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Nav1.7 inhibitor (compound II), a sulfonamide, is a potent Nav1.7 inhibitor. Nav1.7 inhibitor has the potential for a wide range of disorders, particularly pain [1].
Nav1.1 activator 1 (compound 4), a highly potent Nav1.1 activator with BBB penetration, increases decay time constant τ of Nav1.1 currents at 0.03 μM along with significant selectivity against Nav1.2,Nav1.5, and Nav1.6[1].
NAV1 Human Pre-designed siRNA Set A contains three designed siRNAs for NAV1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Nav1.8-IN-7 (Example 116) is a selective Nav1.8 inhibitor. Nav1.8-IN-7 shows an inhibition of >50% with 100 nM for Nav1.8. Nav1.8-IN-7 inhibits hERG with an IC50 of 15.6 μM. Nav1.8-IN-7 has the potential for pain research [1].
Nav1.8-IN-15 (compound 6) is a potent Nav1.8 inhibitor. Nav1.8-IN-15 shows analgesic effect. Nav1.8-IN-15 has the potential for the research of chronic pain [1].
Nav1.8-IN-10 (Compound 6) is a Nav1.8 channel inhibitor. When the concentration is 4 nM, the percentage blocking rate of Nav1.8 channel is 79.4%. Nav1.8-IN-10 can be used in the study of pain disorders [1].
Nav1.8-IN-5 (Example 1) is a voltage-gated sodium channelNav1.8 inhibitor. Nav1.8-IN-5 can be used for Nav1.8-mediated diseases, such as pain and pain-related disorders, as well as cardiovascular diseases (such as atrial fibrillation) research [1].
Nav1.7-IN-8 is a potent blockage of NaV1.7 with high selectivity for the inhibition of NaV1.7 over the subtypes hNaV1.1 and hNaV1.5. Nav1.7-IN-8 inhibits CYP2C9 and CYP3A4 with an IC50 of 0.17 μM and 0.077 μM, respectively. Nav1.7-IN-8 displays significant analgesic effects in rodent models of acute and inflammatory pain [1].
Nav1.8-IN-2 (compound 35A) is a potent Nav1.8 inhibitor with an IC50 value of 0.4 nM. Nav1.8-IN-2 can be used for researching pain disorders, cough disorders, and acute and chronic itch disorders [1].
Nav1.8-IN-6 (Compound 2j) is a novel pyridinone amide Nav1.8 channel inhibitor. The IC50 values in the resting state and semi-activated state are 513.33 and 471.81 nM, respectively. Nav1.8-IN-6 has analgesic activity [1].
Nav1.7-IN-3 is a selective, orally bioavailable voltage-gated sodium channel Nav1.7 inhibitor with an IC50 of 8 nM. Pain relief. Limited CNS penetration [1].
Nav1.7-IN-18 (Compound 31) is a Nav1.7 inhibitor with a Ki value of 4.9 nM and an IC50 of 13 nM, showing analgesic effects in transgenic mice with inherited erythromelalgia (IEM) [1].
Nav1.8-IN-1 (Compound 31) is a potent inhibitor of Na(v)1.8 sodium channel. Nav1.8-IN-1 has the potential for the research of inflammatory and neuropathic pain [1].
Nav1.3 channel inhibitor 1 (compound 15b) is a state-dependent voltage-gated sodium channel Nav1.3 inhibitor (IC50=20 nM). Nav1.3 channel inhibitor 1 can penetrate the blood-brain barrier and can be used in the research of nervous system diseases [1].
Nav1.7-IN-13 (compound 3g) is a sodium channel inhibitor that significantly inhibits Veratridine (HY-N6691)-induced neuronal activity. Nav1.7-IN-13 inhibits total Na+ current in DRG neurons in a concentration-dependent manner; slows down the activation of Navs. Nav1.7-IN-13 significantly alleviated mechanical pain behavior in a rat model of nerve injury (SNI) and had analgesic activity [1].
NaV1.2/1.6 channel blocker-1 is a potent NaV1.2/1.6 channel blocker, with IC50s of 9.8 and 24.4 μM for rNaV1.6 and hNaV1.2, respectively. NaV1.2/1.6 channel blocker-1 can be used for the research of generalized epilepsy [1].
Nav1.7 blocker 1 (example 41) is a Na + channel (Nav) blocker with an IC50 value of 0.037 μM. Nav1.7 blocker 1 can be used for the study of pain, including neuropathic pain, postoperative pain, inflammatory pain, and so on [1].
NaV1.7 inhibitor-1 is an efficacious voltage-gated sodium channel (NaV) 1.7 inhibitor with an IC50 of 0.6 nM for hNaV1.7, exhibits 80-fold selectivity versus hNaV1.5 [1].
GsAF-I is a potent Nav and hERG1 channels blocker with IC50s of 0.36, 0.6, 1.28, 0.33, 1.2, 0.04 and 4.8 μM against Nav1.1,Nav1.2,Nav1.3,Nav1.4,Nav1.6,Nav1.7 and hERG1, respectively [1].
Lu AE98134, an activator of voltage-gated sodium channels, acts as a partly selective Nav1.1 channels positive modulator. Lu AE98134 also increases the activity of Nav1.2 and Nav1.5 channels but not of 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].
ICA-121431 is a nanomolar potent and broad-spectrum voltage-gated sodium channel (Nav) blocker, shows equipotent selectivity for human Nav1.1 and Nav1.3 subtypes with IC50 values of 13 nM and 23 nM, respectively. ICA-121431 shows less potent inhibition of Nav1.2 (IC50=240 nM) and 1,000 fold selectivity against Nav1.4,Nav1.6, and the TTX-resistant human Nav1.5 and Nav1.8 channels (IC50s >10 μM).
GrTx1 is a peptide toxin originally isolated from the venom of the spider Grammostola rosea. GrTx1 blocks sodium channel， with IC50s of 0.63 µM, 0.23 µM, 0.77 µM, 1.29 µM, 0.63 µM and 0.37 µM for Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6 and Nav1.7, repectively [2].GrTx1 can be used for neurological disease research [1].
Huwentoxin-IV is a potent and selective sodium channel blocker, inhibits neuronal Nav1.7, Nav1.2, Nav1.3 and Nav1.4 with IC50s of 26, 150, 338 and 400 nM, respectively. Huwentoxin-IV preferentially blocks peripheral nerve subtype Nav1.7 by binding neurotoxin receptor site 4. Huwentoxin-IV has analgesic effects on animal models of inflammatory and neuropathic pain [1] .
Huwentoxin-IV TFA is a potent and selective sodium channel blocker, inhibits neuronal Nav1.7, Nav1.2, Nav1.3 and Nav1.4 with IC50s of 26, 150, 338 and 400 nM, respectively. Huwentoxin-IV TFA preferentially blocks peripheral nerve subtype Nav1.7 by binding neurotoxin receptor site 4. Huwentoxin-IV TFA has analgesic effects on animal models of inflammatory and neuropathic pain [1] .
Phrixotoxin 3 TFA is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 TFA modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
Phrixotoxin 3 is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
Heteropodatoxin-1 (HpTx1), a spider peptide toxin, is a Kv4.2 current inhibitor. Heteropodatoxin-1 also inhibits Nav1.7 and activates Nav1.9 but does not affect Nav1.8 [1].
LTGO-33 is a potent and selective voltage-gated sodium channel NaV1.8 inhibitor. LTGO-33 inhibits NaV1.8 in the nM potency range and exhibits over 600-fold selectivity against human NaV1.1-NaV1.7 and NaV1.9. LTGO-33 exhibits state-independent inhibition with similar potencies on channels in the closed and inactivated conformations. LTGO-33 inhibits native TTX-R NaV1.8 currents in non-human primate and human DRG neurons, where it reduces action potential firing. LTGO-33 can be used for pain disorders research [1].
Ceratotoxin-1 (CcoTx1), a peptide toxin, is an voltage-gated sodium channel subtypes inhibitor. Ceratotoxin-1 inhibits Nav1.1/β1, Nav1.2/β1, Nav1.4/β1, and Nav1.5/β1 with IC50 of 523 nM, 3 nM, 888 nM, and 323 nM, respectively. Ceratotoxin-1 also inhibits Nav1.8/β1[1].
3'-Methoxydaidzein is a isoflavone and a Sodium Channel inhibitor. 3'-Methoxydaidzein inhibits subtypes NaV1.7, NaV1.8 and NaV1.3 with IC50 of 181 nM, 397 nM, and 505 nM, respectively. 3'-Methoxydaidzein exerts analgesic activity by inhibiting voltage-gated sodium channels [1].
Phlo1a (μ-TrTx-Phlo1a) is a peptide toxin contains 35-amino acid residues. Phlo1b is a selective Nav1.7 inhibitor. Phlo1a has a weak inhibitory effect on Nav1.2 and Nav1.5 [1].
Phrixotoxin 3-NH2 TFA is a derivative of Phrixotoxin 3 TFA (HY-P1218A). Phrixotoxin 3 TFA is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 TFA modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
Phlo1b (μ-TrTx-Phlo1b) is a peptide toxin contains 35-amino acid residues. Phlo1b is a selective Nav1.7 inhibitor. Phlo1b has a weak inhibitory effect on Nav1.2 and Nav1.5 [1].
PF-04856264 is a potent and selective Nav1.7 inhibitor, with IC50s of 28, 131, 19, and 42 nM for human, mouse, cynomolgus monkey and dog Nav1.7, respectively. PF-04856264 has low potency against the rat Nav1.7 channel. PF-04856264 shows analgesic effect [1] .
GTx1-15 is an inhibitor cystine knot (ICK) peptide that inhibits the voltage-dependent calcium channel Cav3.1 and the voltage-dependent sodium channels Nav1.3 and Nav1.7[1].
Funapide (TV 45070; XEN402) is a potent inhibitor of the sodium channel Nav1.7, Nav1.8 and other Nav channels expressed in the peripheral nervous system. Fornabil is an orally effective analgesic agent [1] .
Tap1a (Theraphotoxin-Tap1a) is a spider venom peptide that inhibits sodium channels with IC50s of 80 nM and 301 nM against Nav1.7 and Nav1.1, respectively. Tap1a shows analgesic effects [1].
XPC-5462 is a NaV1.6 and NaV1.2 inhibitor with the IC50s of 10.9 nM and 10.3 nM, respectively. XPC-5462 suppresses epileptiform activity in an ex vivo brain slice seizure model [1].
Methocarbamol is an orally active central muscle relaxant and blocks muscular Nav1.4 channel. Methocarbamol reversibly affects voltage dependence of inactivation of Nav1.4 channel. Methocarbamol has the potential for muscle spasms and pain syndromes research [1] .
(R)-Funapide ((R)-TV 45070) is the less active R-enantiomer of Funapide. Funapide is a potent inhibitor of the sodium channel Nav1.7, Nav1.8 and other Nav channels expressed in the peripheral nervous system. Fornabil is an orally effective analgesic agent [1] .
Analgesic agent-2 is a selective and orally active NaV1.8 Channel inhibitor, with an IC50 of 50.18 nM in HEK293 cells stably expressing human NaV1.8 channel. Analgesic agent-2 has analgesic activity [1].
PF-05661014, a desmethyl analogue of PF-06526290, selectively inhibits Nav1.3 and Nav1.7 currents by stabilizing inactivated channels via interaction with D4 VSD. PF-05661014 can be used for research of sodium channel modulation [1].
ABBV-318 is a potent Nav1.7/ Nav1.8 blocker, with IC50s of 2.8 μM and 3.8 μM for hNav1.7 and hNav1.8, respectively. ABBV-318 can be used for the research of pain [1].
δ-Theraphotoxin-Hm1b is a 42-amino acid peptide isolated from Togo starburst tarantula (Heteroscodra maculata) venom. δ-Theraphotoxin-Hm1b selectively inhibits inactivation of NaV1.1 but have no effect on NaV1.7 [1].
GsAF-II is a peptide toxin that blocks hERG1 subtype potassium channels in a voltage-dependent manner. GsAF-II blocks Nav1.x subtype sodium channels[1].
XPC-6444 is a highly potent, isoform-selective, and CNS-penetrant NaV1.6 inhibitor (IC50=41 nM for hNaV1.6). XPC-6444 also displays potent block of NaV1.2 (IC50=125 nM). XPC-6444 shows anticonvulsant activity [1].
ProTx II is a selective blocker of Nav1.7 sodium channels with an IC50 of 0.3 nM, and is at least 100-fold selective for Nav1.7 over other sodium channel subtypes. ProTx-II inhibits sodium channels by decreasing channel conductance and shifting activation to more positive potentials and blocks action potential propagation in nociceptors [1] .
AZ194 is a first-in-class, orally active inhibitor of CRMP2-Ubc9 interaction and inhibitor of NaV1.7(IC50=1.2 μM). AZ194 blocks SUMOylation of CRMP2 to selectively reduce the amount of surface-expressed NaV1.7. Antinociceptive effects [1].
ProTx II TFA is a selective blocker of Nav1.7 sodium channels with an IC50 of 0.3 nM, and is at least 100-fold selective for Nav1.7 over other sodium channel subtypes. ProTx-II inhibits sodium channels by decreasing channel conductance and shifting activation to more positive potentials and blocks action potential propagation in nociceptors [1] .
Methocarbamol (Standard) is the analytical standard of Methocarbamol. This product is intended for research and analytical applications. Methocarbamol is an orally active central muscle relaxant and blocks muscular Nav1.4 channel. Methocarbamol reversibly affects voltage dependence of inactivation of Nav1.4 channel. Methocarbamol has the potential for muscle spasms and pain syndromes research [1] .
KGP-25 is an inhibitor of voltage-gated sodium channel 1.8 (Nav1.8), which can be used for analgesia by targeting Nav1.8 in the peripheral nervous system (PNS). KGP-25 can also target γ-aminobutyric acid subtype A receptor (GABAA) in the central nervous system (CNS) for general anesthesia [1].
PF-05186462 is a potent and selective inhibitor of human Nav1.7 voltage-dependent sodium channel, with an IC50 of 21 nM. PF-05186462 shows significant selectivity for Nav1.7 versus other sodium channels (Nav 1.1, 1.2, 1.3, 1.4, 1.5, 1.6, and 1.8). PF-05186462 can be used for the research of acute or chronic pain [1].
GX-585 is a sulfonamide analog that acts as a Nav1.7 channel inhibitor, demonstrating analgesic activity in treating neuropathic pain and inflammation.
AM-0466 is a sodium channel inhibitor with nanomolar levels of NaV1.7 inhibitory activity. AM-0466 exhibits potent pharmacodynamic activity in a NaV1.7-dependent histamine-induced itch model. AM-0466 also showed significant analgesic effects in capsaicin-induced pain models. After optimizing its pharmacokinetic properties, AM-0466 was advanced into in vivo targeting and efficacy models for testing [1].
PF-06305591 is a potent and highly selective voltage gated sodium channel NaV1.8 blocker, with an IC50 of 15 nM. An excellent preclinical in vitro ADME and safety profile [1].
GNE-0439 is a novel Nav1.7-selective inhibitor with IC50 of 0.34 uM and inhibits Nav1.5 with an IC50 of 38.3 μM. GNE-0439 inhibits mutant N1742K channels (IC50=0.37 uM) in membrane potential assays. GNE-0439 possesses a carboxylic acid group, binds outside of the channel pore, and is unique compared with known selective VSD4 binders [1].
PF-05150122 is a novel potent and selective human Nav1.7 channel blocker with the activity of inhibiting human pain signaling. PF-05150122 exhibited favorable biopharmacokinetic parameters in microdose studies, providing a basis for exploring its application in acute or chronic pain inhibition. The pharmacokinetic model of PF-05150122 predicted that at the corresponding oral dose, it could effectively reduce the 50% inhibitory concentration (IC50) of Nav1.7, demonstrating its inhibitory potential [1].
PF-06305591 dihydrate is a potent and highly selective voltage gated sodium channel NaV1.8 blocker, with an IC50 of 15 nM. An excellent preclinical in vitro ADME and safety profile [1].
PF-04885614 is a potent NaV1.8 inhibitor, extracted from patent US2018328915. PF-04885614 has potential for neurological and neurodevelopmental diseases treatment [1].
PF-06456384 is a highly potent and selective NaV1.7 inhibitor with an IC50 of 0.01 nM. PF-06456384 has the potential for formalin pain model research [1].
PF-06456384 trihydrochloride is a highly potent and selective NaV1.7 inhibitor with an IC50 of 0.01 nM. PF-06456384 trihydrochloride has the potential for formalin pain model research [1].
Hm1a is a disulfide-rich spider-venom peptide, and a NaV1.1 activator. Hm1a restores the function of inhibitory interneurons in Dravet syndrome (DS) mouse model [1].
Zorevunersen sodium is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen sodium is used for the study of Dravet syndrome.
ST-2560 is a selective inhibitor of the NaV1.7 sodium channel with IC50 value of 39 nM. ST-2560 can be used to study pain behavior and cardiovascular models [1].
PF-05198007 is a potent, orally active and selective arylsulfonamide Nav1.7 inhibitor. PF-05198007 is a compound with a similar pharmacodynamic profile to PF-05089771 [1] .
Suzetrigine phenol is the phenolate form of the sodium channel modulator Suzetrigine (HY-148800). Suzetrigine (VX-548) is an orally active and highly selective inhibitor of NaV1.8 [1] .
AZD-3161 is a potent and selective blocker of NaV1.7 channel, with a pIC50 of 7.1. AZD-3161 can be used for the research of neuropathic and inflammatory pain [1] .
Flecainide acetate (R-818) is a class 1C antiarrhythmic agent especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
Zorevunersen (STK-001) is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen is used for the study of Dravet syndrome.
Cyfluthrin is a type II pyrethroid and has effects on various insects. Cyfluthrin is a modulator of Nav1.8 sodium channels by repetitive stimulation. Cyfluthrin can be applied in agriculture,veterinary, insecticide,pyrethroid and stored product [1] .
OD1 is a scorpion α-toxin that can be isolated from the venom of the Iranian yellow scorpion (Odonthobuthus doriae. OD1 is a modulator of mammalian Nav1.7 (EC50: 4.5 nM) [1] .
GS-462808 is an oral active late sodium current inhibitor (Late INai) of the cardiac Nav1.5 channel with the IC50 of 1.33 μM. GS-462808 can be used for study of arrhythmia [1].
XEN907 is a potent and spirooxindole blocker of NaV1.7, with an IC50 of 3 nM. XEN907 also inhibits CYP3A4 in a recombinant human enzyme assay. XEN907 can be used for the research of pain [1] .
δ-Buthitoxin-Hj2a, a scorpion-venom peptide, is a potent NaV1.1 agonist with an EC50 of 32 nM. δ-Buthitoxin-Hj2a can be used for the Dravet syndrome (DS) research [1].
δ-Buthitoxin-Hj1a, a scorpion-venom peptide, is a potent NaV1.1 agonist with an EC50 of 17nM. δ-Buthitoxin-Hj1a can be used for the Dravet syndrome (DS) research [1].
Phlotoxin-1 (PhlTx1) is a 34-amino acid and 3-disulfide bridge peptide. Phlotoxin-1 can be isolated from Phlogiellus genus spider. Phlotoxin-1 is an antinociceptive agent by inhibiting NaV1.7 channel [1] .
Jingzhaotoxin XI (JZTX-XI) is a sodium conductance inhibitor with an IC50 of 124 nM. Jingzhaotoxin XI slows the fast inactivation (EC50=1.18±0.2 μM) of Nav1.5 expressed in Chinese hamster ovary (CHO-K1) cells [1].
DS-1971a is a potent, selective, and orally active NaV1.7 inhibitor, with IC50s of 22.8 and 59.4 nM for hNaV1.7 and mNaV1.7, respectively. DS-1971a exerts analgesic effects [1].
Suzetrigine (VX-548) is an orally active and highly selective NaV1.8 inhibitor that acts as an analgesic. Suzetrigine is also a blocker of sodium channel protein type 10 subunit alpha. Suzetrigine is promising for research of acute pain after abdominoplasty and bunionectomy [1] .
Jingzhaotoxin-III is a potent and selective blocker of Nav1.5 channels, with an IC50 of 348 nM, and shows no effect on other sodium channel isoforms. Jingzhaotoxin-III can selectively inhibit the activation of cardiac sodium channel but not neuronal subtypes, and hopefully represents an important ligand for discriminating cardiac VGSC subtype [1] .
Flecainide (acetate) (Standard) is the analytical standard of Flecainide (acetate). This product is intended for research and analytical applications. Flecainide acetate (R-818) is a class 1C antiarrhythmic agent especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
AA43279 is an in gamma-aminobutyric acid (GABA) fast-firing interneurons located activator for Nav1.1 channel(SCN1A) with an EC50 of 9.5 μM. AA43279 enhances specific neuronal firing activity in vitro, and exhibits anticonvulsant activity in rat MEST model [1].
δ-Theraphotoxin-Hm1a toxin is a selective Nav1.1 activator. δ-Theraphotoxin-Hm1a toxin elicits pain and touch sensitivity. δ-Theraphotoxin-Hm1a toxin can be used for the research of irritable bowel syndrome [1].
Cn2 toxin TFA (β-Mammal toxin Cn2 TFA) is a single-chain β-scorpion neurotoxic peptide that is the main toxin in scorpion venom. Cn2 toxin (TFA) specifically targets mammalian voltage-gated sodium channels (VGSC) Nav1.6 [1].
Veratridine (3-Veratroylveracevine) is a plant neurotoxin, a voltage-gated sodium channels (VGSCs) agonist. Veratridine inhibits the peak current of Nav1.7, with an IC50 of 18.39 µM. Veratridine regulates sodium ion channels mainly by activating sodium ion channels, preventing channel inactivation and increasing sodium ion flow [1] .
(Rac)-AMG8379 ((Rac)-AMG8380) is a racemate of AMG8379. AMG8379 is a potent, orally active and selective sulfonamide antagonist of NaV1.7, with IC50s of 8.5 and 18.6 nM for hNaV1.7 and mNaV1.7, respectively [1].
Zorevunensen (STK-001) negative control is the negative control form of Zorevunensen (HY-148410). Zorevunensen is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen is used for the study of Dravet syndrome [1] .
Neoline (Bullatine B)) is the active ingredient of the active ingredient (PA), which can be used to cure the disease. Neoline Flow Suppression Nav1.7 Electrical Flow Control (VGSC)，Improve diabetes mechanical pain sensitivity. Neoline has a list of compounds that can be used, research on its use, and the quality of its processing during processing in pain.
GDC-0276 is a potent, selective, reversible and orally active NaV1.7 inhibitor with an IC50 value of 0.4 nM. GDC-0276 is well tolerated and exhibits a good pharmacokinetic profile. GDC-0276 has the potential for the treatment of pain and to address shortcomings of existing pain medications, such as addiction and off-target side effects [1].
AMG8380, an orally active and less active enantiomer of AMG8379, can serves as a negative control. AMG8380 inhibits human and mouse voltage-gated sodium channel NaV1.7 with IC50s of 0.907 and 0.387 μM, respectively. AMG8380 blocks Tetrodotoxin (TTX)-sensitive native channels with an IC50 of 2560 nM [1].
VSTx-3 is a KV channel blocker. VSTx-3 is demonstrated to be a potent, TTX-sensitive sodium channel blocker and especially, a potent blocker of NaV1.8 channels (IC50 0.19 μM for hNaV1.3, 0.43 μM for hNaV1.7 and 0.77 μM for hNaV1.8 channels).
PF 05089771 is a potent, orally active and selective arylsulfonamide Nav1.7 inhibitor, with IC50 values of 11 nM, 12 nM, 13 nM, 171 nM and 8 nM for hNav1.7,cynNav1.7,dogNav1.7,ratNav1.7, and musNav1.7, respectively. PF 05089771 is under the study for pain and diabetic neuropathy [1] .
PF 05089771 tosylate is a potent, orally active and selective arylsulfonamide Nav1.7 inhibitor, with IC50 values of 11 nM, 12 nM, 13 nM, 171 nM and 8 nM for hNav1.7,cynNav1.7,dogNav1.7,ratNav1.7, and musNav1.7, respectively. PF 05089771 is under the study for pain and diabetic neuropathy [1] .
A-803467 is a potent and selective tetrodotoxin-resistant Nav1.8 sodium channel blocker (IC50=8 nM). A-803467 has shown significant anti-nociception in neuropathic and inflammatory pain models. A-803467 enhances the chemosensitivity of conventional anticancer agents through interaction with the ATP-binding cassette subfamily G member 2 (ABCG2) transporter [1] .
AMG8379 is a potent, orally active and selective sulfonamide antagonist of the voltage-gated sodium channel NaV1.7, with IC50s of 8.5 and 18.6 nM for hNaV1.7 and mNaV1.7, respectively. AMG8379 potently and reversibly blocks endogenous Tetrodotoxin (TTX)-sensitive sodium channels in dorsal root ganglia (DRG) neurons with an IC50 of 3.1 nM [1].
DS43260857 is a potentNaV1.7inhibitor, which has a high inhibitory effect on both human and mouse NaV1.7. The IC50 values of DS43260857 for hNaV1.1, hNaV1.5, hNaV1.7, mNaV1.7 are 6.6, 14, 0.015 and 0.061 μM, respectively [1].
Scorpion toxin Tf2 is a β-scorpion toxin, which is firstly identified in the venom of the Brazilian scorpion Tityus fasciolatus. Scorpion toxin Tf2 is a Nav1.3 activator, which is a neuronal voltage-gated sodium (Nav) subtype implicated in epilepsy and nociception. Scorpion toxin Tf2 enhances hNav1.3 activation voltage and opens the channel at resting membrane potentials [1].
Veratridine (Standard) is the analytical standard of Veratridine. This product is intended for research and analytical applications. Veratridine (3-Veratroylveracevine) is a plant neurotoxin, a voltage-gated sodium channels (VGSCs) agonist. Veratridine inhibits the peak current of Nav1.7, with an IC50 of 18.39?μM. Veratridine regulates sodium ion channels mainly by activating sodium ion channels, preventing channel inactivation and increasing sodium ion flow [1] .
VGSC blocker-1 is a potent and small molecule blocker of neonatal isoform of the VGSC subtype, Nav1.5 (nNav1.5). VGSC blocker-1 blocks INa peak currents 34.9% at 1 μM and inhibits cell invasion 0.3% at 1 μM in human breast cancer cell line MDA-MB-231, without affecting the cell viability [1].
ProTx-III is a selective and potent inhibitor of voltage-gated sodium channel Nav1.7, with an IC50 of 2.1 nM. ProTx-III is a spider venom peptide isolated from the venom of the Peruvian green velvet tarantella. ProTx-III has a typical inhibitor cystine knot motif (ICK). ProTx-III is able to reverse the pain response. ProTx-III can be used to study diseases such as chronic pain, epilepsy, and arrhythmia [1].
VGSCs-IN-1 (compound 14), a 2-piperazine analog of Riluzole (HY-B0211), is a human voltage-gated sodium channels (VGSCs) inhibitor. VGSCs-IN-1 shows great Nav1.4 blocking activity. VGSCs-IN-1 has a pKa of 7.6 and a cLog P of 2.4. VGSCs-IN-1 can be used for cell excitability disorders research [1].
Anticonvulsant agent 5 (Compound 5c) exhibits high affinity for GABAA receptors and NaV1.3 receptors. Anticonvulsant agent 5 shows anticonvulsant efficacy in mice psychomotor epilepsy test with an ED50 of 107 mg/kg. Anticonvulsant agent 5 exhibits neuroprotective activity against Kainic acid (HY-N2309) with an IC50 of 113 μM. Anticonvulsant agent 5 is blood-brain barrier (BBB) penetrable [1].
Bifenthrin is a synthetic pyrethroid insecticide. Bifenthrin prolongs the opening time of Nav1.8 sodium channels, leading to membrane depolarization and conductance block in the insect nervous system, thereby disrupting neural function. Bifenthrin was effective in inhibiting A. gambiae (LD50=0.15 ng/mg) and C. quinquefasciatus (LD50=0.16 ng/mg). Bifenthrin has good lethality against susceptible and resistant mosquitoes and is very effective in inhibiting blood sucking and can be developed as a mosquito-removal netting material [1] .
GNE-616 is a highly potent, metabolically stable, orally bioavailable, and subtype selective Nav1.7 inhibitor (Ki of 0.79 nM and Kd of 0.38 nM for hNav1.7) for the treatment of chronic pain. GNE-616 shows >1000 nM Kd and >2500-fold selectivity over hNav1.1, hNav1.3, hNav1.4, and hNav1.5. Selectivity over hNav1.2 and hNav1.6 is more modest at 31- and 73-fold, respectively [1].
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] .
Bifenthrin (Standard) is the analytical standard of Bifenthrin. This product is intended for research and analytical applications. Bifenthrin is a synthetic pyrethroid insecticide. Bifenthrin prolongs the opening time of Nav1.8 sodium channels, leading to membrane depolarization and conductance block in the insect nervous system, thereby disrupting neural function. Bifenthrin was effective in inhibiting A. gambiae (LD50=0.15 ng/mg) and C. quinquefasciatus (LD50=0.16 ng/mg). Bifenthrin has good lethality against susceptible and resistant mosquitoes and is very effective in inhibiting blood sucking and can be developed as a mosquito-removal netting material [1] .
Mambalgin 1 TFA is a selective ASIC1a inhibitor (IC50 values are 192 and 72 nM for human ASIC1a and ASIC1a/1b dimer, respectively). Mambalgin 1 TFA binds to closed/inactive channel. Mambalgin 1 TFA is selective for ASIC1a over ASIC2a, ASIC3, TRPV1, P2X2, 5-HT3, Nav1.8, Cav3.2 and Kv1.2 channels. Mambalgin 1 TFA increases latency of withdrawal response in mouse tail-flick and paw-flick tests.
m3-Huwentoxin IV (m3-HwTx-IV) is a potent NaV inhibitor with IC50s of 3.3, 6.8, 7.2, 8.4, 11.9 and 369 nM against hNaV1.7,hNaV1.6,hNaV1.3,hNaV1.1,hNaV1.2 and hNaV1.4, respectively in QPatch assay. m3-Huwentoxin IV dose-dependently suppresses spontaneous pain induced by the NaV1.7 activator OD1 in a rodent pain model [1].
μ-TRTX-Hd1a, a spider venom, is a selective NaV 1.7 inhibitor. μ-TRTX-Hd1a is a gating modifier that inhibits human NaV 1.7 by interacting with the S3b-S4 paddle motif in channel domain II [1].
AMTB hydrochloride is a selective TRPM8 channel blocker. AMTB hydrochloride inhibits icilin-induced TRPM8 channel activation with a pIC50 of 6.23. AMTB hydrochloride can be used for the research of the overactive bladder and painful bladder syndrome. AMTB hydrochloride is a non-selective inhibitor of voltage-gated sodium channels (NaV) .
Relutrigine (PRAX-562) is an orally active inhibitor of persistent sodium channel. Relutrigine potently and preferentially inhibits persistent INa induced by ATX-II (Nav 1.5 activator) or the SCN8A mutation N1768D with IC50 values of 141 nM and 75 nM, respectively. Relutrigine exhibits potent use-dependent block and reduces neuronal intrinsic excitability. Relutrigine has effective anticonvulsant activity [1].
GFB-8438 is a potent and subtype selective TRPC5 inhibitor, with IC50s of 0.18 and 0.29 μM of hTRPC5 and hTRPC4, respectively. GFB-8438 shows excellent selectivity against TRPC6, other TRP family members, NaV 1.5, as well as limited activity against the hERG channel. GFB-8438 protects mouse podocytes from injury induced by protamine sulfate model [1].
Huwentoxin-IV TFA is a potent and selective sodium channel blocker, inhibits neuronal Nav1.7, Nav1.2, Nav1.3 and Nav1.4 with IC50s of 26, 150, 338 and 400 nM, respectively. Huwentoxin-IV TFA preferentially blocks peripheral nerve subtype Nav1.7 by binding neurotoxin receptor site 4. Huwentoxin-IV TFA has analgesic effects on animal models of inflammatory and neuropathic pain [1] .
Phrixotoxin 3-NH2 TFA is a derivative of Phrixotoxin 3 TFA (HY-P1218A). Phrixotoxin 3 TFA is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 TFA modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
GsAF-I is a potent Nav and hERG1 channels blocker with IC50s of 0.36, 0.6, 1.28, 0.33, 1.2, 0.04 and 4.8 μM against Nav1.1,Nav1.2,Nav1.3,Nav1.4,Nav1.6,Nav1.7 and hERG1, respectively [1].
GrTx1 is a peptide toxin originally isolated from the venom of the spider Grammostola rosea. GrTx1 blocks sodium channel， with IC50s of 0.63 µM, 0.23 µM, 0.77 µM, 1.29 µM, 0.63 µM and 0.37 µM for Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6 and Nav1.7, repectively [2].GrTx1 can be used for neurological disease research [1].
Huwentoxin-IV is a potent and selective sodium channel blocker, inhibits neuronal Nav1.7, Nav1.2, Nav1.3 and Nav1.4 with IC50s of 26, 150, 338 and 400 nM, respectively. Huwentoxin-IV preferentially blocks peripheral nerve subtype Nav1.7 by binding neurotoxin receptor site 4. Huwentoxin-IV has analgesic effects on animal models of inflammatory and neuropathic pain [1] .
Phrixotoxin 3 TFA is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 TFA modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
Phrixotoxin 3 is a potent blocker of voltage-gated sodium channels, with IC50s of 0.6, 42, 72, 288, 610 nM for NaV1.2, NaV1.3, NaV1.4, NaV1.1 and NaV1.5, respectively. Phrixotoxin 3 modulates voltage-gated sodium channels with properties similar to those of typical gating-modifier toxins, both by causing a depolarizing shift in gating kinetics and by blocking the inward component of the sodium current [1].
Heteropodatoxin-1 (HpTx1), a spider peptide toxin, is a Kv4.2 current inhibitor. Heteropodatoxin-1 also inhibits Nav1.7 and activates Nav1.9 but does not affect Nav1.8 [1].
Ceratotoxin-1 (CcoTx1), a peptide toxin, is an voltage-gated sodium channel subtypes inhibitor. Ceratotoxin-1 inhibits Nav1.1/β1, Nav1.2/β1, Nav1.4/β1, and Nav1.5/β1 with IC50 of 523 nM, 3 nM, 888 nM, and 323 nM, respectively. Ceratotoxin-1 also inhibits Nav1.8/β1[1].
Phlo1a (μ-TrTx-Phlo1a) is a peptide toxin contains 35-amino acid residues. Phlo1b is a selective Nav1.7 inhibitor. Phlo1a has a weak inhibitory effect on Nav1.2 and Nav1.5 [1].
Phlo1b (μ-TrTx-Phlo1b) is a peptide toxin contains 35-amino acid residues. Phlo1b is a selective Nav1.7 inhibitor. Phlo1b has a weak inhibitory effect on Nav1.2 and Nav1.5 [1].
GTx1-15 is an inhibitor cystine knot (ICK) peptide that inhibits the voltage-dependent calcium channel Cav3.1 and the voltage-dependent sodium channels Nav1.3 and Nav1.7[1].
Tap1a (Theraphotoxin-Tap1a) is a spider venom peptide that inhibits sodium channels with IC50s of 80 nM and 301 nM against Nav1.7 and Nav1.1, respectively. Tap1a shows analgesic effects [1].
δ-Theraphotoxin-Hm1b is a 42-amino acid peptide isolated from Togo starburst tarantula (Heteroscodra maculata) venom. δ-Theraphotoxin-Hm1b selectively inhibits inactivation of NaV1.1 but have no effect on NaV1.7 [1].
GsAF-II is a peptide toxin that blocks hERG1 subtype potassium channels in a voltage-dependent manner. GsAF-II blocks Nav1.x subtype sodium channels[1].
ProTx II is a selective blocker of Nav1.7 sodium channels with an IC50 of 0.3 nM, and is at least 100-fold selective for Nav1.7 over other sodium channel subtypes. ProTx-II inhibits sodium channels by decreasing channel conductance and shifting activation to more positive potentials and blocks action potential propagation in nociceptors [1] .
ProTx II TFA is a selective blocker of Nav1.7 sodium channels with an IC50 of 0.3 nM, and is at least 100-fold selective for Nav1.7 over other sodium channel subtypes. ProTx-II inhibits sodium channels by decreasing channel conductance and shifting activation to more positive potentials and blocks action potential propagation in nociceptors [1] .
Hm1a is a disulfide-rich spider-venom peptide, and a NaV1.1 activator. Hm1a restores the function of inhibitory interneurons in Dravet syndrome (DS) mouse model [1].
OD1 is a scorpion α-toxin that can be isolated from the venom of the Iranian yellow scorpion (Odonthobuthus doriae. OD1 is a modulator of mammalian Nav1.7 (EC50: 4.5 nM) [1] .
δ-Buthitoxin-Hj2a, a scorpion-venom peptide, is a potent NaV1.1 agonist with an EC50 of 32 nM. δ-Buthitoxin-Hj2a can be used for the Dravet syndrome (DS) research [1].
δ-Buthitoxin-Hj1a, a scorpion-venom peptide, is a potent NaV1.1 agonist with an EC50 of 17nM. δ-Buthitoxin-Hj1a can be used for the Dravet syndrome (DS) research [1].
Phlotoxin-1 (PhlTx1) is a 34-amino acid and 3-disulfide bridge peptide. Phlotoxin-1 can be isolated from Phlogiellus genus spider. Phlotoxin-1 is an antinociceptive agent by inhibiting NaV1.7 channel [1] .
Jingzhaotoxin XI (JZTX-XI) is a sodium conductance inhibitor with an IC50 of 124 nM. Jingzhaotoxin XI slows the fast inactivation (EC50=1.18±0.2 μM) of Nav1.5 expressed in Chinese hamster ovary (CHO-K1) cells [1].
Jingzhaotoxin-III is a potent and selective blocker of Nav1.5 channels, with an IC50 of 348 nM, and shows no effect on other sodium channel isoforms. Jingzhaotoxin-III can selectively inhibit the activation of cardiac sodium channel but not neuronal subtypes, and hopefully represents an important ligand for discriminating cardiac VGSC subtype [1] .
δ-Theraphotoxin-Hm1a toxin is a selective Nav1.1 activator. δ-Theraphotoxin-Hm1a toxin elicits pain and touch sensitivity. δ-Theraphotoxin-Hm1a toxin can be used for the research of irritable bowel syndrome [1].
Cn2 toxin TFA (β-Mammal toxin Cn2 TFA) is a single-chain β-scorpion neurotoxic peptide that is the main toxin in scorpion venom. Cn2 toxin (TFA) specifically targets mammalian voltage-gated sodium channels (VGSC) Nav1.6 [1].
VSTx-3 is a KV channel blocker. VSTx-3 is demonstrated to be a potent, TTX-sensitive sodium channel blocker and especially, a potent blocker of NaV1.8 channels (IC50 0.19 μM for hNaV1.3, 0.43 μM for hNaV1.7 and 0.77 μM for hNaV1.8 channels).
Scorpion toxin Tf2 is a β-scorpion toxin, which is firstly identified in the venom of the Brazilian scorpion Tityus fasciolatus. Scorpion toxin Tf2 is a Nav1.3 activator, which is a neuronal voltage-gated sodium (Nav) subtype implicated in epilepsy and nociception. Scorpion toxin Tf2 enhances hNav1.3 activation voltage and opens the channel at resting membrane potentials [1].
Cd1a is a β-toxin derived from the African spider Ceratogyrus darlingi. Cd1a can regulate calcium ion channels. Cd1a inhibits human calcium ion channels (Cav2.2)(IC502.6 μM) and mouse sodium ion channels (Nav1.7). Cd1a can be used in the development of peripheral pain treatment drugs [1].
ProTx-III is a selective and potent inhibitor of voltage-gated sodium channel Nav1.7, with an IC50 of 2.1 nM. ProTx-III is a spider venom peptide isolated from the venom of the Peruvian green velvet tarantella. ProTx-III has a typical inhibitor cystine knot motif (ICK). ProTx-III is able to reverse the pain response. ProTx-III can be used to study diseases such as chronic pain, epilepsy, and arrhythmia [1].
Mambalgin 1 TFA is a selective ASIC1a inhibitor (IC50 values are 192 and 72 nM for human ASIC1a and ASIC1a/1b dimer, respectively). Mambalgin 1 TFA binds to closed/inactive channel. Mambalgin 1 TFA is selective for ASIC1a over ASIC2a, ASIC3, TRPV1, P2X2, 5-HT3, Nav1.8, Cav3.2 and Kv1.2 channels. Mambalgin 1 TFA increases latency of withdrawal response in mouse tail-flick and paw-flick tests.
m3-Huwentoxin IV (m3-HwTx-IV) is a potent NaV inhibitor with IC50s of 3.3, 6.8, 7.2, 8.4, 11.9 and 369 nM against hNaV1.7,hNaV1.6,hNaV1.3,hNaV1.1,hNaV1.2 and hNaV1.4, respectively in QPatch assay. m3-Huwentoxin IV dose-dependently suppresses spontaneous pain induced by the NaV1.7 activator OD1 in a rodent pain model [1].
μ-TRTX-Hd1a, a spider venom, is a selective NaV 1.7 inhibitor. μ-TRTX-Hd1a is a gating modifier that inhibits human NaV 1.7 by interacting with the S3b-S4 paddle motif in channel domain II [1].
Anti-SCN9a/Nav1.7 Antibody is a human antibody expressed in CHO, targeting SCN9a/Nav1.7. Anti-SCN9a/Nav1.7 Antibody has a huIgG1 heavy chain and a huκ light chain, with a predicted molecular weight (MW) of 150 kDa. The isotype control for Anti-SCN9a/Nav1.7 Antibody can be referenced as Human IgG1 kappa, Isotype Control (HY-P99001).
3'-Methoxydaidzein is a isoflavone and a Sodium Channel inhibitor. 3'-Methoxydaidzein inhibits subtypes NaV1.7, NaV1.8 and NaV1.3 with IC50 of 181 nM, 397 nM, and 505 nM, respectively. 3'-Methoxydaidzein exerts analgesic activity by inhibiting voltage-gated sodium channels [1].
Veratridine (3-Veratroylveracevine) is a plant neurotoxin, a voltage-gated sodium channels (VGSCs) agonist. Veratridine inhibits the peak current of Nav1.7, with an IC50 of 18.39 µM. Veratridine regulates sodium ion channels mainly by activating sodium ion channels, preventing channel inactivation and increasing sodium ion flow [1] .
Neoline (Bullatine B)) is the active ingredient of the active ingredient (PA), which can be used to cure the disease. Neoline Flow Suppression Nav1.7 Electrical Flow Control (VGSC)，Improve diabetes mechanical pain sensitivity. Neoline has a list of compounds that can be used, research on its use, and the quality of its processing during processing in pain.
Veratridine (Standard) is the analytical standard of Veratridine. This product is intended for research and analytical applications. Veratridine (3-Veratroylveracevine) is a plant neurotoxin, a voltage-gated sodium channels (VGSCs) agonist. Veratridine inhibits the peak current of Nav1.7, with an IC50 of 18.39?μM. Veratridine regulates sodium ion channels mainly by activating sodium ion channels, preventing channel inactivation and increasing sodium ion flow [1] .
VSD4-NaV1.7-NaVPas Protein, Human (HEK293, Flag, Strep) is the recombinant human-derived VSD4-NaV1.7-NaVPas, expressed by HEK293 , with Strep, Flag labeled tag. ,
Zorevunersen sodium is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen sodium is used for the study of Dravet syndrome.
NAV1 Human Pre-designed siRNA Set A contains three designed siRNAs for NAV1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Zorevunersen (STK-001) is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen is used for the study of Dravet syndrome.
Zorevunensen (STK-001) negative control is the negative control form of Zorevunensen (HY-148410). Zorevunensen is an antisense oligonucleotide that is intended to increase the level of productive SCN1A mRNA and consequently increase the expression of the sodium channel Nav1.1 protein. Zorevunersen is used for the study of Dravet syndrome [1] .
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