na-1

Tat-NR2B9c (NA-1) is a postsynaptic density-95 (PSD-95) inhibitor with neuroprotective and antiepileptic effects.Tat-NR2B9c inhibits PSD-95d2, PSD-95d1, and PSD-95, which prevents the activation of NMDA-induced NADPH oxidase in neurons, thereby blocking the production of superoxide, which reduces ischemic injury in the acute phase after stroke.

Tat-NR2B9c TFA is a 20-aa peptide, and acts as an inhibitor of postsynaptic density-95 (PSD-95)(EC50 of 6.7 nM for PSD-95d2), and possesses neuroprotective efficacy.

Tat-NR2B9c acetate (NA-1 acetate) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c acetate disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c acetate also inhibits neuronal nitric oxide synthase (nNOS)/PSD-95 interaction, and possesses neuroprotective efficacy.

Thymalfasin (Thymosin α1) (thymosin-alpha 1) is an immunomodulating agent able to enhance the Thl immune response.

Porcine dynorphin A (1-13), a potent endogenous κ opioid receptor agonist, exhibits antinociceptive properties at physiological concentrations and induces acute increases in [Ca2+]i in neurons, akin to those observed with acute NMDA treatment.

Porcine dynorphin A(1-13) acetate (Dynorphin A Porcine Fragment 1-13 acetate) is a potent, endogenous κ opioid receptor agonist and is antinociceptive at physiological concentrations. Exposure to dynorphin A (1-13) causes acute increases in [Ca2+]i in individual neurons similar to increases seen with acute NMDA treatment.

Dynorphin A (1-10) (TFA), an endogenous opioid neuropeptide, binds in the transmembrane domain of the κ-receptor.

Dynorphin A (1-10), an endogenous opioid neuropeptide, interacts with the κ-opioid receptor by binding to its extracellular loop 2 and inhibits NMDA-activated current, demonstrating an IC50 value of 42.0 μM.

Dynorphin A (1-10) acetate is an endogenous opioid neuropeptide, binds to extracellular loop 2 of the κ-opioid receptor. Dynorphin A (1-10) also blocks NMDA-activated current with an IC50 of 42.0 μM.

Transdermal Peptide Disulfide TFA (TD 1 Disulfide(peptide) TFA), an 11-amino acid peptide, specifically binds to the Na+/K+-ATPase beta-subunit (ATP1B1), primarily interacting with its C-terminus, and enhances the transdermal delivery of various macromolecules[1].

γ-1-Melanocyte Stimulating Hormone (MSH), amide, an 11-amino acid peptide, plays a critical role in regulating sodium (Na+) balance and blood pressure by activating melanocortin receptor 3 (MC3-R).

SPAI-1, a peptide isolated from porcine duodenum, serves as a specific inhibitor to monovalent cation transporting ATPases, effectively inhibiting Na+, K+-ATPase and H+, K+-ATPase while stimulating Mg2+-ATPase in vitro [1] [2].

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.

μ-Conotoxin GIIIB, a 22-residue polypeptide derived from the venom of the piscivorous cone snail Conus geographus, serves as an inhibitor of the Na V 1.4 channel, effectively blocking muscle cell contraction [1] [2] [3].

C-Peptide 1 (rat) is a polypeptide isolated from proinsulin. C-Peptide acts as a β-catenin/GSK-3β activator, influences Na/K-ATPase activity, regulates apoptosis, and may improve diabetic neuropathy.

ProTx-III, a spider venom peptide derived from the Peruvian green velvet tarantula, functions as a selective and potent inhibitor of the voltage-gated sodium channel Na v 1.7, exhibiting an IC 50 of 2.1 nM. Characterized by its inhibitor cystine knot motif (ICK), ProTx-III can attenuate the pain response and is applicable in research on chronic pain, epilepsy, and arrhythmia [1].

Crotamine, a 42 amino acid toxin featuring three disulfide bridges, functions as a Na+ channel modulator with analgesic properties. This compound interacts with lipid membranes and exhibits myonecrotic activity, and can be isolated from the venom of Crotalus durissus terrificus [1] [2].

Dc1a, a toxin isolated from the desert bush spider Diguetia canities [1], potently facilitates the opening of the German cockroach Na v channel (BgNa v 1).

Ceratotoxin-2 (CcoTx2) is a voltage-gated sodium channel inhibitor with half maximal inhibitory concentrations (IC50) of 8 nM for Na v 1.2/β 1 and 88 nM for Na v 1.3/β 1 [1].

BmK-M1, a scorpion-derived toxin, consists of a 64-amino acid polypeptide stabilized by four disulfide bridges. This compound functions as an inhibitor of the Na+ channel, classifying it as both a cardiotoxin and a neurotoxin [1].

Theraphotoxin-Tap1a (Tap1a) is a spider venom-derived peptide that acts as an inhibitor of sodium channels, displaying IC50 values of 80 nM for Na v 1.7 and 301 nM for Na v 1.1. It demonstrates analgesic effects [1].

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

Proadrenomedullin (N-20) (ProADM N20) (bovine, porcine) is a peptide known for its strong hypotensive effects and inhibition of catecholamine release from chromaffin cells. It effectively suppresses catecholamine secretion in PC12 pheochromocytoma cells with an IC50 of 350 nM and prevents the desensitization of nicotinic cholinergic agonist-induced catecholamine release and nicotinic signal transduction, with an EC50 of approximately 270 nM for desensitization blockade, as evidenced by inhibited 22 Na+ uptake [1].

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].