Apex Immune Therapeutics Company Overview

MEDIA BACKGROUNDE R Contact: Capwell Communications , media@capwellcomm.com EMBARGOED UNTIL 11 A . M . ET WEDNESDAY, SEPT. 9, 2026. Company F acts • Founded: 2016 • Headquarters: South San Francisco, C A • Employees: Nine , all full - time • Focus: Novel immunotherapies for patients who do not respond to existing immune checkpoint inhibitors Capital R aised • Total to date: $32.05 million o $21.3 million Series A, closed March 2025, led by PharmaEssentia Corporation, with DCI Partners, Taya Venture Capital, KDI Marketing, Huahai US, Hercules BioVenture LP, and TTM 2025 LLC. Judy Swanson invested through TTM 2025 LLC. Her late husband, Robert A. Swanson, co - founded Genentech. o $399,618 NIH SBIR Phase I grant, awarded 2023 o $6 million Pre - A preferred equity, announced March 2021 o $4.35 million prior to Pre - A (Seed round) • Series B is open, with most Series A investors already committed Pipeline • AI - 306, lead program . First - in - class monoclonal antibody that blocks both the enzymatic and non - enzymatic activity of PLA2G2D . IND - enabling development. Cell line development underway, GLP toxicology scheduled to begin late 2026, IND filing targeted for Q2 2027. • MEBA platform, macrophage - engaging bispecific antibodies . S even active programs . AI - 328 is at the cell line development stage; IND filing planned for Q3 2027. • Target discovery platform . Bioinformatics across thousands of RNA - seq transcriptomes spanning more than 20 tumor types, built on a proprietary T - cell gene expression signature. More than 30 novel targets identified. • Patents : Six filed across multiple jurisdictions , including three PLA2G2D patents : 1) Methods and compositions for treating cancer or viral infection with a PLA2G2D antagonist, 2) Anti - PLA2G2D constructs and use thereof, 3) Combination therapy comprising anti - PLA2G2D antibodies and uses thereof. Leadership • Li - Fen Lee, PhD, Founder and Chief Executive Officer. Previously AbbVie, NGM, Pfizer, and the Stanford University School of Medicine faculty. Nature senior and co - corresponding author. • James O’Mara, consulting Chief Business Officer. Previously Ironwood Pharmaceuticals, Neurogastrx, MPM Capital.

• Jason Lih, PhD, VP of Research and Development. Previously the National Cancer Institute, AbbVie, Exelixis, Sana Biotechnology. • Kan V. Lu, PhD, Sr. Director of Biology. Previously Pharmacyclics, an AbbVie company. Nature co - author. • Michihisa Umetani, PhD, Director. Previously the University of Houston faculty. Nature co - author. Board of Directors • Li - Fen Lee, PhD, Founder and Chief Executive Officer, Apeximmune • David Yu, JD, Chief Technology Officer, Dexter Networks • Hsieng Lu, PhD, protein characterization and CMC. Previously Senior Director, Amgen Biologics • Lih - Ling Lin, PhD, Chief Scientific Officer, PharmaEssentia • Ling L ing Liu, DCI Partners • Wei Fan Chen, DCI Partners • Zunlun Wang, CEO and Founder, Stealth startup, Previously CSO RemeGen Scientific Advisory Board • Jenny Ting, PhD, University of North Carolina at Chapel Hill. Past President, American Association of Immunologists. • Dario Vignali , PhD, University of Pittsburgh School of Medicine. Led foundational LAG - 3 work. • Lawrence Steinman, MD, Stanford University. Member, National Academy of Sciences and National Academy of Medicine. • Makoto Murakami, PhD, University of Tokyo. Pioneer of the secreted phospholipase A2 field and a co - author on the Nature paper. • Tony Ho, Chief Scientific Officer & Senior Science Partner, Pivotal Life Sciences. Former Head of R&D at CRISPR Therapeutics , and Head of Oncology Integration & Innovation at AstraZeneca. Breaking News at - a - G lance: S ept. 9, 2026. Researchers have found a molecule in the lymph nodes beside a tumor that disarms immune cells before they reach the cancer, a discovery that may explain why immunotherapy works in only 20% of patients and points toward a way to reach the other 80%. • Publication . Nature , Sept. 9, 2026: “ PLA2G2D in tumour - draining lymph nodes regulates anti - tumour immunity. ” DOI: 10.1038/s41586 - 026 - 10954 - 1 • Two paths, one target . Apeximmune applied a proprietary bioinformatics algorithm to more than 9,000 primary tumor samples from The Cancer Genome Atlas (TCGA), surfacing 70 candidate novel immune checkpoints. PLA2G2D emerged as the top - ranked hit, well ahead of known checkpoints PD - 1 and C TLA - 4 in the same analysis. Erasmus University Medical Center (Erasmus MC) in Rotterdam, the Netherlands, working in parallel and unaware of Apeximmune's program, applied a spatial proteogenomic approach to melanoma patient samples from individuals who had divergent clinical outcomes, and independently identified PLA2G2D as a top hit in the dendritic cell and macrophage populations interacting with CD8+ T - cells in patients with worse outcomes . • A mechanism the field had overlooked . PLA2G2D has long been characterized for its phospholipase activity, and previous efforts to drug the broader sPLA2 family, including terminated late - stage small - molecule programs for inflammation from major pharmaceutical companies , had assumed its enzymatic function was central to its biology. Apeximmune

demonstrated that an enzyme - dead form of PLA2G2D retains potent immunosuppressive activity, establishing that the molecule's role in tumor immune evasion is independent of its enzymatic activity. Apeximmune's anti - PLA2G2D antibody blocks both enzymatic and non - enzymatic functions. • A shot at the patients PD - 1 drugs miss. Anti - PD - 1 therapies have transformed the treatment of certain cancers, but the majority of patients across indications either fail to respond or eventually relapse. Response rates fall to single digits in gastrointestinal cancers and other tumor types . Blockade of PLA2G2D not only restores anti - tumor immunity in preclinical models resistant to anti - PD - 1 therapy but also potentiates the activity of anti - PD - 1 in tumor types that are otherwise unresponsive to checkpoint inhibition. • Where the drug stands. AI - 306 is in IND - enabling development. Cell line development is currently underway, GLP toxicology studies are scheduled to initiate in late 2026, and an IND filing is targeted for Q2 2027. All data are preclinical. No patients have been dosed. • Forward - Looking Statements: This press release contains forward - looking statements, including statements regarding the development of AI - 306, anticipated regulatory milestones including the timing of the IND filing, and the potential clinical and commercial opportunity for PLA2G2D - d irected therapy. Actual results may differ materially from those expressed or implied by these statements as a result of various factors, including the risks inherent in preclinical and clinical drug development. Apeximmune undertakes no obligation to update these statements. K ey T erms • PLA2G2D. Phospholipase A2 group IID. A secreted enzyme made mainly by dendritic cells and macrophages, concentrated in lymph nodes, that dials the immune response down. In tumors it suppresses the T - cells that would otherwise attack cancer. Its immunosuppressive effect does not depend on the enzyme reaction it is named for. • Anti - PD - 1 therapy. Checkpoint inhibitors that release a brake on T - cells so they can recognize and kill tumor cells. Approved anti - PD - 1 drugs include pembrolizumab (Keytruda, Merck) and nivolumab (Opdivo, Bristol Myers Squibb). • Cold tumors. Tumors with few infiltrating T - cells, which makes them largely unresponsive to checkpoint inhibitors. Pancreatic, liver, and microsatellite - stable colorectal and esophageal cancers are common examples. • Tumor - draining lymph node. The lymph node that filters fluid from a tumor. It is where dendritic cells carry tumor fragments and where the anti - tumor immune response is first organized, which makes it the staging ground for any T - cell attack on the cancer. • Enzyme - independent mechanism. PLA2G2D is classified by its phospholipase activity, and the field has long assumed that activity accounts for its immunosuppressive role. Apeximmune tested an enzyme - dead form of the molecule and found that it retained potent immunosuppressive activity, establishing that PLA2G2D suppresses anti - tumor immunity through a function separate from its enzymatic one. AI - 306 blocks both. # # #