the Offering) and will expire on the fifth anniversary of the commencement of sales of the Offering.

Available Information

The SEC maintains an Internet site at www.sec.gov that contains reports, proxy and information statements, and other information regarding issuers that electronically file with the SEC. Our Annual Report on Form 10-K, Quarterly Reports on Form 10-Q, Current Reports on Form 8-K, any amendments to those reports, proxy and registration statements filed or furnished with the SEC, are available on the SEC website. The reports filed with the SEC by our executive officers and directors pursuant to Section 16 under the Exchange Act are also available on the SEC website.

Implications of Being a Smaller Reporting Company

We are a “smaller reporting company,” meaning that the market value of our stock held by non-affiliates is less than $700 million as of our most recently completed second fiscal quarter and our annual revenue was less than $100 million during our most recently completed fiscal year. We may continue to be a smaller reporting company if either (i) the market value of our stock held by nonaffiliates is less than $250 million or (ii) our annual revenue was less than $100 million during the most recently completed fiscal year and the market value of our stock held by non-affiliates is less than $700 million as of our most recently completed second fiscal quarter. As a smaller reporting company, we are permitted and intend to rely on exemptions from certain disclosure requirements that are applicable to other public companies that are not smaller reporting companies.

Implications of Being an Emerging Growth Company

We are an “emerging growth company” as defined in Section 2(a) of the Securities Act of 1933, as amended (the “Securities Act”), as modified by the Jumpstart Our Business Startups Act of 2012 (the “JOBS Act”). As an emerging growth company, we may benefit from specified reduced disclosure and other requirements that are otherwise applicable generally to public companies. These provisions include:

● presentation of only two years of audited financial statements and only two years of related management’s discussion and analysis of financial condition and results of operations in this Annual Report;

● reduced disclosure about our executive compensation arrangements;

● no non-binding stockholder advisory votes on executive compensation or golden parachute arrangements; and

● exemption from the auditor attestation requirement in the assessment of our internal control over financial reporting.

We may benefit from these exemptions until December 31, 2026 or such earlier time that we are no longer an emerging growth company. We will cease to be an emerging growth company upon the earliest of: (1) December 31, 2026; (2) the first fiscal year after our annual gross revenues are $1.235 billion or more; (3) the date on which we have, during the previous three-year period, issued more than $1.0 billion in non-convertible debt securities; or (4) the date on which we are deemed to be a “large accelerated filer” under the Securities Exchange Act of 1934, as amended (the “Exchange Act”). We may choose to benefit from some but not all of these reduced disclosure obligations in future filings. If we do, the information that we provide stockholders may be different than you might get from other public companies in which you hold stock.