GENFLEET-B (02595) announces the publication arrangements for clinical study data related to GFH375 and GFH276.

GENFLEET-B (02595) announces the publication arrangements for clinical study data related to GFH375 and GFH276. GENFLEET-B (02595) announced that the Company will hold an online investor conference on October 15, 2026, to publish preliminary research data on its investigational product GFH375 (KRAS G12D inhibitor) in combination with cetuximab for the treatment of KRAS G12D-mutant solid tumors. The Company's overseas partner Verastem Oncology (Verastem) will hold an online investor conference on October 14, 2026, to present the overseas clinical development progress of GFH375/VS-7375. The preliminary clinical research data on the Company's investigational product GFH276 (Pan RAS inhibitor) as a monotherapy for RAS-mutant solid tumors has been selected as a Late-Breaking Abstract (LBA) for the 2026 European Society for Medical Oncology (ESMO) Annual Congress to be held in Madrid. The Company will hold an online investor conference on October 25, 2026, to further interpret the on-site oral presentation data for GFH276. GenFleet and Verastem have entered into a licensing and early-stage collaborative development agreement for three products developed by GenFleet that target RAS/MAPK-driven cancers. This collaboration grants Verastem an exclusive option to obtain respective licenses for these three products upon successful achievement of pre-defined Phase I clinical trial milestones. In December 2023, Verastem selected GFH375/VS-7375 as the lead program of its collaboration, and in January 2025 obtained the license for GFH375, the first license born under this collaboration framework. These licenses will grant Verastem the development and commercialization rights outside of China, while GenFleet retains such rights within China. GFH276 is an orally available small molecule pan-RAS (ON) inhibitor with a unique mechanism, employing a tri-complex mechanism of action (CypA-GFH276-RAS), which can more efficiently inhibit most activated wild-type/mutant RAS protein subtypes, including the most common KRAS mutants (G12C, G12D, G12V, etc.) as well as NRAS and HRAS subtype proteins.