Parthenon Therapeutics has announced that a collaboration between the company, The University of Texas Health Center at Houston and George Washington University has demonstrated that PRTH-101 potently inhibits the adhesion of collagen receptor discoid in domain receptor-1 expressing cancer cells to collagen substrates and DDR1 autophosphorylation induced by collagen. The drug candidate binds to its target to inhibit DDR1, reversing immune exclusion by disrupting collagen fiber alignment in mouse models. Parthenon recently initiated a Phase 1 first-in-human clinical trial for its lead candidate PRTH-101 in patients with advanced solid tumors.
The Journal for ImmunoTherapy of Cancer (JITC) has published results from a study conducted by Parthenon Therapeutics, The University of Texas Health Center at Houston (UTHealth Houston), and George Washington University on the effects of PRTH-101 on DDR1 inhibition. The study found that PRTH-101 was able to potently inhibit the adhesion of cancer cells expressing DDR1 to collagen substrates, which disrupts the physical barrier formed by aligned collagen fibers in tumors. This reversal of immune exclusion allows T-cells to enter and attack