n-type calcium channel

N-type calcium channel blocker-1 is an orally active analgesic agent with a high affinity for functionally blocking N-type calcium channels.

PD0176078 () is a newly blocker of N-type Calcium channel.

JNJ-26489112 is a CNS-active agent and inhibitor of voltage-gated Na+ channels and N-type Ca2+ channels with broad-spectrum anticonvulsant activity in rodents and can be used to study neurological disorders.

Cilnidipine (FRC-8653)(FRC8653) is a dual L- and N-type calcium channel blocker and displays antihypertensive, sympatholytic and neuroprotective activity.

Ca2+ channel agonist 1 is an agonist of N-type Ca2+ channel and an inhibitor of Cdk2 (EC50s: 14.23 μM and 3.34 μM) and is used as a potential treatment for motor nerve terminal dysfunction.

Cav 2.2 blocker 1 is an N-type calcium channel (Cav 2.2; IC50: 1 nM) blocker for the treatment of pain.

GV-58 is a selective N- and P/Q-type Ca2+ channels agonist (EC50: 7.21/8.81 uM for N-type/P-Q-type Ca2+ channel). The inhibitory of GV-58 is 20-fold fewer for CDK kinases activity.

Norverapamil hydrochloride (D591 hydrochloride) ((±)-Norverapamil hydrochloride) is an N-demethylated metabolite of Verapamil and it is an L-type calcium channel blocker and a P-glycoprotein (P-gp) function inhibitor.

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.

PD-151307 is used as an N-type calcium channel blocker.

sFTX-3.3 is a calcium ion channel antagonist, exhibiting IC50 values of approximately 0.24 mM and 0.70 mM against P-type and N-type channels respectively.

MONIRO-1 is a T- and N-type calcium channel blocker that acts on hCav2.2 (IC50: 34 μM), hCav3.1 (IC50: 3.3 μM), hCav3.2 (IC50: 1.7 μM) and hCav3.3 (IC50: 7.2 μM).

Azelnidipine, (S)-, is an L-type calcium channel blocker (CCB). Studies have shown that in patients with hypertension (HT) and heart failure preserved ejection fraction (HFpEF), azelnidipine improved the severity of HF and cardiac sympathetic nerve activity compared with cilnidipine, an N-type CCB (Cat#326734).

Azelnidipine, (R)-, is an L-type calcium channel blocker (CCB). Studies have shown that in patients with hypertension (HT) and heart failure preserved ejection fraction (HFpEF), azelnidipine improved the severity of HF and cardiac sympathetic nerve activity compared with cilnidipine, an N-type CCB (Cat#326734).

Ginsenoside Rf (Panaxoside Rf) is a trace component of ginseng root. Ginsenoside Rf inhibits N-type Ca2+ channel.

A-1048400 is a potent and selective N-type and T-type calcium channel blocker.

Efonidipine HCl (NZ-105) serves as both a T-type and L-type calcium channel blocker. This compound, distinct from other calcium channel blockers, notably increases N(6), 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced StAR mRNA and DHEA-S production in NCI-H295R adrenocortical carcinoma cells, actions reflective of adrenocorticotropic hormone. Efonidipine uniquely inhibits calcium channels by merging tonic and use-dependent blocking methods. Its inhibitory concentrations (IC50) for I(Ca(T)) and I(Ca(L)) are 0.35 micromol l and 1.8 nmol l, respectively. Clinically, efonidipine administered to hypertensive patients undergoing chronic hemodialysis (20-60 mg, twice daily) demonstrated comparable blood pressure control to amlodipine (2.5-7.5 mg, once daily) over a 12-week period without significantly altering pulse rate. Furthermore, efonidipine significantly improved left ventricular ejection fraction in heart failure models without affecting blood pressure, in addition to lowering the heart rate by about 10%.

NP118809 (39-1B4) is a potent N-type calcium channel blocker(IC50 : 0.11 μM).

Huwentoxin XVI TFA, a potent analgesic derived from the Chinese tarantula Ornithoctonus huwena, acts as a highly reversible and selective antagonist of mammalian N-type calcium channels (IC 50 of ~60 nM), with no impact on voltage-gated T-type calcium channels, potassium channels, or sodium channels [1].

α-Conotoxin PeIA is an analgesic that inhibits nAChRs α6β4, α9α10, and α3β2, and potently inhibits the N-type calcium channel through GABAB receptor activation [1] [2] [3].

Tat-CBD3 is a chemical compound inhibiting the interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2), as well as the interaction between CRMP2 and the NMDA receptor NR2B subunit. At a concentration of 10 µM, Tat-CBD3 reduces the Cav2.2-CRMP2 interaction by 43% in cell-free assays and impedes the NMDA receptor NR2B subunit-CRMP2 interaction in immunoprecipitation assays. It lowers voltage-induced calcium currents by about 60% in primary rat dorsal root ganglion (DRG) neurons and decreases glutamate-induced cytosolic calcium level rises in primary rat hippocampal neurons. When administered at 20 mg/kg, Tat-CBD3 lessens infarct volume in a rat model of cerebral ischemia following middle cerebral artery occlusion (MCAO). Additionally, intrathecal delivery of Tat-CBD3 at a dose of 20 µg/5 µl mitigates carrageenan-induced thermal hypersensitivity in rats.

Tat-CBD3A6K, a peptide derivative of the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2) interaction inhibitor Tat-CBD3, has demonstrated efficacy in a rat model of antiretroviral neuropathic pain caused by stavudine (d4T). Administered at 10 mg/kg, it preserves paw withdrawal threshold, indicating pain relief, and reduces the number of action potentials in dorsal root ganglia (DRG) neurons from affected rats. Additionally, a 30 µM/animal dural dose of Tat-CBD3A6K lessens meningeal blood flow escalation triggered by capsaicin, showcasing its potential in managing neuropathic pain and inflammation.

Myr-Tat-CBD3 is a chemical compound that serves as an inhibitor of the protein-protein interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2). This compound effectively disrupts the Cav2.2-CRMP2 interaction by about 81% at a 10 µM concentration and demonstrates an inhibitory concentration 50 (IC50) value of approximately 2.8 µM against potassium-induced calcium influx in primary rat dorsal root ganglion (DRG) neurons. Furthermore, at a concentration of 20 µM, Myr-Tat-CBD3 specifically inhibits calcium currents without affecting sodium currents in primary DRG neurons. Additionally, intrathecal administration of 20 µg/5 µl of Myr-Tat-CBD3 effectively mitigates carrageenan-induced declines in paw withdrawal latencies in rats, indicating its potential for pain relief. The compound also notably reduces cue-induced reinstatement of cocaine-seeking behavior in rats, suggesting therapeutic potential in addiction treatment.

ML-252 is a potent, selective inhibitor of the Kv7.2 voltage-gated potassium channel, demonstrating an IC50 value of 69 nM in patch clamp assays. It exists as the (S)-enantiomer, which is significantly more effective than both its (R)-enantiomer counterpart and the racemic mixture, with respective IC50 values of 944 nM and 160 nM. ML-252 exhibits high selectivity for Kv7.2 over other potassium channel subtypes and shows minimal activity against more than 68 G protein-coupled receptors, various transporters, L- and N-type calcium channels, K_ATP, and hERG potassium channels. However, it does inhibit the melatonin MT1 receptor by 61% at a 10 µM concentration.