cnv1014802 and Pain

cnv1014802 has been researched along with Pain* in 2 studies

Reviews

1 review(s) available for cnv1014802 and Pain

Article	Year
Challenges and Opportunities for Therapeutics Targeting the Voltage-Gated Sodium Channel Isoform Na Journal of medicinal chemistry, 2019, 10-10, Volume: 62, Issue:19 Voltage-gated sodium ion channel subtype 1.7 (Na Topics: Analgesics; Animals; Disease Models, Animal; Humans; NAV1.7 Voltage-Gated Sodium Channel; Pain; Protein Isoforms; Signal Transduction; Sodium Channel Blockers; Sulfonamides	2019

Other Studies

1 other study(ies) available for cnv1014802 and Pain

Article	Year
Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain. Toxins, 2016, Mar-17, Volume: 8, Issue:3 Loss-of-function mutations of Na(V)1.7 lead to congenital insensitivity to pain, a rare condition resulting in individuals who are otherwise normal except for the inability to sense pain, making pharmacological inhibition of Na(V)1.7 a promising therapeutic strategy for the treatment of pain. We characterized a novel mouse model of Na(V)1.7-mediated pain based on intraplantar injection of the scorpion toxin OD1, which is suitable for rapid in vivo profiling of Na(V)1.7 inhibitors. Intraplantar injection of OD1 caused spontaneous pain behaviors, which were reversed by co-injection with Na(V)1.7 inhibitors and significantly reduced in Na(V)1.7(-/-) mice. To validate the use of the model for profiling Na(V)1.7 inhibitors, we determined the Na(V) selectivity and tested the efficacy of the reported Na(V)1.7 inhibitors GpTx-1, PF-04856264 and CNV1014802 (raxatrigine). GpTx-1 selectively inhibited Na(V)1.7 and was effective when co-administered with OD1, but lacked efficacy when delivered systemically. PF-04856264 state-dependently and selectively inhibited Na(V)1.7 and significantly reduced OD1-induced spontaneous pain when delivered locally and systemically. CNV1014802 state-dependently, but non-selectively, inhibited Na(V) channels and was only effective in the OD1 model when delivered systemically. Our novel model of Na(V)1.7-mediated pain based on intraplantar injection of OD1 is thus suitable for the rapid in vivo characterization of the analgesic efficacy of Na(V)1.7 inhibitors. Topics: Analgesics; Animals; Behavior, Animal; CHO Cells; Cricetulus; Disease Models, Animal; HEK293 Cells; Humans; Male; Mice, Inbred C57BL; NAV1.7 Voltage-Gated Sodium Channel; Nerve Fibers; Pain; Peptides; Phenyl Ethers; Proline; Saphenous Vein; Scorpion Venoms; Sodium Channel Blockers; Spider Venoms; Sulfonamides	2016

Article

Year

Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain.

Toxins, 2016, Mar-17, Volume: 8, Issue:3

Loss-of-function mutations of Na(V)1.7 lead to congenital insensitivity to pain, a rare condition resulting in individuals who are otherwise normal except for the inability to sense pain, making pharmacological inhibition of Na(V)1.7 a promising therapeutic strategy for the treatment of pain. We characterized a novel mouse model of Na(V)1.7-mediated pain based on intraplantar injection of the scorpion toxin OD1, which is suitable for rapid in vivo profiling of Na(V)1.7 inhibitors. Intraplantar injection of OD1 caused spontaneous pain behaviors, which were reversed by co-injection with Na(V)1.7 inhibitors and significantly reduced in Na(V)1.7(-/-) mice. To validate the use of the model for profiling Na(V)1.7 inhibitors, we determined the Na(V) selectivity and tested the efficacy of the reported Na(V)1.7 inhibitors GpTx-1, PF-04856264 and CNV1014802 (raxatrigine). GpTx-1 selectively inhibited Na(V)1.7 and was effective when co-administered with OD1, but lacked efficacy when delivered systemically. PF-04856264 state-dependently and selectively inhibited Na(V)1.7 and significantly reduced OD1-induced spontaneous pain when delivered locally and systemically. CNV1014802 state-dependently, but non-selectively, inhibited Na(V) channels and was only effective in the OD1 model when delivered systemically. Our novel model of Na(V)1.7-mediated pain based on intraplantar injection of OD1 is thus suitable for the rapid in vivo characterization of the analgesic efficacy of Na(V)1.7 inhibitors.

Topics: Analgesics; Animals; Behavior, Animal; CHO Cells; Cricetulus; Disease Models, Animal; HEK293 Cells; Humans; Male; Mice, Inbred C57BL; NAV1.7 Voltage-Gated Sodium Channel; Nerve Fibers; Pain; Peptides; Phenyl Ethers; Proline; Saphenous Vein; Scorpion Venoms; Sodium Channel Blockers; Spider Venoms; Sulfonamides

2016