Proto-oncogene tyrosine-protein kinase receptor Ret (RET) and 5'-AMP-activated protein kinase catalytic subunit alpha-1 (AMPKα1) (RET and AMPKα1)

The target "RET and AMPKα1" refers to two distinct molecular entities: the Proto-oncogene tyrosine-protein kinase receptor Ret (RET) and the 5'-AMP-activated protein kinase catalytic subunit alpha-1 (AMPKα1). RET is a transmembrane receptor tyrosine kinase (RTK) that is essential for the development of the enteric nervous system and the kidneys, but its oncogenic activation through fusions or point mutations is a primary driver in medullary thyroid cancer and a subset of non-small cell lung cancers (UniProt P07949). Therapeutic intervention for RET-driven malignancies involves highly selective small-molecule inhibitors such as selpercatinib and pralsetinib, which effectively block downstream signaling to inhibit tumor growth (PubMed 32814019). In contrast, AMPKα1 is a catalytic subunit of the heterotrimeric AMPK complex, which functions as a master energy sensor to maintain cellular ATP levels by activating catabolic pathways and inhibiting anabolic processes (UniProt Q13131). While AMPK is a major target for metabolic diseases like type 2 diabetes (e.g., via metformin), it is also being investigated for its role in cancer metabolism and as a potential therapeutic checkpoint (PubMed 22230683). Because these are two separate proteins with distinct biological roles and therapeutic contexts, they are not typically grouped as a single target entity.

Other names

RETCDHF12CDHR16PTCRET51PRKAA1AMPK alpha 15'-AMP-activated protein kinase catalytic subunit alpha-1

Inhibition of RET tyrosine kinase activity and activation of the AMPK metabolic pathway