Manidipine is a calcium channel blocker that is used clinically as an antihypertensive. Target: Calcium ChannelManidipine is a dihydropyridine calcium antagonist, which causes systemic vasodilation by inhibiting the voltage-dependent calcium inward currents in smooth muscle cells. Manidipine was well tolerated in clinical trials, with most adverse effects related to vasodilation [1]. Manidipine is a lipophilic, third-generation dihydropyridine calcium channel antagonist with a high degree of selectivity for the vasculature, thereby inducing marked peripheral vasodilation with negligible cardiodepression. manidipine represents a first-line treatment option for patients with essential mild-to-moderate hypertension [2]. Manidipine has neutral effects on glucose and lipid metabolism and is generally well tolerated. Manidipine thus represents a first-line option for lowering BP in patients with mild-to-moderate hypertension [3].
Isradipine-d3 (PN 200-110-d3) is the deuterium labeled Isradipine. Isradipine (PN 200-110) is an orally active L-type calcium channel blocker. Isradipine, as a powerful peripheral vasodilator, is a dihydropyridine calcium antagonist with selective actions on the heart as well as the peripheral circulation. Isradipine is a potentially viable neuroprotective agent for Parkinson's disease[1][2][3].
VK-II-36 is a carvedilol analog that suppresses sarcoplasmic reticulum Ca2+release but does not block the β-receptor.VK-II-36 inhibits triggered activities evoked by both early and delayed after depolarizations[1].
L-Phenylalanine-3-13C ((S)-2-Amino-3-phenylpropionic acid-3-13C) is the 13C-labeled L-Phenylalanine. L-Phenylalanine ((S)-2-Amino-3-phenylpropionic acid) is an essential amino acid isolated from Escherichia coli. L-Phenylalanine is a α2δ subunit of voltage-dependent Ca+ channels antagonist with a Ki of 980 nM. L-phenylalanine is a competitive antagonist for the glycine- and glutamate-binding sites of N-methyl-D-aspartate receptors (NMDARs) (KB of 573 μM ) and non-NMDARs, respectively. L-Phenylalanine is widely used in the production of food flavors and pharmaceuticals[1][2][3][4].
Catharanthine Sulfate ((+)-3,4-Didehydrocoronaridine Sulfate) is an alkaloid isolated from Madagascar periwinkle, inhibits voltage-operated L-type Ca2+ channel, with anti-cancer and blood pressure-lowering activities[1].
JTV-519 free base (K201 free base) is a Ca2+-dependent blocker of sarcoplasmic reticulum Ca2+-stimulated ATPase (SERCA) and a partial agonist of ryanodine receptors in striated muscle. Cardioprotective agent[1].
MONIRO-1 is a T-type and N-type calcium channel blocker with IC50 values of 34, 3.3, 1.7 and 7.2 µM against hCav2.2, hCav3.1, hCav3.2 and hCav3.3, respectively[1].
Nilvadipine is a potent calcium channel antagonist, and the IC50 value is around 0.1 nM.
Lercanidipine-d3 hydrochloride is the deuterium labeled Lercanidipine. Lercanidipine is a lipophilic third-generation dihydropyridine-calcium channel blocker (DHP-CCB). Lercanidipine has long lasting antihypertensive action and reno-protective effect[1][2][3].
Amlodipine is a long-acting calcium channel blocker.Target: Calcium ChannelAmlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the movement of calcium ions into vascular smooth muscle cells and cardiac muscle cells. Experimental data suggest amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects, or decreased heart muscle contractility, can be detected in vitro, but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa = 8.6), and its interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect. Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure. From Wikipedia.
ω-Conotoxin GVIA is an inhibitor of the N-type Ca2+ channel[1].
Amlodipine maleate is a long-acting calcium channel blocker.Target: Calcium ChannelAmlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the movement of calcium ions into vascular smooth muscle cells and cardiac muscle cells. Experimental data suggest amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects, or decreased heart muscle contractility, can be detected in vitro, but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa = 8.6), and its interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect. Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure. From Wikipedia.
Nicardipine(YC-93) is a calcium channel blocker that has been widely used to control blood pressure in severe hypertension following events such as ischemic stroke, traumatic brain injury, and intracerebral hemorrhage.
HUP30 is a vasodilating agent. HUP30 stimulates soluble guanylyl cyclase, activate K+ channels, and blocks extracellular Ca2+ influx[1].
Norbormide shows vasoconstrictor activity by blocking calcium channel. The activity of Norbormide is species- and tissue-specific, endothelium independent, and is restricted to the peripheral arteries of rat. Norbormide is also a toxicant, and the oral LD50s in mouse, hamster, guinea pig and rabbit are 2250, 140, 620, and 1000 mg/kg[1].
Cinnarizine is an antihistamine and a calcium channel blocker, promote cerebral blood flow, used to treat cerebral apoplexy, post-trauma cerebral symptoms, and cerebral arteriosclerosis.
Nifedipine is a potent calcium channel blocker and drug of choice for cardiac insufficiencies.
ω-Agatoxin IVA is a potent, selective P/Q type Ca2+ channel blocker with IC50s of 2 nM and 90 nM for P-type and Q-type Ca2+ channels, respectively. ω-Agatoxin IVA (IC50, 30-225 nM) inhibits glutamate exocytosis and calcium influx elicited by high potassium. ω-Agatoxin IVA also blocks the high potassium-induced release of serotonin and norepinephrine. ω-Agatoxin IVA has no effect on L-type or N-type calcium channels[1][2].
Hyperforin is a transient receptor canonical 6 (TRPC6) channels activator. Hyperforin modulates Ca2+ levels by activating Ca2+-conducting non-selective canonical TRPC6 channels. Hyperforin also shows diverse pharmacological activities including anti-depression, anti-tumor, anti-dementia, anti-diabetes. Hyperforin modulates γδ T cells to secret IL-17α, improves Imiquimod (HY-B0180)-induced psoriasis-like mice model[1][2][3][4][5].
Flunarizine is a selective calcium entry blocker.Target: Calcium ChannelFlunarizine is a drug classified as a calcium channel blocker. Flunarizine is a non-selective calcium entry blocker with other actions including histamine H1 receptor blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy. It may help to reduce the severity and duration of attacks of paralysis associated with the more serious form of alternating hemiplegia, as well as being effective in rapid onset dystonia-parkinsonism (RDP). From Wikipedia.
ω-Grammotoxin SIA (GrTx) is P/Q and N-type voltage-gated Calcium channels inhibitor. ω-Grammotoxin SIA is also a protein toxin that can be obtained from spider venom. ω-Grammotoxin SIA has the potential to study neurological diseases as well as cardiovascular diseases[1].
Bevantolol hydrochloride is a selective β1 and α1-adrenergic receptor antagonist with pKi values of 7.83, 6.9 in rat cerebral cortex, respectively. Bevantolol hydrochloride is a potent Ca2+ antagonist[1][2].
ω-Conotoxin SO3 is a blocker of N-type voltage-sensitive calcium channel. ω-Conotoxin SO3 is an analgesicω-conotoxin that can be isolated from the venom of C. striatus[1][2].
Gabapentin-d6 (hydrochloride) is deuterium labeled Gabapentin (hydrochloride).
Amlodipine mesylate, an antianginal agent and an orally active dihydropyridine calcium channel blocker, works by blocking the voltage-dependent L-type calcium channels, thereby inhibiting the initial influx of calcium. Amlodipine mesylate can be used for the research of high blood pressure and cancer[1][2][3].
ILS-920 is a nonimmunosuppressive Rapamycin analog with reduced immunosuppressive activity and potent neuroprotective activity. ILS-920 binds selectively to the immunophilin FKBP52 and to the β1-subunit of L-type voltage-gated calcium channels (VGCC). ILS-920 shows 200-fold selectivity for FKBP52 versus FKBP12[1].
(R)-Lercanidipine hydrochloride is the R-enantiomer of Lercanidipine. (R)-lercanidipine hydrochloride is a calcium channel blocker[1].
Etripamil (MSP-2017) is a short-acting L-type calcium-channel antagonist with a rapid onset of action designed for intranasal administration, used to treat Paroxysmal Supraventricular Tachycardia (PSVT). Etripamil (MSP-2017) slows atrioventricular nodal conduction and prolongs atrioventricular nodal refractory periods by inhibiting calcium ion influx through the calcium slow channels in the atrioventricular node cells[1][2].
Ibutilide Fumarate is a Class III antiarrhythmic agent that is indicated for acute cardioconversion of atrial fibrillation and atrial flutter of a recent onset to sinus rhythm.Target: Calcium ChannelIbutilide is the first 'pure' class III antiarrhythmic drug to become available. Its predominant action is prolongation of the myocardial action potential duration. Intravenous ibutilide 0.01 to 0.025 mg/kg or 1 to 2 mg successfully converted atrial flutter or fibrillation to sinus rhythm in 33 to 49% of patients in 2 placebo-controlled trials involving 439 patients with sustained arrhythmia [1]. Ibutilide appears to be an effective alternative method for rapid conversion of recent-onset AF or AFl. The drug may be particularly useful in patients who have undergone recent cardiac surgery or those who are not ideal candidates for DCC [2].
Zonisamide sodium is a 1,2 benzisoxazole derivative and the first agent of this chemical class to be developed as an antiepileptic drug.Target: Calcium channel inhibitor; Sodium channel inhibitorZonisamide sodium is a sulfonamide anticonvulsant approved for use as an adjunctive therapy in adults with partial-onset seizures for adults; infantile spasm, mixed seizure types of Lennox-Gastaut syndrome, myoclonic, and generalized tonic clonic seizure. Zonisamide sodium is a 1,2 benzisoxazole derivative and the first agent of this chemical class to be developed as an antiepileptic drug. It has shown activity in various animal models of epilepsy, and although a detailed mode of action awaits clarification it appears to block the propagation/spread of seizure discharges and to suppress the epileptogenic focus [1].Zonisamide sodium 500 mg/day was significantly superior to placebo in reducing the frequency of complex partial seizures (-51% versus -16%), all partial seizures and all seizures, with dose-dependent benefit provided over a 100-500 mg/day dose range. Supporting trials have confirmed significant increases in reduction in median seizure frequency (up to 41%) and responder rates (35-42%) compared with placebo following zonisamide sodium 400-600 mg/day, enabling 20-27% of patients to attain >or=75% reduction in seizure frequency [2].Clinical indications: Epilepsy; Lewy body dementia; Parkinsons diseaseToxicity: Anorexia; Somnolence; Dizziness; Irritability; Confusional state; Depression; Diplopia; Memory impairment