BridgeBio spins out KRAS-focused cancer newco with $200M from VCs

02 May 2024
Phase 1Phase 2
With its hands full bringing a series of late-stage cardiorenal and genetic disorder assets over the finish line, BridgeBio has decided to spin out a new unit dedicated to advancing a trio of its early cancer programmes.
The move will transform BridgeBio’s former TheRas subsidiary into a standalone company, dubbed BridgeBio Oncology Therapeutics (BBOT) – which raised $200 million in private funding on Thursday.
The round was led by Cormorant Asset Management and co-led by Omega Funds. The oversubscribed financing also saw participation from affiliates of Deerfield Management, Google Ventures, EcoR1 Capital, Wellington Management, Enavate Sciences, Surveyor Capital, Aisling Capital, Casdin Capital, and Longwood Fund.
Eli Wallace, formerly CEO of oncology R&D at BridgeBio, will helm the new company alongside Pedro Beltran, who will serve as chief scientific officer and previously was head of oncology biology.
Innovative KRAS inhibition
BBOT’s lead candidate, KRAS G12C inhibitorKRAS G12C inhibitor BBO-8520, was recently cleared for in-human testing. Enrollment is underway for the Phase I ONKORAS-101 trial in patients with KRAS G12C mutant non-small-cell lung cancerKRAS G12C mutant non-small-cell lung cancer, who will receive either BBO-8520 monotherapy or in combination with Merck & Co’s PD-1 inhibitor Keytruda (pembrolizumab).
The company plans to file with the FDA this quarter to start a trial of its second candidate, BBO-10203. The compound was designed to block interactions between PI3Kα and RAS, inhibiting PI3Kα/AKT effector signalling in tumours while bypassing glucose metabolic signalling to avoid hyperglycemia.
The final programme is BBO-11818, a pan-KRAS inhibitor that targets both the “on” and “off” states of KRAS G12X. It’s expected to enter the clinic next year.
Additionally, BBOT also aims to discover new programmes that target other oncogenic drivers within the RAS and PI3K pathways.
“BBOT’s innovative chemical biology approaches to inhibit a wide spectrum of KRAS mutations in both the ‘on’ and ‘off’ states, as well as bypass mechanisms exploiting PI3K signalling, promise to transform the treatment of this important class of cancers,” said Cormorant’s Raymond Kelleher.
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