As the world’s first GDF15/IL-6 bispecific antibody, GFS202A demonstrated a favorable safety/tolerability profile in preliminary phase I data, alongside promising efficacy for cancer cachexia and robust pharmacodynamic properties.
TARGET-D 201 is an open-label, multi-center study in the U.S. to evaluate both the monotherapy and in combination with full-dose cetuximab in patients with second-line metastatic PDAC. The study also evaluates the combination with cetuximab in the first-line PDAC setting.
The oral KRAS G12D (ON/OFF) inhibitor was previously granted with FDA’s FTD for the treatment of KRAS G12D-mutant pancreatic ductal adenocarcinoma (PDAC) in 2025. Besides, GFH375 received the first two Breakthrough Therapy Designations in China for monotherapy treating G12D-mutant pancreatic cancer and NSCLC respectively.
GenFleet Therapeutics（2595.HK） announced the updated clinical data of GFH375 monotherapy treating KRAS G12D-mutant solid tumors were presented in the oral abstract session at the 2026 American Society of Clinical Oncology (ASCO) annual meeting on June 1 local time.
Additionally, preliminary clinical data of GFS202A, the world’s first GDF15/IL-6 bispecific antibody developed for cachexia, will be unveiled in a poster session during the conference. The 2026 ASCO annual meeting is slated to take place in Chicago, USA, from May 29 to June 2 local time.
The studies highlighted the potent and differentiated profile of GFH375, an oral KRAS G12D (ON/OFF) inhibitor, demonstrating superior anti-tumor activity, enhanced potency and selectivity, and more durable pathway suppression compared with other KRAS/RAS inhibitors across animal models and cellular assays.
GFS784 links a molecular glue Pan RAS (ON) inhibitor to cetuximab. Preclinical studies showed potent activity in RAS mutant models, both DXd sensitive and DXd resistant models, as well as anti tumor efficacy in EGFR mutant and TKI resistant models, supporting its potential as a monotherapy to deliver superior benefit compared with double-agent combination regimens.
Preclinical research showed at one-third the dosage of RMC 6236, GFH276 exerted comparable or enhanced tumor growth inhibition (TGI) in multiple RAS-mutant tumor models.
