Our Targets

UDT1: undisclosed target1 / [Our targets are in blue]

Effect of A2A /A2B AdoRs, EP4 and UDT1 activation on immune cells

We target novel GPCR immune checkpoints in the TME that are upregulated on multiple immune cells and are also involved in ATP (A2A and A2B AdoRs) and lipid (EP4, UDT1) metabolic pathways. Activation of those GPCRs increases cAMP, which plays a central role in suppressing antigen presentation, T effector function and stimulation of immunosuppressive cells leading to tumor immune evasion. Our targets also include metabolic checkpoints (undisclosed target 2) inhibitors that have the potential of reinvigorating antitumor immunity and thus enhance the efficacy of our GPCR immune checkpoint inhibitors and anti-PD-1 when used in combination therapy.

In preclinical animal models, we have demonstrated that our lead GPCR antagonists are highly efficacious in inhibiting ATP (A2A and A2B) and lipid (EP4, UDT1) immune checkpoint pathways and consequently restoring antitumor immunity and attenuating tumor growth.