Identification of NFAT5 as a novel target for preventing KRAS targeted therapy resistance

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Inhibiting NFAT5 attenuates pancreatitis-induced resistance to KRAS inhibition and extends mouse survival. 

Invention Summary:

Resistance to KRAS targeted therapy in cancers involves epithelial-to-mesenchymal transition (EMT), which poses challenges for effective targeting. However, the mechanism underlying EMT associated KRAS resistance and potential target treatments for KRAS inhibitor resistance cancers are still urgent to be known.  

Rutgers researchers delineated the molecular and cellular mechanisms and found the druggable target for this process, thereby providing a potential treatment for KRAS resistance tumors. TGFβ triggers EMT and resistance by activating key mediators via inducing the formation of novel protein complexes. NFAT5 is one of the major components in the protein complex and their pre-clinical data showed that KRAS resistance is mitigated by inhibiting NFAT5. Their invention elucidates the role of TGFβ signaling in EMT-associated KRAS therapy resistance and identifies NFAT5 as a druggable target. 

Market Applications:

• Targeted therapy for KRAS resistance cancers. 

• Targeted therapy for pancreatic cancer.  

Advantages:

• Unique block for EMT-driven KRAS resistance pathway. 

• Less side effects than broad TGFβ receptor blockers. 

Publication/s: https://pubmed.ncbi.nlm.nih.gov/39432061/ 

Intellectual Property & Development Status: Provisional application filed. Patent pending. Available for licensing and/or research collaboration. For any business development and other collaborative partnerships, contact:  marketingbd@research.rutgers.edu