A ProxAI modulator selectively intercepts an undruggable kinase-effector interface in immune cells, leaving the target's remaining functions intact. One design round. No natural template. In under three months.
A kinase driving inflammation presents a broad, flat interaction surface with no conventional druggable pocket. It engages effector substrates through this interface, making selective inhibition with traditional small molecules particularly challenging.
ProxAI designed a 90-amino-acid minibinder modulator in a single round with no structural template. It engages the exact kinase interface inhibiting by steric hindrance the effector phosphorylation.
In immune cells, the engineered modulator suppressed the inflammatory pathway by 82% without disrupting the kinase's other functions, a level of selectivity that separates function-specific modulation from blunt inhibition. Developed in collaboration with Université de Montréal; patent pending.
Readout: suppression of a downstream inflammatory-pathway effector measured in immune cells by western blot and qPCR. Selectivity refers to retention of the target’s remaining functions in the same assay context. Design of modulators with no natural template; single, unoptimized design round; proof of concept, not a validated therapeutic. Developed in collaboration with Université de Montréal; patent pending. Specific target identity withheld pending publication and IP; claims reflect internal data and are subject to scientific review.
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