TC-N 1752_product_DataBase

Bioactivity

TC-N 1752 is a potent and orally active inhibitor of Nav1.7, with IC50s of 0.17 μM, 0.3 μM, 0.4 μM, 1.1 μM and 2.2 μM at hNav1.7, hNav1.3, hNav1.4, hNaV1.5 and rNav1.8, respectively. TC-N 1752 also inhibits tetrodotoxin-sensitive sodium channels. TC-N 1752 shows analgesic efficacy in the Formalin model of pain[1][2][3].

Invitro

TC-N 1752 (compound 52) state-dependently inhibits Nav1.7, with IC50 of 170 nM on channels that are 20% inactivated and IC50 of 3.6 μM on fully noninactivated channels[1].TC-N 1752 inhibits hNav1.7, hNav1.8, hNav1.9, rNav1.9, and mNav1.9 with IC50s of 0.2, 0.1, 1.6, 0.5 and 1.4 μM, respectively[2].

In Vivo

TC-N 1752 (compound 52) (3-30 mg/kg; p.o.) dose-dependently shows analgesic effect in the Formalin model[1].TC-N 1752 (3-30 mg/kg; p.o.) decreases thermal hyperalgesia produced by inflammation[3].TC-N 1752 (5 mg/mL; 500 μL; i.v.) attenuates complete Freund’s adjuvant (CFA)-induced sensitization of C-fiber nociceptors[3]. Animal Model:

Name

TC-N 1752

CAS

1211866-85-1

Formula

C25H27F3N6O3

Molar Mass

516.52

Appearance

Solid

Transport

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Reference

[1]. Bregman H, et, al. Identification of a potent, state-dependent inhibitor of Nav1.7 with oral efficacy in the formalin model of persistent pain. J Med Chem. 2011 Jul 14;54(13):4427-45. [2]. Lin Z, et, al. Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells. PLoS One. 2016 Aug 24;11(8):e0161450. [3]. Matson DJ, et, al. Inhibition of Inactive States of Tetrodotoxin-Sensitive Sodium Channels Reduces Spontaneous Firing of C-Fiber Nociceptors and Produces Analgesia in Formalin and Complete Freund's Adjuvant Models of Pain. PLoS One. 2015 Sep 17;10(9):e013

PeptideDB

TC-N 1752

CAS: 1211866-85-1 F: C25H27F3N6O3 W: 516.52