transformative medicines against kinase-addicted cancers
Motivation
Unless we target the mechanics foundational to evasive tumor response, hallmarks of cancers will continue to drive resistance to therapy
Approach
Redesign small-molecule inhibitors from the ground up, and intercept kinases early and upstream of escape points
Mission
Transform the treatment landscape for patients battling aggressive tumors, one pioneering kinase drug at a time
=> first-in-class MoA denies tumors access to escape routes
=> potent, ultra-selective, and prolonged target engagement
=> durable efficacy in the face of evasive tumor response
=> small molecule kinase inhibitors and ADCs
=> standalone therapies (and combinations)
=> efficacious, tolerable, with lasting effect
Empowered by our purpose-built library of bivalent probes, we develop small-molecule therapeutics that engage disease-driving kinases where they are most vulnerable: their idle OFF-states.
This has multiple advantages over inhibiting the catalytic function of the ON-state: unmatched selectivity, full depth of inhibition, and unprecedented durability in the face of adaptive tumor response.
Where classical kinase inhibitors facilitate escape to treatment, our compounds deny tumors access to their preferred escape routes.
Platform and Discovery Engine
powered by
bivalent chemistry, large-scale compute, tunable biology
Provides exclusive access to first-in-class MoA
turns target kinase off, takes it out of circulation, prevents reentry
Generates assets with single-agent profiles
for standalone therapies and logical combinations
Broadly applicable across clinically validated kinases
directly expandable to CDKs (CMGC), ERBBs (TK), RAFs (TKL)
Our CDK2i lead program demonstrates the capability of our platform and engine at
unlocking vast therapeutic value among clinically validated kinases by interepting them in their OFF-states