This technology identifies Delta-2-tubulin (D2) as a therapeutic target and biomarker for peripheral neuropathy.
Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent neurological complication associated with chemotherapy and can be induced by multiple anticancer drugs. The pathogenesis of CIPN remains largely unknown, and current therapies, such as opioid analgesics, antidepressants, and anticonvulsants, provide only limited symptomatic relief. As a result, there is a critical need to identify therapeutic targets and biomarkers for the treatment and prevention of CIPN.
This technology identifies Delta-2-tubulin (D2) as both a biomarker and therapeutic target for peripheral neuropathy. D2 is formed from the irreversible modification of α-tubulin in sensory neurons, causing multiple cellular perturbations. In preclinical models of chemotherapy-induced peripheral neuropathy (CIPN), overexpression of D2 was found to suppress mitochondrial respiration, inhibit transient receptor potential (TRP) channel function, upregulate the mitochondrial anchor syntaphilin, and directly impair axonal mitochondrial motility. Collectively, these effects contribute to sensory neuron axonopathy. Thus, D2 serves as both a therapeutic target and biomarker for determining the risk of developing peripheral neuropathy.
This technology has been validated in vivo with mouse models of CIPN.
Patent Pending(WO/2026/107492)
IR CU25119, CU18162
Licensing Contact: Kristin Neuman