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Ref-Nr: TA-TA04745


A strategy to quantify activity-conformations of mutated and cancer relevant RAF kinases in vivo. The full-length kinase is the basis for an extendable cell-based reporter platform which enables noninvasive recordings of open (active) and closed (inactive) RAF conformations following dose- and time-dependent exposure with approved drugs or promising lead molecules.


Tumors originate from a collection of oncogenic BRAF mutations which diminish the auto-inhibitory kinase conformation and promote RAS-uncoupled proliferative RAF-MEK-ERK signaling. The most common oncogenic BRAF mutation (V600E) has become the prime target for therapeutic intervention. Therapeutic effects are often temporary and proposed drug resistance mechanism involve alterations of molecular interactions of RAF provoking MAP-kinase reactivation. There is a need for cell-based technologies to systematically evaluate mode of action and efficacies of lead molecules acting on mutated RAF conformations/activities.


We present a kinase reporter toolbox to implement various BRAF mutations to systematically profile and compare target specificity, pharmacodynamics and efficacies of clinical BRAF inhibitors in vivo. This technology has implications for the more rational development of kinase drugs in the context of personalized medicine and combinational kinase inhibitor drug therapy.


  • Biosensor for analysing full length kinase:drug interactions
  • Extendable for other RAF isoforms & kinases
  • Drug screening using wt and mutant RAF in vivo
  • Chance to identify allosteric modulators of kinases


  • About 50 % of melanomas harbor activating BRAF mutations (300 different RAF mutations have been identified and can be tested).
  • Personalized medicine – the right drug for the right RAF mutation
  • Leopard & Noonan syndrome

Dr. David Lederbauer
+43 512 507-34403
Universität Innsbruck; ICT-Technologiepark, Technikerstraße 21a
6020 Innsbruck


  • EP anhängig


Cancer, RAF kinase, BRAF, RAF mutation

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