Mutant RAS peptide antigen

Mutant RAS peptide antigens are short amino acid sequences derived from oncogenic mutations in RAS family proteins (KRAS, HRAS, NRAS), most notably missense changes at codons G12, G13, and Q61[2][3][6]. These mutations drive constitutive, deregulated signaling that underlies tumorigenesis in multiple cancers, especially lung, pancreatic, and colorectal[1][2][3][4][6]. The mutated peptides are processed within tumor cells and presented on their surface by class I human leukocyte antigen (HLA) molecules as neoantigens, enabling recognition and killing by cytotoxic CD8+ T cells[2][3][5]. The antigenicity and specificity of these peptides, particularly for common HLA alleles (A*02:01, A*03:01, A*11:01, B*07:02), support their development as targets for cancer vaccines, adoptive T cell therapies, and bispecific antibodies that redirect T cells or immune effectors against tumors[2][3][5]. Therapies targeting mutant RAS peptide antigens are an active research frontier and address the longstanding challenge of “undruggable” RAS mutations[2][3][5][6]. Key hurdles include HLA restriction, immune evasion, and minimizing off-target toxicity[2][5][6].

Other names

Mutant RAS neoantigenRAS mutant peptide epitopemRAS peptideMutant KRAS peptideRAS mutation-derived peptideG12-mutant RAS peptide

Direct inhibition of mutant RAS signaling (by small molecule inhibitors); Immune-mediated elimination of tumor cells expressing mutant RAS epitopes (via peptide vaccines, adoptive T cell therapy, bispecific antibodies)