TAMPA – October 29, 2026 -- Akari Therapeutics (Nasdaq: AKTX) has filed international patent application PCT/US2026/45955, adding claims on how its PH1 payload modulates alternative splicing across multiple cancer-driving genes.
The filing expands the company's intellectual property around PH1, a splicing-modulating payload derived from its proprietary Thailanstatin platform, and around PH1-based antibody drug conjugates (ADCs). Akari contrasts PH1 with conventional ADC payloads that rely on tubulin inhibition, such as vedotin, or DNA damage, such as topoisomerase I inhibitors.
Application claims PH1 shifts VEGF-A splicing to block tumor blood supply
The claims cover PH1 altering VEGF-A splicing in cancer cells. The shift moves from a pro-angiogenic isoform to the anti-angiogenic VEGF-165b isoform, which prevents blood vessel recruitment to tumors.
PH1 converts FAS to a cell-surface form that exposes tumors to immune attack
Cancer cells produce soluble versions of the death receptor FAS to evade immune cells carrying the FAS ligand. According to the filing, PH1 changed FAS splicing to a transmembrane isoform anchored on the cell surface, making the cells susceptible to immune cell-mediated death.
PH1 reduces both wild-type AR and AR-V7 in prostate cancer cells
In prostate cancer cells, PH1 lowered levels of wild-type androgen receptor (WT-AR) and the oncogenic splice variant AR-V7. AR-V7 drives tumor growth in metastatic castration-resistant prostate cancer, where hormone ablation therapy has failed.
CEO Abizer Gaslightwala said the claims support PH1 as a platform payload for ADCs across multiple tumor targets and cancer types, and that Akari is building an "increasingly robust" IP foundation.
Lead candidate AKTX-101 targets first-in-human trial by mid-2027
Akari's lead candidate, AKTX-101, targets the Trop2 receptor with a proprietary linker. The company has started IND-enabling studies and aims to begin a first-in-human trial by mid-2027. A second candidate, AKTX-102, pairs PH1 with a novel antibody construct directed at CEACAM5, a tumor antigen expressed across multiple solid tumors.