channels

GsMTx4 TFA (1209500-46-8 free base) (GsMTx4 TFA) is a spider venom peptide that selectively inhibits cationic permeable mechanically-sensitive channels (MSCs) belonging to the Piezo and TRP channel families.

Oligopeptide-68 Acetate is a peptide. It is a novel whitening ingredient that mimics the binding of TGF-β to cell surface receptors to reduce induced and hereditary pigmentation by inhibiting MITF intramolecular channels to achieve whitening and brightening effects.

CALP3 acetate is a potent Ca2+ channel blocker that activates EF hand motifs of Ca2+-binding proteins. CALP3 acetate can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin (CaM), Ca2+ channels and pumps.

Apamin acetate (Apamine acetate) is a selective Ca2+-activated blocker of K+ (SK) channels, an 18-amino acid peptide neurotoxin found in bee toxins.Apamin acetate enhances synapse growth and regeneration following laceration injury to cortical neurons.Apamin acetate has anti-inflammatory and anti-fibrotic effects.

CALP1 acetate is a calmodulin (CaM) agonist (Kd of 88 µM) that binds to the CaM EF-hand/Ca2+-binding site. CALP1 blocks calcium influx and apoptosis (IC50 of 44.78 µM) by inhibiting the open of calcium channel. CALP1 blocks glutamate receptor channels and blocks a store-operated nonselective cation channel. CALP1 activates CaM-dependent phosphodiesterase activity.

Ziconotide Acetate (107452-89-1 free base) (Prialt) is an analgesic agent and has been used to treat neuropathic and non-neuropathic pain. Ziconotide Acetate (107452-89-1 free base) acts by binding to N-type calcium channels situated on the terminal part of primary afferent neurons of the nociceptive pathway therefore reducing synaptic transmission with potent antinociceptive effects.

TAT-Gap19 TFA, a Cx mimetic peptide and specific connexin43 hemichannel (Cx43 HC) inhibitor, does not inhibit the corresponding Cx43 gap junction channels (GJCs). It crosses the blood-brain barrier and has been shown to alleviate liver fibrosis in mice [1] [2] [3].

Apamin (Apamine) is an 18 amino acid peptide neurotoxin found in apitoxin (bee venom), is known as a specifically selective blocker of Ca2+-activated K+ (SK) channels and exhibits anti-inflammatory and anti-fibrotic activity. Apamin is a bee venom compone

Calciseptine, a neurotoxin isolated from the Black Mamba (Dendroaspis p. polylepis) venom, comprises 60 amino acids and is stabilized by four disulfide bonds. It specifically targets and blocks L-type calcium channels [1].

VSTx-3 is a potassium voltage-gated channel (K_V) blocker, which has also been shown to be a potent tetrodotoxin-sensitive (TTX-sensitive) sodium channel inhibitor, with particular efficacy against NaV1.8 channels, as evidenced by its half-maximal inhibitory concentration (IC_50) values of 0.19 μM for hNaV1.3, 0.43 μM for hNaV1.7, and 0.77 μM for hNaV1.8 channels.

Neurotoxin that blocks neuromuscular transmission via irreversible inhibition of nicotinic ACh receptors (nAChRs). Prevents opening of nicotinic receptor-associated ion channels and is selective for α7 receptors over α3β4 receptors (IC50 values are 1.6 nM

Iota-conotoxin RXIA, an agonist of voltage-gated sodium channels (Na v 1.2, 1.6, 1.7), has been shown to induce repetitive action potentials and seizure in the motor axons of frogs following intracranial injection in mice [1].

Cn2 toxin, a β-toxin, interacts with the voltage-sensing domain of voltage-gated sodium channels (NaV) [1].

Peptide neurotoxin; selectively and reversibly blocks N-type calcium channels (IC50 = 0.15 nM). Reduces (RS)-3,5-DHPG -induced long term depression in vivo.

Potent and selective KV11.1 (hERG) channel blocker. Selective for KV11.1 over a panel of 14 other potassium channels. Dose-dependently prolongs QTc interval in isolated rabbit heart.

Chlorotoxin is a 36-amino acid peptide found in the venom of the deathstalker scorpion (Leiurus quinquestriatus) which blocks small-conductance chloride channels.

Iberiotoxin (TFA) is a selective inhibitor of high conductance Ca2+-activated K+ channels, exhibiting a dissociation constant (Kd) of approximately 1 nM, yet it does not inhibit other types of voltage-dependent ion channels [1] [2] [3].

Tityustoxin-Kα (TsTx-Kα) acts as an inhibitor of potassium voltage-gated channels, exhibiting a dose-dependent blockade of the sustained outward current in cultured hippocampal neurons [1].

ATX-II TFA, a specific Na+ channel modulator toxin, is derived from the venom of the sea anemone (Anemonia sulcata). This compound impedes the inactivation of Na+ channels and has been associated with arrhythmogenesis in the pulmonary vein and atrial fibrillation [1] [2]. It interacts with halothane, caffeine, and ryanodine in this modulation.

Potent KV1.3 channel blocker (IC50 = 36 pM). Displays no effect at calcium-activated channels. Reduces VEGF-induced transmembrane calcium influxes and nitric oxide production in human endothelial cells.

NaV1.5 channels blocker

Selective CaV3.1 channel blocker (IC50 values are 0.2 and 31.8 μM for hCaV3.1 and hCaV3.2 respectively). Also reversibly inhibits NaV1.8 and blocks KV2.1 channels.

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

Gap19 TFA is a selective and potent blocker of connexin 43 (Cx43) hemichannels, originating from nine amino acids within the Cx43 cytoplasmic loop (CL). It operates by hindering intramolecular interactions between the C-terminus (CT) and the CL, effectively inhibiting hemichannel activity without affecting GJ channels or Cx40/pannexin-1 hemichannels. This peptide offers protective benefits for the myocardium.

Very high affinity ClC-2 blocker (apparent KD ~ 50 pM). Slows ClC-2 activation and inhibits slow-gating but does not inhibit open ClC-2 channels. Selective for ClC-2 over other ClC family members (ClC-0, ClC-1, ClC-3 and ClC-4), CFTR, GABAC, CaCC and KV1.

Peptide neurotoxin; wide spectrum blocker of N, P and Q type calcium channels.

Kaliotoxin is an inhibitor of neuronal BK-type peptide groups and specifically inhibits Kv channels and calcium-activated potassium channels. Kaliotoxin has research significance on the regulation of cell membrane potential and neuronal excitability. The product number is T37808 and the CAS number is 145199-73-1

Cell-permeable calmodulin (CaM) agonist that binds to the EF-hand/Ca2+-binding site; produces CaM-dependent activation of phosphodiesterase. Also binds to cytoplasmic sites on other Ca2+ channels, including NMDA and HIV-1 gp120-activated channels, inhibit

ω-Agatoxin IVA TFA is a potent selective inhibitor of P/Q type Ca2+ (Cav2.1) channels, exhibiting IC50 values of 2 nM for P-type and 90 nM for Q-type channels. It effectively inhibits glutamate exocytosis and calcium influx induced by high potassium, with IC50 ranging from 30 to 225 nM. Additionally, this compound blocks high potassium-induced serotonin and norepinephrine release, while having no impact on L-type or N-type calcium channels [1][2].

Kurtoxin is a selective Cav3 (T-type) voltage-gated Ca2+ channel gating inhibitor, exhibiting a dissociation constant (Kd) of 15 nM for the Cav3.1 (α1G T-type) Ca2+ channel. The compound demonstrates high-affinity interactions with native neuronal high-threshold L-type, N-type, and P-type Ca2+ channels in both central and peripheral neurons, while also displaying cross-reactivity with the voltage-gated Na+ channel [1].

ATX-II, an Na+ channel modulator toxin derived from the sea anemone (Anemonia sulcata), causes delayed inactivation of the Na+ channels and has been linked to pulmonary vein arrhythmogenesis and atrial fibrillation [1] [2]. It exhibits interaction with halothane, caffeine, and ryanodine.

Ergtoxin-1, a potassium channel blocker isolated from the venom of the Mexican scorpion Centruroides noxius, inhibits ERG-K+ channels in nerve, heart, and endocrine cells [1].

TRPC1/6 and Piezo2 inhibitor. Exhibits same effect as L-enantiomer, GsMTx4 (Cat. No. 4912) on TRPC channels. Inhibits mechanosensitive currents by ~70%. Protects against myocardial infarction in mouse ischemia/reperfusion model. Resistant to proteolytic digestion.

Selective blocker of CaV2.1 P/Q-type calcium channels.

Nociceptin (1-13), amide is a potent ORL1 (OP4) receptor agonist with a pEC50 of 7.9 for mouse vas deferens and a Ki of 0.75 nM for binding to rat forebrain membranes.

Acid-sensing ion channel 3 (ASIC3) channel blocker (IC50 values are 63 and 175 nM for homomeric rat and human ASIC3 channels). Also inhibits NaV1.8 and NaV1.2 channels (IC50 values are 55 and 114 nM respectively). Demonstrates analgesic properties against

Imperatoxin A, a peptide toxin sourced from the African scorpion Pandinus imperator, functions as an activator of Ca2+-release channels/ryanodine receptors (RyRs), facilitating increased Ca2+ flow from the sarcoplasmic reticulum into the cell [1].

Tamapin TFA, a venom peptide isolated from the Indian red scorpion (Mesobuthus tamulus) [1], selectively targets and blocks small conductance Ca(2+)-activated K(+) (SK) channels, particularly the SK2 subtype (Potassium Channel). It is known to inhibit SK channel-mediated currents in the hippocampal pyramidal neurons.

Phrixotoxin 2 selectively blocks the KV 4.2 and KV 4.3 channels, demonstrating high specificity in its interaction with these voltage-gated ion channels [1].

MitTx-alpha, a component of the complex MitTx, acts as a powerful and enduring agonist specifically targeting acid-sensing ion channels (ASICs), with a pronounced selectivity for ASIC1 under neutral pH conditions. At lower pH levels (pH<6.5), MitTx significantly amplifies (over 100-fold) the activation of ASIC2a channels induced by protons [1].

Huwentoxin I (HWTX-I) is a peptide toxin that targets and inhibits both voltage-gated sodium channels and N-type calcium channels. It effectively inhibits sodium channels in the rat hippocampus and cockroach dorsal unpaired median (DUM) neurons, displaying IC50 values of 66.1 nM and 4.80 nM, respectively [1].

μ-Conotoxin Sx IIIA is a biologically active peptide that functions as a blocker of NaV1.4 channels.

Aam-KTX, a toxic peptide sourced from Mesobuthus eupeus scorpion venom, acts as a selective K_v channel inhibitor, exhibiting IC_50 values of 1.1 nM for K_v1.3 channels and >750 nM for K_v1.1 channels. This compound shows promise for research in autoimmune diseases [1].

Hemitoxin, a scorpion-venom peptide, functions as a K+ channel blocker and selectively inhibits rat Kv1.1, Kv1.2, and Kv1.3 channels expressed in Xenopus oocytes, with respective IC50 values of 13 nM, 16 nM, and 2 nM [1].

Jingzhaotoxin-X (JZTX-X) selectively inhibits Kv4.2 and Kv4.3 potassium channels, resulting in prolonged mechanical hyperalgesia [1].

CALP3 TFA is a potent Ca2+ channel blocker that activates EF-hand motifs of Ca2+-binding proteins. It can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin, Ca2+ channels, and pumps.

Potent and reversible Kv3.4 potassium channel blocker (IC50 = 47 nM); also attenuates inactivation of sodium currents by acting on Nav1.7 and Nav1.3 channels. Enhances TTX-sensitive sodium currents in rat small dorsal root ganglion neurons. Neuroprotective.

D-GsMTx4 TFA, a selective spider venom peptide, is a TRPC1/6 and Piezo2 inhibitor that inhibits cation-permeable mechanosensitive channels (MSCs) belonging to the Piezo and TRP channel families, blocks cation-selective stretch-activated channels (SACs), and attenuates lysophosphatidylcholine (LPC)-induced astrocyte toxicity and microglia reactivity. toxicity and microglia reactivity.D-GsMTx4 TFA prevented myocardial infarction in a mouse model of ischemia/reperfusion and can be used to characterize the role of excitatory MSCs in normal physiology and pathology.

Potent rat Nav1.7, human Nav1.4 and rat Nav1.6 channel activator (EC50 values are 7, 10 and 47 nM, respectively). Exhibits minimal activation at mammalian Nav1.2, Nav1.3 and Nav1.5 (EC50 values >3 μM). Inhibits fast inactivation on all channels. Increases

Apamin TFA (Apamine TFA) is a toxin found in bee venom. It is a potent blocker of small conductance Ca2+-activated K+ (SK, KCa2) channels that is more effective at SK2 than SK1 and SK3.