On October 1, 2026 Akari Therapeutics, Plc (Nasdaq: AKTX), an oncology biotechnology company developing antibody drug conjugates (ADCs) with a novel RNA splicing disrupting payload, reported the filing of PCT/US2026/45955, expanding the Company’s growing intellectual property portfolio around its novel splicing-modulating payload, PH1 and PH1-based ADCs.

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Alternative splicing enables cells to generate different proteins from a single gene. Cancer cells can exploit this process to produce protein variants called ‘isoforms’ that support tumor growth, proliferation and survival and promote resistance to therapy. This PCT filing expands Akari’s current patent portfolio 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. Accordingly, Akari’s payload PH1 uses a differentiated approach compared with traditional ADC payloads that primarily rely on tubulin inhibition (i.e., vedotin) or DNA damage as (i.e., topoisomerase I Inhibitors) 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:

Inhibiting Angiogenesis: PH1 altered VEGF-A splicing, shifting cancer cells from a VEGF-A isoform with the ability to supply tumors with blood vessels bringing in nutrients and oxygen (pro-angiogenic) toward the VEGF-165b isoform that prevented 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: Cancer cells produce soluble versions of the death receptor FAS to prevent immune cells expressing the FAS ligand from recognizing the cancer cell and killing it. PH1 altered 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.
Disrupting hormone and oncogenic signaling in prostate cancer: 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 (after hormone ablation therapy fails).
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.

Abizer Gaslightwala, President and Chief Executive Officer of Akari Therapeutics, commented, "This PCT filing represents another important expansion of our intellectual property portfolio and further demonstrates the differentiated potential of PH1 as a novel ADC payload with unique properties vs. current ADC payloads. These claims illustrate PH1’s potential to impact multiple fundamental mechanisms that cancer tumors use to survive and spread, including angiogenesis, oncogene signaling and avoiding programmed cell death. We believe the breadth of this biology further supports the potential of PH1 as a platform payload for the development of differentiated ADCs across multiple tumor targets and cancer types. As we continue to expand our understanding of PH1, we are building an increasingly robust intellectual property foundation for our novel PH1 payload and ADC portfolio."

(Press release, Akari Therapeutics, OCT 1, 2026, View Source [SID1234671211])