Infinity Pharma (INFI) Presented Encouraging Data for IPI-926 at AACR
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Infinity Pharmaceuticals, Inc. (Nasdaq: INFI) has presented new preclinical data for saridegib (IPI-926), its novel oral molecule that inhibits Smoothened, a key component of the Hedgehog pathway.
Data presented showed the anti-tumor activity of saridegib in models of residual disease, in which malignant cells remain present after primary treatment. Importantly, these data show that the ability of saridegib to delay tumor recurrence is time dependent and provide rationale for the development of saridegib in residual disease settings, such as ovarian cancer and small cell lung cancer. These data were presented during a mini symposium session at the American Association for Cancer Research (AACR) 103rd Annual Meeting in Chicago, Illinois (Abstract #979).
Saridegib has been previously shown to delay tumor recurrence following cytoreduction (tumor shrinkage caused by treatment with chemotherapy or targeted therapy) in multiple preclinical models of residual disease, including ovarian, prostate and lung cancer.1,2,3,4 New preclinical data presented today support these findings and show that cytoreduction leads to temporal changes in the tumor microenvironment, as well as upregulation of the Hedgehog ligand and pathway signaling in the tumor cells and surrounding stromal cells, respectively. These new data also suggest that saridegib treatment inhibits the observed Hedgehog pathway activation and may delay tumor recurrence by increasing necrosis, or tumor cell death, post-therapy. Saridegib showed the greatest inhibition of tumor regrowth when administered within 10 days of completing primary therapy, suggesting that there may be a window of activity during which the effects of saridegib are greatest.
Data presented showed the anti-tumor activity of saridegib in models of residual disease, in which malignant cells remain present after primary treatment. Importantly, these data show that the ability of saridegib to delay tumor recurrence is time dependent and provide rationale for the development of saridegib in residual disease settings, such as ovarian cancer and small cell lung cancer. These data were presented during a mini symposium session at the American Association for Cancer Research (AACR) 103rd Annual Meeting in Chicago, Illinois (Abstract #979).
Saridegib has been previously shown to delay tumor recurrence following cytoreduction (tumor shrinkage caused by treatment with chemotherapy or targeted therapy) in multiple preclinical models of residual disease, including ovarian, prostate and lung cancer.1,2,3,4 New preclinical data presented today support these findings and show that cytoreduction leads to temporal changes in the tumor microenvironment, as well as upregulation of the Hedgehog ligand and pathway signaling in the tumor cells and surrounding stromal cells, respectively. These new data also suggest that saridegib treatment inhibits the observed Hedgehog pathway activation and may delay tumor recurrence by increasing necrosis, or tumor cell death, post-therapy. Saridegib showed the greatest inhibition of tumor regrowth when administered within 10 days of completing primary therapy, suggesting that there may be a window of activity during which the effects of saridegib are greatest.
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