Inhibiting FST-IGF1R interaction for neuropathic pain

Inhibiting the interaction between the glycoprotein FST, which is upregulated in the dorsal root ganglion of mice with nerve injury, and the growth factor receptor IGF1R could help treat neuropathic pain by decreasing the binding pair's enhancement of voltage-gated sodium channel activity and IGF1R-induced ERK/AKT signaling in neurons, thus preventing neuronal hyperexcitability.

In a mouse spinal nerve ligation model of neuropathic pain, systemic heterozygosity or induced intrathecal knockout of FST, or intrathecal injection of an FST-targeting siRNA or antibody, decreased allodynia and hypersensitivity to heat compared with normal FST expression or a control siRNA or antibody, respectively. ...