This technology selectively targets NRAS mutants in melanomas through depalmitoylation modulation, which can be used to treat cutaneous melanomas and other pathophysiological conditions.
NRAS mutations are implicated in 15-20% of melanomas. Despite the significance of this mutation, targeting NRAS proteins has proven challenging due to undruggable sites on the protein surface. Thus, current treatments for NRAS-mutant melanomas focus on broad targeting of signaling pathways, which can have limited specificity and efficacy. Existing therapies also struggle to effectively modulate the palmitoylation cycle that governs NRAS membrane association. A more targeted and precise method to disrupt NRAS signaling could improve treatment efficacy and patient outcomes.
This technology selectively targets NRAS-mutant proteins by modulating their palmitoylation cycle, disrupting NRAS membrane association and downstream signaling. By incorporating a feedback loop based on ERK phosphorylation, the technology selectively affects NRAS mutants without interfering with normal cellular processes. This approach ensures that NRAS signaling is disrupted in cancerous cells while minimizing effects on healthy tissue.
This technology has been validated in rat hippocampal neurons.
Patent Pending
IR CU24204
Licensing Contact: Kristin Neuman