An ADC with a novel RNA spliceosome modulating payload PH1 paired with a KRAS inhibitor demonstrates synergistic cytotoxic activity against KRAS G12D and G12C- driven pancreatic cancer models



Data supports the broader applicability of targeting RNA splicing to attack difficult-to-treat KRAS-driven cancers

Findings featured in ASCO 2026 online abstract further differentiate AKTX-101 from TROP2 ADCs utilizing Topoisomerase I inhibitor payloads

 

TAMPA, Fla. and LONDON, May 21, 2026 (GLOBE NEWSWIRE) -- Akari Therapeutics, Plc (NASDAQ:AKTX), an oncology biotechnology company developing antibody drug conjugates (ADCs) with a novel RNA splicing modulator payload, today announced positive preclinical data featured in an online abstract released in connection with the American Society of Clinical Oncology (ASCO) Annual Meeting 2026 highlighting synergistic cytotoxic activity of AKTX-101 in combination with KRAS inhibition in KRAS-mutated pancreatic cancer models. Access the abstract here.

The data further expands the potential opportunity for Akari's lead TROP2-targeting ADC, AKTX-101, and its proprietary RNA spliceosome-modulating payload beyond the Company's current Phase 1 development plan and supports the broader applicability of targeting RNA splicing as a potential way to treat difficult-to-treat KRAS-driven cancers.

The ASCO abstract evaluated the activity of AKTX-101 in combination with adagrasib, a KRAS inhibitor, across pancreatic cancer cell lines harboring KRAS G12D and KRAS G12C. In these studies, the combination of AKTX-101 and adagrasib demonstrated synergistic cell killing in KRAS mutant cell lines driven by G12C and G12D. This synergistic inhibition was not observed with the comparator first-in-class topoisomerase I-targeting TROP2 ADCs. Instead, these ADCs exhibited antagonism when paired with adagrasib. These results suggest that AKTX-101 synergy with KRAS inhibitor may be linked to the novel biology of PH1 targeting RNA splicing. The synergy was explained by PH1's unique ability target pre-mRNA transcripts for degradation, including those bearing KRAS mutations driving these cancer models.