Post by Gary G. Altman

CEO of Cambium Oncology. Our drug is efficacious in models of prostate and KRAS-G12D PDAC; designed to make aza last longer in TP53-mutant AML, and extend durability of FLT3-therapy.

Our drug is a first-in-class VIP/VPAC1 antagonist that works outside the PD-1/PD-L1 pathway and reaches an immune compartment that PD-1/PD-L1 blockade misses. · Designed to extend azacitidine (HMA) durability in TP53-mutant AML — the subset where current options fail fastest. · Designed to extend the durability of FLT3-targeted therapy. · Efficacy in preclinical models of prostate cancer and KRAS-G12D pancreatic cancer. · Single-agent, T-cell–mediated anti-leukemic activity across multiple murine AML models.