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Acquired Resistance in Clinically Relevant Kinases

Acquired resistance with TKI therapy has been defined as disease progression after initial clinical benefit and can be attributed to selection of biological variants during TKI exposure. The development of next generation TKIs has proven to be very successful in mutant EGFR and ALK targeted therapies. Using our EPriL platform NTRC Therapeutics focuses on the discovery and development of next-generation kinase inhibitors to treat acquired drug resistance.


Next Generation Kinase Inhibitors

Wild-type and mutant forms of target are inhibited by EPriLs

Kinase Target

Uninhibited state of kinase
leads to aberrant signalling

Signalling on

1st Generation
Kinase Inhibitor

Target is inhibited by
first generation drug

Signalling off

Acquired Resistance

Resistance mutations emerge that weaken binding of
first generation drug

Signalling on


Next generation EPriLs bind
wild type and mutant forms
of the target

Signalling off

EPriL/Degrader Platform Technologies

NTRC - Our Science - Visual

EPriL Chemistry

  • Our proprietary Energetically Privileged Ligands (EPriLs) are designed to interact with specific kinases with optimal entropic and enthalpic energy contributions

BTK Kinase

Binding Kinetics

  • EPriLs have prolonged target residence times on their target kinase and are better suited to target acquired resistance caused by mutations in the target kinases

LCK Kinase

Target Occupancy

  • Due to their enhanced target residency EPriLs have be applied in affinity based probes, that aid in the determination of target occupancy in tumors in phase 1 trials

LCK Kinase

EPriL Degraders

  • Our unique EPriL concept can be easily expanded to effective E3 ligase mediated degraders