voltage-sensitive

Tetracaine hydrochloride (Amethocalne HCl) (Pontocaine), a potent local anaesthetic, is a channel function allosteric inhibitor. It is primarily used as an antipruritic and topically in ophthalmology, and it has been used for surface and spinal anesthesia.

Cyfluthrin binds to voltage-sensitive sodium channel such as Nav 1.8 sodium channel and modify their gating kinetics, thereby disrupting nerve function of pests.

Divalproex Sodium (Valproate semisodium) binds to and inhibits gamma-aminobutyric acid (GABA) transaminase and its anticonvulsant activity may be exerted by increasing brain concentration of GABA and by inhibiting enzymes that catabolize GABA or block the reuptake of GABA into glia and nerve endings. It also is an HDAC inhibitor， Comprised of sodium valproate and valproic acid with anticonvulsant and antiepileptic activities. Divalproex may also work by suppressing repetitive neuronal firing through the inhibition of voltage-sensitive sodium channels.

Methyl homoveratrate, a McN5691 (RWJ-26240) metabolite detected in vivo in plasma, urine, and fecal extracts, functions as a voltage-sensitive calcium channel blocker.

Topiramate lithium (McN 4853) is a broad-spectrum antiepileptic compound with GluR5 receptor antagonistic properties. Its mechanism of action includes enhancing GABAergic activity, inhibiting kainate AMPA receptors, voltage-sensitive sodium and calcium channels, and increasing potassium conductance. Additionally, this compound inhibits carbonic anhydrase. [1][2][3]

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.

QAQ dichloride is a photoswitchable compound that blocks voltage-gated Na v and K v channels. Its channel-blocking activity is observed in the trans form of the azobenzene photoswitch, while the cis form does not exhibit this effect. This compound is membrane-impermeant and selectively enters pain-sensing neurons expressing endogenous import channels. QAQ dichloride functions as a light-sensitive analgesic and provides a valuable tool for investigating signaling mechanisms involved in acute and chronic pain [1] [2].

Brevetoxin-3 (PbTx-3) is a potent allosteric activator of voltage-gated Na+ channels, exhibiting a high affinity for site 5 and inhibiting the inactivation of these channels.

PD 173212 is a blocker that blocks N-type voltage sensitive calcium channel (Cav2.2). PD173212 (0.0017-1.7 μmol kg, Intraperitoneal Injection.) dose-dependently reduced DNBS-induced visceral hypersensitivity in mice.

ω-Conotoxin CVIA, a 27-amino acid neuropeptide, functions as a blocker of voltage-sensitive calcium channels (VSCCs) [1].

Hainantoxin-IV acts as a specific antagonist for tetrodotoxin-sensitive (TTX-S) voltage-gated sodium channels, with His28 and Lys32 being critical residues for binding to the target. This compound also features an inhibitor cystine knot motif [1].

ω-Conotoxin SO3 is an analgesic peptide that functions as an antagonist to N-type voltage-sensitive calcium channels, and can be isolated from the venom of Conus striatus [1] [2].

Methylamine occurs endogenously from amine catabolism and its tissue levels increase in some pathological conditions, including diabetes. Interestingly, methylamine and ammonia levels are reciprocally controlled by a semicarbazide-sensitive amine oxidase activity that deaminates methylamine to formaldehyde with the production of ammonia and hydrogen peroxide. Methylamine also targets the voltage-operated neuronal potassium channels, probably inducing the release of neurotransmitter(s).

Hardwickiic acid ((-)-Hardwickiic acid) is a natural compound derived from Pulicaria gnaphalodes with anti-injury receptor properties. It blocks tetrodotoxin-sensitive voltage-dependent sodium channels and exhibits anti-inflammatory and insecticidal activity.

Oe-9000 is a blocker of voltage-gated Na(+) currents in neurons. It reversibly reduces rapidly activating and inactivating TTX-sensitive (TTX-S) Na(+) currents as well as slowly activating and inactivating tetrodotoxin-resistant (TTX-R) Na(+) currents at

Jingzhaotoxin-IX is a C-terminally amidated peptide neurotoxin consisting of 35 amino acid residues. It inhibits both tetrodotoxin-resistant and tetrodotoxin-sensitive isoforms of voltage-gated sodium channels, as well as the Kv2.1 channel. However, Jingzhaotoxin-IX does not affect the delayed rectifier potassium channels Kv1.1, Kv1.2, and Kv1.3 [1].

mHuwentoxin-IV, a naturally modified form of Huwentoxin-IV, selectively inhibits tetrodotoxin-sensitive (TTX-S) voltage-gated sodium channels in dorsal root ganglion neurons with an IC50 value of 54.16 nM. Notably, the inhibitory effect of mHuwentoxin-IV on these sodium channels is unaffected by strong depolarization voltages [1].