Ion Channel Modulators

ATX-II is a selective sodium channel modulator toxin. ATX-II enhances late sodium current, prevents full sodium channel inactivation, and generates persistent current fractions. ATX-II has pro-arrhythmic effect. ATX-II slows intrinsic heart rate, prolongs QT interval and sinus node recovery time, and causes sinus pauses and arrests. ATX-II can be used for the research of atrial fibrillation, long QT syndrome, and long QT3 syndrome.

BeKm-1 is a HERG (human ether-a-go-go-related gene) blocking compound. BeKm-1 can be used for the research of heart disease.

Charybdotoxin TFA, a 37-amino acid peptide, is a K⁺ channel blocker.

CALP3, a Ca²⁺-like peptide, is a potent Ca²⁺ channel blocker that activates EF hand motifs of Ca²⁺-binding proteins. CALP3 can functionally mimic increased [Ca²⁺]_i by modulating the activity of Calmodulin (CaM), Ca²⁺ channels and pumps. CALP3 has the potential in controlling apoptosis in diseases such as AIDS or neuronal loss due to ischemia.

Poneratoxin acetate is the acetate salt form of Poneratoxin (HY-P10234). Poneratoxin acetate is the modulator for voltage-gated sodium channel (NaV, EC₅₀ for NaV1.6 and NaV1.7 is 97 nM and 2.3 µM), that lowers the voltage threshold for activation and inhibits the inactivation of channels, enhances the excitability of neurons, and leads to the transmission of pain signals.

Guangxitoxin 1E TFA is the TFA salt form of Guangxitoxin 1E (HY-P1427). Guangxitoxin 1E TFA is a peptide toxin and a selective inhibitor for voltage-gated potassium channel K_V2.1 and K_V2.2 with IC₅₀ of 1-3 nM. Guangxitoxin 1E TFA enhances glucose-stimulated intracellular calcium ion oscillations and increases insulin secretion in a glucose-dependent manner.

Heteropodatoxin-2 (TFA), a peptides of 30-amino acid, is a heteropodatoxin. Heteropodatoxin-2 blocks Kv4.2 current expressed in Xenopus laevis oocytes in a voltage-dependent manner, with less block at more positive potentials.

Dendrotoxin K TFA is a Kv1.1 channel blocker. Dendrotoxin K TFA determines glutamate release in CA3 neurons in a time-dependent manner through the control of the presynaptic spike waveform.

Transdermal Peptide Disulfide TFA (TD 1 Disulfide(peptide) TFA) is a 11-amino acid peptide, binds to Na⁺/K⁺-ATPase beta-subunit (ATP1B1), and mainly interacts with the C-terminus of ATP1B1. Transdermal Peptide Disulfide TFA can enhance the transdermal delivery of many macromolecules.

Dendrotoxin-I (DTX-I) TFA is a potent K⁺ channel blocker with IC₅₀s of 0.13-50 nM for voltage-gated potassium channel subunits K_V1.1, K_V1.2 and K_V1.6. Dendrotoxin-I TFA, a neurotoxin, has the potential for cancer research.

CALP1 TFA is a calmodulin (CaM) agonist (K_d of 88 µM) with binding to the CaM EF-hand/Ca²⁺-binding site. CALP1 TFA blocks calcium influx and apoptosis (IC₅₀ of 44.78 µM) through inhibition of calcium channel opening. CALP1 TFA blocks glutamate receptor channels and blocks a store-operated nonselective cation channel. CALP1 TFA activates CaM-dependent phosphodiesterase activity.

MitTx is a complex formed by MitTx-α and MitTx-β. MitTx is an ASIC1 channel activator with EC₅₀ values of 9.4 and 23 nM for ASIC1a and ASIC1b isoforms, respectively. MitTx is highly selective for ASIC1 isoforms at neutral pH. Under acidic conditions, MitTx greatly enhances proton-evoked ASIC2a channel activation.

ω-Agatoxin IVA is a potent, selective P/Q type Ca²⁺ (Cav2.1) channel blocker with IC₅₀ values of 2 nM and 90 nM. ω-Agatoxin IVA inhibits glutamate exocytosis and calcium influx elicited by high potassium. ω-Agatoxin IVA inhibits Capsaicin (HY-10448)-induced CGRP release and vasodilation. ω-Agatoxin IVA can be used for the research of neurological and cardiovascular disease.

CALP2 TFA is a calmodulin (CaM) antagonist (K_d of 7.9 µM) with high affinity for binding to the CaM EF-hand/Ca²⁺-binding site. CALP2 TFA inhibits CaM-dependent phosphodiesterase activity and increases intracellular Ca²⁺ concentrations. CALP2 TFA potently inhibits of adhesion and degranulation. CALP2 TFA is also a strong activator of alveolar macrophages.

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.

Chlorotoxin TFA is a peptide isolated from the venom of the scorpion Leiurus quinquestriatus, acts as a chloride channel blocker. Anti-cancer activity.

Ssm Spooky Toxin TFA is found in Scolopendra mutilans that potently inhibits KCNQ (voltage-gated potassium channel family 7) channels, with IC₅₀s of 2.8 μM, 5.26 μM and 0.1-0.3 M for Kv7.4, Kv1.3, and Shal channel, respectivily. Ssm Spooky Toxin TFA inhibits cytokine generation by specifically acting on the KV1.3 channel in T cells. Ssm Spooky Toxin TFA plays an essential role in the centipede’s circulatory system .

Atrial natriuretic factor (1-28) (human, porcine) TFA exhibits blood pressure lowering activity by increasing sodium and urine excretion. Atrial natriuretic factor (1-28) (human, porcine) TFA inhibits the release of pituitary adrenocorticotropic hormone (ACTH) and beta-endorphin through inhibition of pro-opiomelanocortin (POMC) expression. Atrial natriuretic factor (1-28) (human, porcine) TFA increases cGMP levels in RMIC cells with an IC₅₀ of 1.2 nM.

Imperatoxin A TFA is a peptide toxin derived from the venom of the African scorpion Pandinus imperator. Imperatoxin A TFA is a Ca²⁺-release channels/ryanodine receptors (RyRs) activator. Imperatoxin A TFA enhances the influx of Ca²⁺ from the sarcoplasmatic reticulum into the cell.

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.