Business
BridgeBio Pharma Announces Progress in its KRAS Portfolio, New Gene Therapy Programs, and Updates on Advancements Across its R&D Pipeline Targeting Genetic Diseases and Cancers
PALO ALTO, Calif., Oct. 12, 2021 /PRNewswire/ -- BridgeBio Pharma, Inc. (Nasdaq: BBIO), a commercial-stage biopharmaceutical company that focuses on genetic

About this update from Bridgebio Pharma, Inc.
[{"type":"text","content":"PALO ALTO, Calif., Oct. 12, 2021 /PRNewswire/ -- BridgeBio Pharma, Inc. (Nasdaq: BBIO), a commercial-stage biopharmaceutical company that focuses on genetic diseases and cancers, is announcing meaningful progress in its KRAS cancer portfolio, new programs in gene therapy, and advancements in cardiorenal and early-stage Mendelian programs at its second annual R&D Day today. BridgeBio will also discuss how it is broadening the scope of its R&D engine with the launch of its new early-stage research institute, BridgeBioX.\n\n \n \n \n \n \n \n\n \nBridgeBio's R&D Day will feature presentations by Neil Kumar, Ph.D., BridgeBio founder and CEO; Richard Scheller, Ph.D., chairman of R&D at BridgeBio; Charles Homcy, M.D., chairman of pharmaceuticals at BridgeBio; Uma Sinha, Ph.D., chief scientific officer at BridgeBio; and scientists and physicians leading BridgeBio's drug discovery and development programs. \nBridgeBio has more than 30 programs in its pipeline for patients living with genetic diseases and genetically-driven cancers. Fourteen of those programs are being advanced in the clinic or commercial setting, and earlier this year BridgeBio received its first two U.S. Food and Drug Administration (FDA) drug approvals.\nR&D Day pipeline news and updates:\nBridgeBio Precision Oncology\nKRAS inhibitors for KRAS cancers: BridgeBio announces its discovery of next-generation G12C dual inhibitors, the first-known compounds that directly bind and inhibit KRAS in both its active (GTP bound) and inactive (GDP bound) conformations driven by insights from its molecular dynamics platform. This unique mechanism of action (MOA) is differentiated in preclinical models from first generation compounds, which only bind inactive KRAS. RAS is one of the most well-known oncogenic drivers with approximately 30% of all cancers being driven by RAS mutations, including large proportions of lung, colorectal and pancreatic tumors. In preclinical models, BridgeBio compounds showed rapid and complete modification of active (GTP bound) KRAS, which is not observed with first generation compounds. BridgeBio compounds were shown to be >500 fold more potent in inhibiting KRAS:RAF effector binding and more potent at inhibiting downstream signaling than first generation inhibitors. In cellular resistance models, BridgeBio's dual KRAS inhibitors were shown to be >35x mo...