Immunotherapeutic agent and biosensor for KRASG12V mutation in tumor cells.
- First in class, targeted immunotherapy for patients presented with KRASG12V mutation.
- Attenuates immune suppression associated with KRASG12V-positive cancers.
The KRASG12V mutation, representing 85% of all cancer mutations, is implicated in a wide variety of cancers including lung, pancreatic, thyroid, and colorectal cancers and is presented in 3.08% of all cancer patients. KRAS mutations account for about 1 million deaths per year. However, no drugs are available for treating patients with KRAS mutations. This suggests an urgent unmet clinical need for cancer therapeutics specifically targeting oncogenic KRAS mutations.
Emory inventors have discovered that KRASG12V drives tumorigenesis in part through suppressing the JAK1-mediated immune response pathway. The inventors have constructed a small 8-mer peptide (“RasKi”) and showed that disruption of KRASG12V-JAK1 interaction enhances killing of KRASG12V-carrying cancer cells by restoring IFNγ-JAK1 mediated immune response. Thus, the KRASG12V-JAK1 interaction may represent a promising molecular target for therapeutic discovery and development. RasKi and its derivatives may serve as candidates for the development of the next generation of KRASG12V-targeted anticancer immune therapeutic agents for cancers with KRASG12V mutation.
In vitro study showing the interaction between KRASG12V and JAK1.
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