Press Release

EMBARGOED UNTIL 11 A.M. ET WEDNESDAY, SEPT . 9, 2026 Two Independent Research Teams Converge on Novel Immune Checkpoint PLA2G2D as a Path to Overcome Anti - PD - 1 Resistance in Cancer Nature publication validates Apeximmune ’ s novel target and reveals an enzyme - independent mechanism the field had overlooked; company’s first - in - class anti - PLA2G2D antibody AI - 306 advancing toward IND filing in Q2 2027 SOUTH SAN FRANCISCO, Calif. (Sept. 9, 2026) – Apeximmune Therapeutics, Inc. , an IND - stage immuno - oncology company, today announced the publication of research in Nature validating PLA2G2D as a novel and mechanistically distinct immune checkpoint capable of addressing resistance to anti - PD - 1 therapy. The publication represents the convergence of two ind ependent research programs – one led by Apeximmune, the other by researchers at Erasmus University Medical Center ( Erasmus MC ) in Rotterdam, the Netherlands – that arrived at the same target using fundamentally different scientific approaches. 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. Ove rcoming this resistance remains one of the most significant unmet needs in oncology. 1 Two paths, one target. Apeximmune and Erasmus MC reached p hospholipase A2 group IID ( PLA2G2D) by markedly different routes. Apeximmune's team, led by founder and CEO , Li - Fen Lee, PhD, 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 CTLA - 4 in the same analysis. Erasmus MC, 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. Their analysis 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. Beyond identifying the target, the Apeximmune team uncovered a mechanism that had eluded prior investigators. PLA2G2D has long been characterized for its phospholipase activity, and previous efforts to drug the broader sPLA2 family, including terminated l ate - 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.