ArticleMolecular therapy. Oncology2026
Targeting LKB1-inactivated lung cancers with a stapled peptide inhibitor of the CRTC-CREB pathway.
Article in Molecular therapy. Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Non-small cell lung cancers (NSCLCs) with inactivation of the tumor suppressor LKB1 are common and respond poorly to current therapies. We previously identified aberrant activation of the CRTC-CREB transcriptional pathway as a key driver of malignancy in LKB1-deficient lung cancer. In this study, we developed stabilized α-helical peptides, termed stabilized alpha helices of the CREB binding domain (SAH-CBDs), which were designed to disrupt the CRTC-CREB protein-protein interaction. SAH-CBD peptides adopt a stable, bioactive α-helical conformation, bind directly to CREB, and effectively block CRTC-CREB complex formation
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