Akari Therapeutics Expands Patent Portfolio with Novel ADC Payload

TAMPA, Fla. and LONDON, Oct. 01, 2026 /CourierPR/ -- Akari Therapeutics, Plc, an oncology biotechnology company, has expanded its intellectual property portfolio with the filing of PCT/US2026/45955. This filing covers the unique ability of the company’s PH1 payload to disrupt multiple cancer-driving pathways in addition to its overall cytotoxic mechanism. The new patent application expands Akari’s current portfolio, which includes claims relating to its proprietary Thailanstatin payload ADCs and the payload’s ability to disrupt alternatively spliced protein isoforms that many cancers use to survive, proliferate, and spread.

Alternative splicing, a process that enables cells to generate different proteins from a single gene, is exploited by cancer cells to produce protein variants called ‘isoforms’ that support tumor growth, proliferation, and survival. PH1, Akari’s novel splicing-modulating payload, uses a differentiated approach compared to traditional ADC payloads that primarily rely on tubulin inhibition or DNA damage as mechanisms of action. The new PCT application includes claims relating to PH1’s modulation of alternative splicing involving multiple genes associated with tumor progression, including pathways involved in angiogenesis, programmed cell death, and hormone and oncogenic signaling in prostate cancer.

Inhibiting angiogenesis, PH1 alters VEGF-A splicing, shifting cancer cells from a VEGF-A isoform that supports tumor growth by supplying tumors with blood vessels bringing in nutrients and oxygen (pro-angiogenic) toward the VEGF-165b isoform that prevents blood vessel recruitment to tumors (anti-angiogenic). This switch may disrupt the ability of tumors to recruit the blood vessels necessary to support their growth and spread.

Facilitating programmed cell death of the tumor, PH1 alters the splicing of FAS to a version that would be anchored on cell surfaces (transmembrane isoform), making the cancer cells susceptible to immune cell-mediated cell death. In prostate cancer cells, PH1 demonstrated reductions in both wild-type androgen receptor (WT-AR) and the oncogenic splice variant AR-V7. WT-AR plays an important role in hormone-dependent prostate cancer, while AR-V7 is a signaling oncogene that drives tumor growth in metastatic castration-resistant prostate cancer.

Together, these collective findings further demonstrate the versatility of PH1’s mechanism of action and its potential to disrupt different alternative splicing pathways that different cancers rely upon for survival, growth, and metastasis.

Akari’s lead candidate, AKTX-101, targets the Trop2 receptor on cancer cells with a proprietary linker, enabling it to deliver its novel PH1 payload directly into the tumor with minimal off-target effects. Unlike current ADCs that use microtubule inhibitors and DNA-damaging agents as their payloads, PH1 is a novel payload that is a spliceosome modulator designed to disrupt RNA splicing within cancer cells. This splicing modulation has been shown in preclinical animal models to induce cancer cell death while activating both the innate and adaptive immune systems to drive robust and durable activity.

Additionally, Akari is developing AKTX-102, an ADC candidate targeting CEACAM5 (Carcinoembryonic Antigen-related Cell Adhesion Molecule-5), a well-validated tumor antigen broadly expressed across multiple solid tumors. AKTX-102 is designed to leverage Akari’s proprietary PH1 spliceosome-modulating payload and a novel antibody construct to enable differentiated tumor cell killing and immune activation. The company has initiated IND enabling studies for AKTX-101 with a goal of starting its First-In-Human trial by mid-2027.