ST-2560, a selective inhibitor of the Na1.7 sodium channel, affects nocifensive and cardiovascular reflexes in non-human primates.

Background And Purpose: The voltage-gated sodium channel isoform Na1.7 is a high-interest target for the development of non-opioid analgesics due to its preferential expression in pain-sensing neurons. Na1.

Discovery of Selective Inhibitors of Na1.7 Templated on Saxitoxin as Therapeutics for Pain.

The voltage-gated sodium channel isoform Na1.7 has drawn widespread interest as a target for non-opioid, investigational new drugs to treat pain. Selectivity over homologous, off-target sodium channel isoforms, which are expressed in peripheral motor neurons, the central nervous system, skeletal muscle and the heart, poses a significant challenge to the development of small molecule inhibitors of Na1.

Antinociceptive properties of an isoform-selective inhibitor of Nav1.7 derived from saxitoxin in mouse models of pain.

The voltage-gated sodium channel Nav1.7 is highly expressed in nociceptive afferents and is critically involved in pain signal transmission. Nav1.

Discovery of a selective, state-independent inhibitor of Na1.7 by modification of guanidinium toxins.

The voltage-gated sodium channel isoform Na1.7 is highly expressed in dorsal root ganglion neurons and is obligatory for nociceptive signal transmission. Genetic gain-of-function and loss-of-function Na1.

Challenges and Opportunities for Therapeutics Targeting the Voltage-Gated Sodium Channel Isoform Na1.7.

Voltage-gated sodium ion channel subtype 1.7 (Na1.7) is a high interest target for the discovery of non-opioid analgesics.