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Phlotoxin-1 (PhlTx1) 是一种含有 34 个氨基酸和 3-二硫键的多肽。Phlotoxin-1 可以从<i>Phlogiellus</i>属蜘蛛中分离出来。Phlotoxin-1 是一种通过抑制 <b>NaV1.7</b> 通道而发挥作用的抗伤害试剂。
" in MedChemExpress (MCE) Product Catalog:
3
Isotope-Labeled Compounds
Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
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- HY-13985
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Sodium Channel
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Neurological Disease
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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].
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- HY-126429
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5160
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PhlTx1
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Sodium Channel
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Inflammation/Immunology
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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] .
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- HY-RS09046
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Small Interfering RNA (siRNA)
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Others
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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.
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NAV1 Human Pre-designed siRNA Set A
NAV1 Human Pre-designed siRNA Set A
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- HY-160588
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Sodium Channel
Potassium Channel
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Neurological Disease
|
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].
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-
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- HY-160589
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Sodium Channel
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Neurological Disease
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Nav1.8-IN-8 (Compound A11) is a Nav1.8 channel inhibitor. Nav1.8-IN-8 may prevent associated diseases mediated by sodium ion channels (NaV) .
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-
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- HY-160591
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Sodium Channel
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Neurological Disease
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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].
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- HY-160593
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-
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- HY-162246
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Sodium Channel
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Cardiovascular Disease
Neurological Disease
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Nav1.8-IN-5 (Example 1) is a voltage-gated sodium channel Nav1.8 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].
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- HY-160592
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Sodium Channel
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Neurological Disease
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Nav1.8-IN-11 (Example 1) is a Nav1.8 channel inhibitor with a IC50 value of 0.1 nM. Nav1.8-IN-11 can be used in the study of pain disorders [1].
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- HY-155635
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Sodium Channel
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Infection
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Nav1.8-IN-4 (compound 9a) is a Nav1.8 channel inhibitor (IC50=0.014 μM). Nav1.8-IN-4 can be used for research on pain-related diseases [1].
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- HY-141547
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Sodium Channel
Cytochrome P450
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Inflammation/Immunology
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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].
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- HY-116194
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-
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- HY-143481
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Sodium Channel
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Neurological Disease
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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].
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- HY-102998
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-
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- HY-161272
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Sodium Channel
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Neurological Disease
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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].
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- HY-101789
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Sodium Channel
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Neurological Disease
|
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].
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- HY-132133
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-
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- HY-155058
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Sodium Channel
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Neurological Disease
|
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].
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- HY-19366
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Nav1.7-IN-2 is an inhibitor of voltage-gated sodium channels (Nav), in particular Nav 1.7, with IC50 of 80 nM.
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- HY-162347
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Sodium Channel
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Neurological Disease
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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].
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- HY-152166
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Sodium Channel
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Neurological Disease
|
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].
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- HY-160663
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Sodium Channel
|
Neurological Disease
Inflammation/Immunology
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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].
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- HY-119934
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5795
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Sodium Channel
Potassium Channel
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Neurological Disease
|
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].
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- HY-133910
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Sodium Channel
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Neurological Disease
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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].
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- HY-16787
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Sodium Channel
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Cardiovascular Disease
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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).
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- HY-P5164
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Sodium Channel
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Neurological Disease
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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].
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- HY-125079
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-
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- HY-P1220
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P1220A
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P1218A
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Sodium Channel
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Neurological Disease
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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].
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- HY-P1218
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Sodium Channel
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Neurological Disease
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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].
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- HY-126985
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Anhydroepitetrodotoxin
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Sodium Channel
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Neurological Disease
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4,9-Anhydrotetrodotoxin is a selective voltage-gated sodium channel (VGSC) inhibitor that blocks Nav1.1 and Nav1.6 in human brain and induces a hyperpolarizing shift in the voltage dependence of inactivated Nav1.6 [1].
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- HY-P5786
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-
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- HY-103623
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-
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- HY-157802
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5811
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CcoTx1; β-TRTX-cm1a
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Sodium Channel
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Neurological Disease
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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].
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- HY-101383
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Sodium Channel
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Neurological Disease
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PF-01247324 is a selective and orally bioavailable Nav1.8 channel blocker with an IC50 of 196 nM for recombinant human Nav1.8 channel.
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- HY-N1847
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5801
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μ-TrTx-Phlo1a
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Sodium Channel
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Neurological Disease
|
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].
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- HY-100727
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-
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- HY-P5800
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μ-TrTx-Phlo1b
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Sodium Channel
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Neurological Disease
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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].
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- HY-12811
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P5793
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-
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- HY-P5865
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Theraphotoxin-Tap1a; TRTX-Tap1a; µ/ω-TRTX-Tap1a
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Sodium Channel
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Neurological Disease
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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].
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- HY-157786
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Sodium Channel
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Neurological Disease
|
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].
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- HY-B0262
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Sodium Channel
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Neurological Disease
|
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] .
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- HY-149944
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Sodium Channel
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Inflammation/Immunology
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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].
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-
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- HY-P5810
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CcoTx2; β-TRTX-cm1b
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Sodium Channel
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Neurological Disease
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Ceratotoxin-2 (CcoTx2) is a voltage-gated sodium channel blocker with IC50s of 8 nM and 88 nM against Nav1.2/β1 and Nav1.3/β1, respectively [1].
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- HY-16723
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- HY-146069
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Sodium Channel
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Neurological Disease
|
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].
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- HY-105283
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-
- HY-P1681
-
-
- HY-112279
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-
- HY-P5336
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- HY-B0262S1
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Sodium Channel
|
Neurological Disease
|
Methocarbamol-d3 is the deuterium labeled Methocarbamol. 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][2][3].
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- HY-P5781
-
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Sodium Channel
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Neurological Disease
|
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].
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- HY-P5177
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-
- HY-P5861
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- HY-128772
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Sodium Channel
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Neurological Disease
|
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].
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- HY-P1221
-
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Sodium Channel
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Neurological Disease
|
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] .
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- HY-145169
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Sodium Channel
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Neurological Disease
|
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].
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- HY-P1221A
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Sodium Channel
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Neurological Disease
|
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] .
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- HY-122001
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Sodium Channel
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Neurological Disease
|
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].
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- HY-12796
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Vixotrigine; GSK-1014802; CNV1014802
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Sodium Channel
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Neurological Disease
|
Raxatrigine (GSK-1014802) is a novel small molecule state-dependent sodium channel blocker; Nav1.7 sodium channel inhibitor.
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- HY-12796A
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Vixotrigine hydrochloride; GSK-1014802 hydrochloride; CNV1014802 hydrochloride
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Sodium Channel
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Neurological Disease
|
Raxatrigine hydrochloride (GSK-1014802 hydrochloride) is a novel small molecule state-dependent sodium channel blocker; Nav1.7 sodium channel inhibitor.
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- HY-131870
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-
- HY-B0262S2
-
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Isotope-Labeled Compounds
Sodium Channel
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Neurological Disease
|
Methocarbamol- 13C,d3 is the 13C- and deuterium labeled Methocarbamol. 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][2][3].
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- HY-139081
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-
- HY-P5808A
-
-
- HY-P5809
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-
- HY-155236
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-
- HY-B0262S
-
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Sodium Channel
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Metabolic Disease
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Methocarbamol-d5 is deuterium labeled Methocarbamol. Methocarbamol is an orally active central muscle relaxant and blocks muscular Nav1.4 channel[1].
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- HY-16723A
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(R)-TV 45070; (R)-XEN402
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Sodium Channel
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Neurological Disease
|
(R)-Funapide ((R)-TV 45070) is the less active R-enantiomer of Funapide. Funapide is a potent Nav1.7 sodium channel blocker that can be used for pain research [1].
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- HY-139346
-
-
- HY-114301
-
|
Sodium Channel
|
Neurological Disease
|
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].
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- HY-123824
-
|
Sodium Channel
|
Neurological Disease
|
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].
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-
- HY-114301A
-
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Sodium Channel
|
Neurological Disease
|
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].
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- HY-110325
-
|
Sodium Channel
|
Neurological Disease
|
PF-04885614 is a potent NaV1.8 inhibitor, extracted from patent US2018328915. PF-04885614 has potential for neurological and neurodevelopmental diseases treatment [1].
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- HY-118952
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|
Sodium Channel
|
Neurological Disease
|
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].
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- HY-118952A
-
|
Sodium Channel
|
Neurological Disease
|
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].
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-
- HY-118048
-
|
Sodium Channel
|
Neurological Disease
|
NAV 26 (compound 26) is a selective voltage-gated sodium channel Nav1.7 blocker with an IC50 of 0.37 μM. NAV 26 can be used for pain research [1].
|
-
- HY-123825
-
-
- HY-P5183
-
|
Sodium Channel
|
Neurological Disease
|
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].
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- HY-148410A
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STK-001 sodium
|
Sodium Channel
|
Others
|
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.
|
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- HY-157784
-
|
Sodium Channel
|
Neurological Disease
|
XPC-7724 is a selective Nav1.6 channel inhibitor with a IC50 value of 0.078 μM. XPC-7724 can be used in the study of neurological diseases [1].
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-
- HY-18689
-
|
iGluR
|
Neurological Disease
|
SYM2206 is a potent and non-competitive AMPA receptor antagonist, with an IC50 of 1.6 μM. SYM2206 blocks Nav1.6-mediated persistent currents [1] .
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- HY-12883A
-
|
Sodium Channel
|
Neurological Disease
|
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] .
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-
- HY-117714
-
|
Sodium Channel
|
Neurological Disease
|
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] .
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-
- HY-148800
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VX-548
|
Sodium Channel
|
Neurological Disease
|
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 [1] .
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- HY-17429
-
R-818
|
Sodium Channel
|
Cardiovascular Disease
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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.
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- HY-148410
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STK-001
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Sodium Channel
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Others
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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.
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- HY-B1837
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Sodium Channel
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Infection
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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] .
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- HY-P1443
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Sodium Channel
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Cancer
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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] .
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- HY-19958
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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] .
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- HY-P1952A
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Sodium Channel
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Neurological Disease
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µ-Conotoxin-CnIIIC acetate, a 22-residue conopeptide, is a potent antagonist of the voltage-gated NaV1.4 sodium channel with an IC50 of 1.3 nM acting at the neuromuscular junction. µ-Conotoxin-CnIIIC acetate has myorelaxant and analgesic effects [1].
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- HY-P5783
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5784
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Sodium Channel
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Neurological Disease
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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].
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Cat. No. |
Product Name |
Target |
Research Area |
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- HY-P5160
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PhlTx1
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Sodium Channel
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Inflammation/Immunology
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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] .
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- HY-P5795
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Sodium Channel
Potassium Channel
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Neurological Disease
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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].
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- HY-P5164
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Sodium Channel
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Neurological Disease
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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].
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- HY-P1220
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P1220A
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P1218A
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Sodium Channel
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Neurological Disease
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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].
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- HY-P1218
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5786
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- HY-P5811
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CcoTx1; β-TRTX-cm1a
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5801
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μ-TrTx-Phlo1a
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5800
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μ-TrTx-Phlo1b
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5793
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- HY-P5865
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Theraphotoxin-Tap1a; TRTX-Tap1a; µ/ω-TRTX-Tap1a
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5810
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CcoTx2; β-TRTX-cm1b
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Sodium Channel
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Neurological Disease
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Ceratotoxin-2 (CcoTx2) is a voltage-gated sodium channel blocker with IC50s of 8 nM and 88 nM against Nav1.2/β1 and Nav1.3/β1, respectively [1].
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- HY-P1681
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- HY-P5336
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- HY-P5781
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Sodium Channel
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Neurological Disease
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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].
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- HY-P5177
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- HY-P5861
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- HY-P1221
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P1221A
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Sodium Channel
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Neurological Disease
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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] .
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- HY-P5808A
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- HY-P5809
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- HY-P5183
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Sodium Channel
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Neurological Disease
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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].
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- HY-P1443
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Sodium Channel
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Cancer
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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] .
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- HY-P1952A
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Sodium Channel
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Neurological Disease
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µ-Conotoxin-CnIIIC acetate, a 22-residue conopeptide, is a potent antagonist of the voltage-gated NaV1.4 sodium channel with an IC50 of 1.3 nM acting at the neuromuscular junction. µ-Conotoxin-CnIIIC acetate has myorelaxant and analgesic effects [1].
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- HY-P5783
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|
Sodium Channel
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Neurological Disease
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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].
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- HY-P5784
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|
Sodium Channel
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Neurological Disease
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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].
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- HY-P5808
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Peptides
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Neurological Disease
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lota-conotoxin RXIA is an agonist of voltage-gated
sodium channels (Nav1.2, 1.6, 1.7). Iota-conotoxin RXIA
can induce repetitive action potential and seizure in motor axons of frogs
after intracranial injection in mice [1].
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Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
Cat. No. |
Product Name |
Chemical Structure |
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- HY-B0262S1
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Methocarbamol-d3 is the deuterium labeled Methocarbamol. 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][2][3].
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- HY-B0262S2
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Methocarbamol- 13C,d3 is the 13C- and deuterium labeled Methocarbamol. 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][2][3].
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- HY-B0262S
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Methocarbamol-d5 is deuterium labeled Methocarbamol. Methocarbamol is an orally active central muscle relaxant and blocks muscular Nav1.4 channel[1].
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