• Pipeline
  • Program Target
    PD-L1 x LAG-3
  • Disease Indication
    Solid Tumor
  • Development Stage
    Clinical Development
    (Phase 1)
ABL501 is a bispecific antibody capable of blocking the PD-L1 and LAG-3 immune checkpoint pathways, overcoming the current limitations of conventional PD-(L)1 therapy based around resistance to PD-L1 and low response rates. ABL501 demonstrates a higher efficacy over LAG-3 alone, PD-L1 alone, and the combination of LAG-3 and PD-L1, and shows superior performance compared to competing substances.

Mechanism of action

ABL501 is a bispecific antibody targeting LAG-3 and PD-L1 and blocks the interaction of LAG3-MHCII and PD-1-PD-L1,
releasing T cells from tumor-mediated suppression

Mechanism of action
좌우스크롤 Mechanism of action

Higher T cell activation than combination of LAG-3 and PD-L1 antibodies

ABL501 induced superior T cell activation compared to the combination of LAG-3 and PD-L1 antibodies as indicated in PBMC-based IL-2 expression assays and dual blockade reporter assays

Strong tumor killing effect of ABL501 compared with Atezolizumab

ABL501 induced stronger cytotoxic activity on NSCLC cells in the presence of tumor-matched patient PBMCs

Potent inhibition on tumor progression

ABL501 exhibited dose-dependent tumor growth inhibition

Phase 1 clinical study

Monotherapy dose escalation is ongoing with support of Korea Drug Development Fund funded by Ministry of Science and ICT, Ministry of Trade, Industry, and Energy, and Ministry of Health and Welfare (HN21C0979000021, Republic of Korea).