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Pathways Recommended:	Membrane Transporter/Ion Channel

Results for "

Nav channel function

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Apoptosis (4) ATP Synthase (4) Autophagy (4) Environmental Pollutants (2) Ferroptosis (4) Glutathione Peroxidase (4) Insecticide (1) Isotope-Labeled Compounds (1) Mitophagy (4) NOD-like Receptor (NLR) (4) PINK1/Parkin (4) Reactive Oxygen Species (ROS) (3) Reference Standards (2) Sodium Channel (9)
By Research Areas:	Cardiovascular Disease (4) Infection (1) Inflammation/Immunology (4) Neurological Disease (9)

Inhibitors & Agonists

Screening Libraries

Peptides

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-17355A

Dexpramipexole dihydrochloride 2 Publications Verification (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride	ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS)	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the *Na_v1.8* sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .

HY-B0824

Bifenthrin 1 Publications Verification	Environmental Pollutants Sodium Channel	Neurological Disease
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 .

HY-17355B

Dexpramipexole 2 Publications Verification (R)-Pramipexole; R-(+)-Pramipexole; KNS-760704	PINK1/Parkin Glutathione Peroxidase Sodium Channel ATP Synthase NOD-like Receptor (NLR) Mitophagy Ferroptosis Autophagy Apoptosis Reactive Oxygen Species (ROS)	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Dexpramipexole ((R)-Pramipexole) is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the *Na_v1.8* sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .

HY-133910

Lu AE98134 1 Publications Verification	Sodium Channel	Neurological Disease
Lu AE98134, an activator of voltage-gated sodium channels, acts as a partly selective **Na_v1.1 channels** positive modulator. Lu AE98134 also increases the activity of Na_v1.2 and Na_v1.5 channels but not of Na_v1.4, Na_v1.6 and Na_v1.7 channels. Lu AE98134 can be used to analyze pathophysiological functions of the Na_v1.1 channel in various central nervous system diseases, including cognitive restoring in schizophrenia, et al .

HY-P5152

Scorpion toxin Tf2	Sodium Channel	Neurological Disease
Scorpion toxin Tf2 is a selective human voltage-gated sodium channel Nav1.3 (hNav1.3) activator. Scorpion toxin Tf2 selectively shifts the channel's activation voltage to more negative values, enabling channel opening at resting membrane potentials. Scorpion toxin Tf2 can be used for the research of epilepsy, nociception (after spinal cord injury) .

HY-17355BS

Dexpramipexole-d3 dihydrochloride (R)-Pramipexole-d₃ dihydrochloride; R-(+)-Pramipexole-d₃ dihydrochloride; KNS-760704-d₃ dihydrochloride	Isotope-Labeled Compounds ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS)	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Dexpramipexole-d₃ ((R)-Pramipexole-d₃) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the *Na_v1.8* sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

HY-B0824R

Bifenthrin (Standard)	Reference Standards Sodium Channel	Neurological Disease
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 .

HY-17355AR

Dexpramipexole dihydrochloride (Standard) (R)-Pramipexole dihydrochloride (Standard); R-(+)-Pramipexole dihydrochloride (Standard); KNS-760704 dihydrochloride (Standard)	Reference Standards ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis	Cardiovascular Disease Neurological Disease Inflammation/Immunology
Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the *Na_v1.8* sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

HY-W040171

Tefluthrin	Insecticide Sodium Channel Environmental Pollutants	Infection Neurological Disease
Tefluthrin is a pyrethroid insecticide. Tefluthrin prolongs the opening time of **Nav1.6 sodium channels*, leading to membrane depolarization and conductance block in the insect nervous system, thereby disrupting neural function* .

Cat. No.	Product Name

HY-L923

Ion Channel Lead-like Compound Library	9000 compounds
Ion channels are key proteins on the cell membrane that regulate the flow of ions across membranes. They participate in nearly all physiological processes, including nerve conduction, muscle contraction, heart rhythm, and pain perception. Abnormalities in their function can lead to various serious diseases such as arrhythmia, epilepsy, hypertension, neuropathic pain, and cancer. Therefore, ion channels are highly valuable drug targets—over 15% of approved drugs target ion channels currently, demonstrating their irreplaceable therapeutic value in cardiovascular, neurological, and analgesic fields. MCE has collected a library of over 5,000 reported ion channel-related bioactive compounds targeting major sites such as Na+ channels, K+ channels, Ca2+ channels, GABA receptors, iGluRs, and others. Using AI models, these compounds are characterized through both 2D representations (molecular fingerprints, pharmacophores) and 3D representations (3D conformation) to screen for a collection of lead-like compounds highly similar to known active molecules. Additionally, an hERG channel prediction algorithm integrating XGB and ISE mapping strategy is employed to assess and exclude potential cardiotoxicity in the library.. This step significantly reduces safety risks in subsequent screenings, particularly for ion channel drug development related to cardiovascular systems (e.g., Nav1.5, Cav1.2), effectively minimizing failures due to hERG inhibition and serving as a valuable tool for ion channel drug screening.

Ion Channel Lead-like Compound Library

9000 compounds

Ion channels are key proteins on the cell membrane that regulate the flow of ions across membranes. They participate in nearly all physiological processes, including nerve conduction, muscle contraction, heart rhythm, and pain perception. Abnormalities in their function can lead to various serious diseases such as arrhythmia, epilepsy, hypertension, neuropathic pain, and cancer. Therefore, ion channels are highly valuable drug targets—over 15% of approved drugs target ion channels currently, demonstrating their irreplaceable therapeutic value in cardiovascular, neurological, and analgesic fields.

MCE has collected a library of over 5,000 reported ion channel-related bioactive compounds targeting major sites such as Na+ channels, K+ channels, Ca2+ channels, GABA receptors, iGluRs, and others. Using AI models, these compounds are characterized through both 2D representations (molecular fingerprints, pharmacophores) and 3D representations (3D conformation) to screen for a collection of lead-like compounds highly similar to known active molecules. Additionally, an hERG channel prediction algorithm integrating XGB and ISE mapping strategy is employed to assess and exclude potential cardiotoxicity in the library.. This step significantly reduces safety risks in subsequent screenings, particularly for ion channel drug development related to cardiovascular systems (e.g., Nav1.5, Cav1.2), effectively minimizing failures due to hERG inhibition and serving as a valuable tool for ion channel drug screening.

Cat. No.	Product Name	Target	Research Area

HY-P5152

Scorpion toxin Tf2	Sodium Channel	Neurological Disease
Scorpion toxin Tf2 is a selective human voltage-gated sodium channel Nav1.3 (hNav1.3) activator. Scorpion toxin Tf2 selectively shifts the channel's activation voltage to more negative values, enabling channel opening at resting membrane potentials. Scorpion toxin Tf2 can be used for the research of epilepsy, nociception (after spinal cord injury) .

Cat. No.	Product Name	Chemical Structure

HY-17355BS

Dexpramipexole-d3 dihydrochloride
Dexpramipexole-d₃ ((R)-Pramipexole-d₃) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the *Na_v1.8* sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

Dexpramipexole-d3 dihydrochloride

Dexpramipexole-d₃ ((R)-Pramipexole-d₃) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Na_v1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.

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