nav1.1

Nav1.1 activator 1 is a highly potent activator of Nav1.1 with BBB penetration.

Nav1.1-IN-B is a selective NaV1.1 inhibitor which reduces visceral hypersensitivity.

Lu AE98134, an activator of voltage-gated sodium channels, acts as a partly selective positive modulator of Nav1.1 channels and also increases the activity of Nav1.2 and Nav1.5 channels while not affecting Nav1.4, Nav1.6, and Nav1.7 channels. Lu AE98134 can be used to analyze pathophysiological functions of the Nav1.1 channel in various central nervous system diseases, including cognitive restoring in schizophrenia, et al[1].

GDC-0310 is a selective, orally available Nav1.7 inhibitor with an IC50 of 0.6 nM for human Nav1.7, suitable for pain research.

AA43279 is a novel selective Nav1.1 activator, increasing the firing activity of parvalbumin-expressing, fast-spiking GABAergic interneurons and increasing the spontaneous inhibitory post-synaptic currents (sIPSCs) recorded from pyramidal neurons.

ICA-121431 (2,2-Diphenyl-N-[4-(thiazol-2-ylsulfamoyl) is a nanomolar potent small molecule Nav1.7 channel inhibitor with IC50 of 19 nM for rat Nav1.7, with little or no activity against human Nav1.5 or Nav1.7 channels.

PF-05089771 is a voltage-gated sodium channel 1.7 (Nav1.7) blocker (IC50: 11, 16, 33, and 20 nM for 5N11S, 5A11L, 5A11S, and 5A11L Nav1.7 splice variants, respectively). It is selective for Nav1.7 over Nav1.1-1.6 and 1.8 channels (IC50: 0.11-25 μM), L-typ

Phrixotoxin 3 TFA is a potent inhibitor of voltage-gated sodium channels, with IC50 values of 0.6 nM for NaV1.2, 42 nM for NaV1.3, 72 nM for NaV1.4, 288 nM for NaV1.1, and 610 nM for NaV1.5. This compound modulates the activity of these channels similarly to traditional gating-modifier toxins, inducing a depolarizing shift in gating kinetics and obstructing the inward sodium current.

GrTx1, a peptide toxin derived from Grammostola rosea spider venom, selectively inhibits sodium channels Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6, and Nav1.7, with IC50 values of 0.63 µM, 0.23 µM, 0.77 µM, 1.29 µM, 0.63 µM, and 0.37 µM, respectively [2]. This compound has applications in neurological disease research [1].

Hm1a, a disulfide-rich spider-venom peptide and NaV1.1 activator, reestablishes the function of inhibitory interneurons in a Dravet syndrome (DS) mouse model [1].

δ-Theraphotoxin-Hm1b, a 42-amino acid peptide derived from the Togo starburst tarantula (Heteroscodra maculata) venom, selectively inhibits the inactivation of NaV1.1 channels without affecting NaV1.7 channels [1].

δ-Theraphotoxin-Hm1a is a selective NaV1.1 activator that induces pain and touch sensitivity, with potential applications in irritable bowel syndrome research [1].

δ-Buthitoxin-Hj2a, a potent scorpion-venom peptide, acts as a NaV1.1 agonist with an EC50 value of 32 nM and is employed in Dravet syndrome (DS) research [1].

δ-Buthitoxin-Hj1a, a scorpion-venom peptide, functions as a potent agonist for the NaV1.1 channel with an EC50 value of 17 nM, and is applicable in research on Dravet syndrome (DS) [1].

GsAF-I is a potent blocker of Na_v and hERG1 channels, exhibiting half-maximal inhibitory concentrations (IC50s) of 0.36 μM (Na_v 1.1), 0.6 μM (Na_v 1.2), 1.28 μM (Na_v 1.3), 0.33 μM (Na_v 1.4), 1.2 μM (Na_v 1.6), 0.04 μM (Na_v 1.7), and 4.8 μM (hERG1) [1].

Ceratotoxin-1 (CcoTx1) is a peptide toxin that functions as an inhibitor of various voltage-gated sodium channel subtypes. It selectively inhibits Nav1.1/β1, Nav1.2/β1, Nav1.4/β1, and Nav1.5/β1 with IC50 values of 523 nM, 3 nM, 888 nM, and 323 nM, respectively. Additionally, Ceratotoxin-1 is known to inhibit Nav1.8/β1 [1].

Theraphotoxin-Tap1a (Tap1a) is a spider venom-derived peptide that acts as an inhibitor of sodium channels, displaying IC50 values of 80 nM for Na v 1.7 and 301 nM for Na v 1.1. It demonstrates analgesic effects [1].

LTGO-33 is a species-specific inhibitor of the voltage-gated sodium channel NaV1.8, inhibiting NaV1.8, NaV1.1-NaV1.7, and NaV1.9.LTGO-33 inhibits wild-type and multiple NaV1.8 variants associated with human pain disorders and can be used for the study of pain.hBChE-IN-2 is a low affinity Nurr1 agonist.

Potent blocker of voltage-gated sodium channels (IC50 values are 0.6, 42, and 72 nM for NaV1.2, NaV1.3 and NaV1.5 respectively). Blocks inward sodium currents in a voltage-dependent manner.

Potent Nav1.7 blocker (IC50 = 2.5 nM). Also inhibits Nav1.1, Nav1.2, Nav1.3 and Nav1.6 in the nanomolar range. Exhibits no effects on Cav channels or nAChR at 5 μM. Demonstrates analgesic activity in vivo; antagonizes effects of scorpion-venom toxin OD1 a