Targeted immunotherapy and companion biosensing approach for cancers harboring the KRASG12V mutation.
KRAS mutations are among the most common cancer-driving alterations and are found across major tumor types, including lung, pancreatic, colorectal, and thyroid cancers. The KRASG12V mutation alone represents 85% of all cancer mutations, yet there are currently no approved drugs that directly address this mutation. With growing interest and investment in precision oncology and immunotherapy, there is a strong unmet need for mutation-specific therapies that can expand treatment options and improve patient outcomes for KRAS-driven cancers.
Emory researchers have identified a previously unexploited interaction involving the KRASG12V mutant protein that plays a role in suppressing the immune system’s ability to attack cancer cells. By disrupting this interaction using a proprietary peptide-based inhibitor, the technology restores immune signaling and enhances cancel cell killing in KRASG12V-positive tumors. This approach introduces a new therapeutic target and modality for KRAS-mutant cancers and provides a foundation for developing next-generation immunotherapies with strong differentiation from existing oncology pipelines.
In vitro studies completed with co-culture data showing interaction between KRASG12V and JAK1.