Kirsten rat sarcoma viral oncogene homolog G12D mutant mRNA (KRAS G12D mutant mRNA)

KRAS G12D mutant mRNA refers to the messenger RNA encoding the Kirsten rat sarcoma viral oncogene homolog (KRAS) protein with a glycine-to-aspartic acid mutation at codon 12 (G12D). KRAS is a small GTPase involved in cellular signal transduction; the G12D mutation is one of the most common oncogenic alterations in human cancers, especially pancreatic, colorectal, and lung carcinomas[3][4][7]. The G12D mutation impairs intrinsic GTPase activity and disrupts regulation by GTPase-activating proteins, resulting in constitutive signaling that drives uncontrolled cell proliferation, survival, and oncogenic transformation[2][4][6][7]. While the protein is the usual therapeutic target, the mRNA may also be targeted by RNA-based drugs, though most biochemical and structural studies focus on the mutant protein. Clarifying note: The query uses “KRAS G12D mutant mRNA” as the target, which is uncommon in drug discovery; typically, the term refers to the encoded **protein** as the target. Most drugs, structural data, and biological functions pertain to the KRAS G12D mutant protein, not directly to its mRNA. Only RNA-targeting drugs (e.g., siRNA, antisense oligonucleotides) would act on the mRNA. If structured information about the KRAS G12D mutant protein is required, remove “mRNA” from the target name[4].

Other names

KRAS G12D mutantKRAS (G12D) mutantK-Ras G12D variantKRAS Gly12Asp mutantOncogenic KRAS G12D

Allosteric inhibition of mutant KRAS protein activity (e.g., by occupying the switch II pocket)[1][4]; Disruption of protein–protein interactions; Inhibition of GTPase signaling; mRNA degradation/inhibition (for oligonucleotide drugs targeting mRNA).