Junshi Bio, Antengene pair PD-1/VEGF bispecific with oral CD73 inhibitor in China-focused deal

Shanghai Junshi Biosciences Co., Ltd (HKEX: 1877; SSE: 688180) and Antengene Corporation Ltd (SEHK: 6996.HK) entered into a strategic clinical collaboration to evaluate the combination of JS207, a PD-1/VEGF bispecific antibody developed by Junshi Biosciences, with ATG-037, an oral CD73 inhibitor developed by Antengene, in patients with solid tumors in Chinese Mainland. The partnership is structured as a clinical evaluation agreement aimed at identifying synergistic anti-tumor activity across multiple tumor types, with no financial terms were not disclosed.

The collaboration pairs two clinical-stage oncology assets with complementary mechanisms. JS207 simultaneously targets PD-1 and VEGF-A, combining immune checkpoint blockade with anti-angiogenic activity in a single molecule. ATG-037 inhibits CD73, an enzyme that generates immunosuppressive adenosine in the tumor microenvironment. Together, the companies describe the regimen as a “triple-axis” strategy designed to modulate immune checkpoint signaling, angiogenesis, and the adenosine pathway.

The rationale for PD-1/VEGF + CD73 combo

JS207 is a recombinant humanized anti-PD-1/VEGF bispecific antibody that binds PD-1 and VEGF-A simultaneously, blocking PD-1 interaction with PD-L1 and PD-L2 while neutralizing VEGF receptor binding. Its anti-PD-1 component is based on the Fab structure of toripalimab, Junshi’s approved anti-PD-1 monoclonal antibody, which has received marketing authorization in more than 40 countries and regions, including China, the US, and EU.

ATG-037 is an orally administered small-molecule CD73 inhibitor positioned by Antengene as having potential advantages over antibody-based CD73 inhibitors, including stronger inhibition of cell-surface CD73 enzymatic activity, improved tissue penetration, and avoidance of the “hook effect” associated with antibody approaches.

The scientific rationale for the collaboration rests on the intersection of three pathways contributing to immune evasion and tumor progression. CD73-generated adenosine suppresses anti-tumor immune responses and promotes angiogenesis, including through VEGF signaling, and has been implicated in resistance to anti-VEGF therapies. CD73 inhibition has also demonstrated synergy with anti-PD-1 therapies in both clinical and preclinical settings.

Combining ATG-037 with JS207 is therefore intended to address overlapping biology simultaneously. By pairing CD73 blockade with dual PD-1/VEGF inhibition, the companies aim to deepen responses, improve durability of benefit, and potentially overcome resistance mechanisms that limit single-pathway approaches. The strategy reflects a broader industry shift toward multi-target regimens designed to address the complexity of the tumor microenvironment.