PRIMARY ENDPOINT
55%
ORR (BICR-confirmed)
Naïve 50% · Treated 60%
Abion’s drug discovery begins with the biological mechanisms that enable cancer to evade existing therapies and develop resistance.
Building on this understanding, we deploy four therapeutic modalities—small molecules, antibodies, bispecific antibodies, and antibody–cytokine fusions—to address c-MET–mediated resistance to targeted therapies, Claudin-3 as a historically difficult-to-drug antibody target, and acquired resistance and limited durability of response to TROP2-directed ADCs. Each program is designed from the early stages of development alongside a biomarker strategy to identify patients most likely to benefit.
The lead iRAC candidate — a TROP2-directed antibody fused to interferon-β, designed for tumours that have progressed on ADC therapy.
A first-in-class human antibody against claudin-3, a tight-junction protein overexpressed across solid tumours.
An oral, selective c-MET inhibitor in Phase 2 for NSCLC driven by MET exon 14 skipping and MET amplification.
PRIMARY ENDPOINT
55%
ORR (BICR-confirmed)
Naïve 50% · Treated 60%
DISEASE CONTROL
83%
DCR vs. ~80% for approved peers
PROGRESSION-FREE
8.54mo
median PFS tepo 8.5 · cap 6.7 · savo 6.9
DURABILITY ★
19.4mo
median DoR (naïve) — longest reported in class
iRAC — interferon-β, delivered where it matters.
While conventional interferons activate immune responses and relevant systemic toxicity, But Abion’s iRAC targets the tumor specifically, increasing signals exclusively within the tumor itself
We are building a Korea-originated global oncology model — combining Abion´s discovery engine with partners platform-commercialization, CMC, and global BD capabilities.