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BridgeBio Announces Clinical Collaboration with Bristol Myers Squibb to Study BBP-398, a Potentially Best-in-class SHP2 Inhibitor, in Combination with OPDIVO® (nivolumab) in Advanced Solid Tumors with KRAS Mutations
- First clinical combination study set to evaluate safety and preliminary efficacy in non-small cell lung cancer with KRAS mutations PALO ALTO, Calif., July
About this update from Bridgebio Pharma, Inc.
[{"type":"text","content":"- First clinical combination study set to evaluate safety and preliminary efficacy in non-small cell lung cancer with KRAS mutations\n\n\nPALO ALTO, Calif., July 27, 2021 /PRNewswire/ -- BridgeBio Pharma, Inc. (Nasdaq: BBIO) (BridgeBio), a commercial-stage biopharmaceutical company founded to discover, create, test and deliver meaningful medicines for patients with genetic diseases and cancers with clear genetic drivers, today announced a non-exclusive, co-funded clinical collaboration with Bristol Myers Squibb to evaluate the combination of BBP-398, a potentially best-in-class SHP2 inhibitor, with OPDIVO® (nivolumab) in patients with advanced solid tumors with KRAS mutations with the hope of providing an effective new treatment option for patients with difficult-to-treat cancers. \n\n \n \n \n \n \n \n\n \nThe collaboration will also include the initiation of a Phase 1/2 study to evaluate the safety and preliminary efficacy of BBP-398 in combination with both OPDIVO as doublet therapy, and OPDIVO plus a KRASG12C inhibitor as triplet therapy in non-small cell lung cancer (NSCLC) with KRAS mutations, as first- and second-line treatment options. Under the terms of the non-exclusive collaboration, BridgeBio will sponsor the study and Bristol Myers Squibb will provide nivolumab. Both BridgeBio and Bristol Myers Squibb will share the cost of clinical development activities for the combination trial.\nSHP2 is a protein-tyrosine phosphatase that links growth factor, cytokine and integrin signaling with the downstream RAS/ERK MAPK pathway to regulate cellular proliferation and survival. Overactivity of the SHP2 pathway, often driven by distinct genetic mutations, is a critical contributor to many forms of cancer, and is a mechanism of resistance to several targeted therapies.\n\"Cancers that are driven by hyperactive MAPK signaling, including certain RAS mutations such as KRASG12C, may be sensitive to SHP2 inhibition,\" said Frank McCormick, Ph.D., chairman of oncology at BridgeBio. \"With this collaboration, we hope to better elucidate our SHP2 inhibitor's ability to enhance immuno-oncology and other targeted therapies to potentially provide options for patients with difficult-to-treat cancers as quickly and safely as possible.\"\nKRAS mutations occur in approximately 27% of NSCLC cases and approximately 17% of malignant solid tumors. ...