EPriL inhibitors are being developed to target (mutant) kinases with aberrant signaling and (tumor) restricted expression.
Crossfire’s Energetically Privileged Ligands (EPriLs) are non-covalently binding, but designed to have a long, covalent-like, residence time on target kinases. EPriL-based Inhibitors show prolonged signaling inhibition compared to other non-covalent inhibitors in clinical development. By targeting both wild-type and mutated forms of a kinase, our inhibitors reduce the risk of tumor escape through acquired mutations. Furthermore, EPriL-based inhibitors maintain high selectivity over other kinases of the kinome (off-target kinases) reducing the risk of toxicity in non-cancerous cells and tissues.
Our BTK inhibitor (NTRC 12026-0) is our most advanced internal program, with clinical trials planned Q3-Q4 2024. NTRC 12026-0 is being developed as a potential best-in class non-covalent inhibitor, targeting both wild type BTK and all clinically relevant BTK mutant variants.