Data presented demonstrate that a single administration of IPI-926 in a preclinical model of human pancreatic cancer results in rapid and sustained Hedgehog pathway inhibition in the stromal cells, as measured by Gli1 expression, a downstream mediator of Hedgehog signaling, said Infinity.
These findings suggest that IPI-926 inhibits tumor growth by down-regulating Hedgehog signaling to tumor associated stroma. Data reported also show that in a preclinical model of human pancreatic cancer, daily administration of IPI-926 results in significant tumor growth inhibition when compared to vehicle controls.
Infinity has presented preclinical data showing that in a novel model of medulloblastoma, IPI-926 demonstrated excellent oral bioavailability, a long plasma half-life and duration of action, and good distribution to tumor tissue. In addition, daily oral administration of IPI-926 in this model led to dose-dependent inhibition of tumor growth, with tumor regression seen at higher doses.
Additional data demonstrated that IPI-926 delayed tumor growth following chemotherapy in a preclinical model of small cell lung cancer (SCLC). In this model, following tumor debulking with a treatment regimen similar to that used clinically in patients with SCLC, once-daily oral administration of IPI-926 led to a statistically significant delay in tumor re-growth as compared to vehicle control.
Julian Adams, president of R&D and chief scientific officer at Infinity, said: “Our Hedgehog program is further evidence of Infinity’s ongoing commitment to emerging cancer targets, and to those patients in need of better therapies. We look forward to learning more about IPI-926 as we pursue Phase I evaluation of this novel anti-cancer compound.”