CilnidipineBlocker of Dual L- and N-type calcium channel CAS# 132203-70-4 |
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Quality Control & MSDS
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| Cas No. | 132203-70-4 | SDF | Download SDF |
| PubChem ID | 5282138 | Appearance | Powder |
| Formula | C27H28N2O7 | M.Wt | 492.52 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Atelec; Cinalong; Siscard; FRC 8653 | ||
| Solubility | DMSO : ≥ 100 mg/mL (203.04 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 3-O-(2-methoxyethyl) 5-O-[(E)-3-phenylprop-2-enyl] 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate | ||
| SMILES | CC1=C(C(C(=C(N1)C)C(=O)OCC=CC2=CC=CC=C2)C3=CC(=CC=C3)[N+](=O)[O-])C(=O)OCCOC | ||
| Standard InChIKey | KJEBULYHNRNJTE-DHZHZOJOSA-N | ||
| Standard InChI | InChI=1S/C27H28N2O7/c1-18-23(26(30)35-14-8-11-20-9-5-4-6-10-20)25(21-12-7-13-22(17-21)29(32)33)24(19(2)28-18)27(31)36-16-15-34-3/h4-13,17,25,28H,14-16H2,1-3H3/b11-8+ | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Cilnidipine is a unique L-type and N-type calcium channel blocker, used for high blood pressure treatment.Dual L- and N-type calcium channel blocker that displays antihypertensive, sympatholytic and neuroprotective activity. Lowers mean blood pressure and reduces the size of cerebral infarction in the rat model of focal brain ischemia.Cilnidipine (10 mM) suppresses the elevation of the ratio induced by 40 mM KCl, and this suppression is effectively inhibited after the treatment with omega-conotoxin GVIA.Cilnidipine reduces Ca(2+) influx via N-type Ca(2+) channels after NMDA receptors activation and then protects neurons against ischemia-reperfusion injury in the rat retina in vivo. Cilnidipine significantly prevents the increase in desmin staining and restores the glomerular podocin and nephrin expression compared with amlodipine in spontaneously hypertensive rat/ND mcr-cp (SHR/ND). Cilnidipine also prevents the increase in renal angiotensin II content, the expression and membrane translocation of NADPH oxidase subunits and dihydroethidium staining in SHR/ND. Cilnidipine (30 mg/kg/d as food admix) treatment suppresses the increase in systolic blood pressure in Dahl salt-sensitive rats. Cilnidipine inhibits the increase in blood urea nitrogen and decrease in creatinine clearance as well as progression of glomerular sclerosis. Cilnidipine reduces plasma norepinephrine level and plasma rennin activity compared with vehicle-treated Dahl S rats. Cilnidipine suppresses the pressor response induced by sympathetic nerve stimulation and angiotensin II in pithed rats. Cilnidipine or omega-conotoxin MVIIA decreases mean blood pressure, but slightly increases heart rate in anesthetized rats. Cilnidipine can affect sympathetic N-type Ca(2+) channels in addition to vascular L-type Ca(2+) channels in antihypertensive doses in the rat in vivo. |
Cilnidipine Dilution Calculator
Cilnidipine Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.0304 mL | 10.1519 mL | 20.3037 mL | 40.6075 mL | 50.7594 mL |
| 5 mM | 0.4061 mL | 2.0304 mL | 4.0607 mL | 8.1215 mL | 10.1519 mL |
| 10 mM | 0.203 mL | 1.0152 mL | 2.0304 mL | 4.0607 mL | 5.0759 mL |
| 50 mM | 0.0406 mL | 0.203 mL | 0.4061 mL | 0.8121 mL | 1.0152 mL |
| 100 mM | 0.0203 mL | 0.1015 mL | 0.203 mL | 0.4061 mL | 0.5076 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Dual L- and N-type calcium channel blocker that displays antihypertensive, sympatholytic and neuroprotective activity. Lowers mean blood pressure and reduces the size of cerebral infarction in the rat model of focal brain ischemia.
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Effects of Cilnidipine on Heart Rate and Uric Acid Metabolism in Patients With Essential Hypertension.[Pubmed:28197287]
Cardiol Res. 2016 Oct;7(5):167-172.
BACKGROUND: The relation between hypertension and hyperuricemia has been established by epidemiological studies. Calcium channel blockers are one of the first-line drugs for newly diagnosed patients with essential hypertension. Cilnidipine is a new calcium channel blocker acting by blocking both L- and N-type calcium channels. The aim of this study was to compare the effectiveness of amlodipine and Cilnidipine in patients with essential hypertension and their effects on heart rate and serum uric acid levels. METHODS: Out of 100 enrolled patients, 92 completed the study. They were randomly assigned to amlodipine (N = 47) and Cilnidipine (N = 45) groups. Cilnidipine was started at 10 mg/day and then adjusted to 5 - 20 mg/day, and amlodipine was started at 5 mg/day and then adjusted to 2.5 - 10 mg/day. RESULTS: After 24 weeks of study, patients in Cilnidipine groups showed significant reduction in heart rate and serum uric acid levels from baseline (P = 0.00). CONCLUSION: In clinical setting where both hypertension and hyperuricemia exist, Cilnidipine can be a promising drug of choice.
Cilnidipine: Next Generation Calcium Channel Blocker.[Pubmed:27734656]
J Assoc Physicians India. 2016 Apr;64(4):95-99.
Hypertension is one of the most common conditions seen in primary care and a major public health problem in India. It can lead to various complications if not detected early and treated appropriately. As per the latest Eighth Joint National Committee (JNC 8) the goal BP in most hypertensive patients age <60 years should be <140/90 mmHg and treatment can be started by selecting drugs from among 4 specific medication classes i.e. angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), calcium channel blocker (CCB) or diuretics. CCB is one of the first line drugs in the management of hypertension. Among CCB, Cilnidipine is a unique Ca2+ channel blocker as it has inhibitory action on the sympathetic N-type Ca2+ channels along with its effect on L-type Ca2+ channels. This article focuses on the current status of Cilnidipine in the management of hypertension and co-morbidities. Cilnidipine by attenuating norepinephrine release from sympathetic nerve endings leads to vasodilatation, decreases heart rate and increases renal blood flow. Cilnidipine has an advantage of causing less reflex tachycardia, less pedal edema and better control of proteinuria in comparison to L-type CCB. By causing dilatation of efferent arteriole, it causes less damage to glomeruli and suppresses podocyte injury. Cilnidipine also increases insulin sensitivity. Therefore, Cilnidipine as CCB can be a good choice in hypertensive patients with diabetes, chronic kidney disease and in patients developing pedal edema with other CCB.
N- and L-type calcium channels blocker cilnidipine ameliorates neuropathic pain.[Pubmed:27823932]
Eur J Pharmacol. 2016 Dec 15;793:66-75.
Cilnidipine is a dihydropyridine derivative that inhibits N-type and L-type voltage-gated Ca(2+) channels (VDCCs). We recently reported that a selective N-type VDCC blocker attenuated the spinal long-term potentiation (LTP) of C-fiber-evoked field potentials recorded in the spinal dorsal horn of rats, which served as a model for examining synaptic function during central pain sensitization. In this study, we investigated the effects of Cilnidipine on the changes related to neuropathic pain induced by nerve injury. Mechanical allodynia and hyperalgesia were evaluated by von Frey test and pin prick test, respectively. Spinal LTP of C-fiber-evoked field potentials were evaluated by in vivo electrophysiology. Intrathecally administrated Cilnidipine attenuated mechanical allodynia and hyperalgesia in the spared nerve injury mouse model. Using in vivo electrophysiology in rats, Cilnidipine (10microm) administered spinally inhibited the induction and maintenance of high-frequency stimulation-induced LTP of C-fiber-evoked field potentials, while basal C-fiber-evoked field potentials in naive rats were unaffected. The basal C-fiber-evoked field potentials in nerve-injured rats were strongly inhibited by Cilnidipine. Treatment with a specific N-type VDCC blocker, omega-conotoxin GVIA, which reportedly attenuates C-fiber-evoked field potentials both before and after the induction of LTP, attenuated mechanical allodynia and hyperalgesia in nerve-injured mice. By contrast, an L-type VDCC blocker, nicardipine attenuated only mechanical hyperalgesia, but not mechanical allodynia in nerve-injured mice, and also attenuated the established LTP of C-fiber-evoked field potentials in rats. These results suggested that N-type and L-type VDCC blockers may effectively alleviate the hyperalgesia and allodynia associated with neuropathic pain without affecting normal pain perception.
Neuroprotective effects of a dual L/N-type Ca(2+) channel blocker cilnidipine in the rat focal brain ischemia model.[Pubmed:15340224]
Biol Pharm Bull. 2004 Sep;27(9):1388-91.
Although a blockade or lack of N-type Ca(2+) channels has been reported to suppress neuronal pathological processes in several animal models of pain and ischemic brain injury, information is still limited regarding the neuroprotective effects of a dual L/N-type Ca(2+) channel blocker, Cilnidipine. In this study, we assessed the effects of Cilnidipine in the rat focal brain ischemia model to analyze its potential utility for hypertensive patients with cerebral infarction. In an anesthetized rat model, cerebral vasodilator actions of Cilnidipine were detected at hypotensive doses, which was less potent than those of an L-type Ca(2+) channel blocker, nilvadipine. In the rat focal brain ischemia model, an anti-hypertensive and anti-sympathetic dose of Cilnidipine could reduce the size of cerebral infarction, whereas an equipotent hypotensive dose of nilvadipine failed to affect it. These results suggest that N-type Ca(2+) channel-blocking profile of Cilnidipine may contribute its neuroprotective action in the animal focal brain ischemia model. Thus, treatment of hypertension with Cilnidipine may prevent severe consequences after brain attack.
Preferential inhibition of L- and N-type calcium channels in the rat hippocampal neurons by cilnidipine.[Pubmed:10784100]
Brain Res. 2000 Jan 31;854(1-2):6-10.
The effect of a dihydropyridine Ca2+ antagonist, Cilnidipine, on voltage-dependent Ca2+ channels was studied in acutely dissociated rat CA1 pyramidal neurons using the nystatin-perforated patch recording configuration under voltage-clamp conditions. Cilnidipine had no effect on low-voltage-activated (LVA) Ca2+ channels at the low concentrations under 10(-6) M. On the other hand, Cilnidipine inhibited the high-voltage-activated (HVA) Ca2+ current (I(Ca)) in a concentration-dependent manner and the inhibition curve showed a step-wise pattern; Cilnidipine selectively reduced only L-type HVA I(Ca) at the low concentrations under 10(-7) and 10(-6) M Cilnidipine blocked not only L- but also N-type HVA I(Ca). At the high concentration over 10(-6) M Cilnidipine non-selectively blocked the T-type LVA and P/Q- and R-type HVA Ca2+ channels. This is the first report that Cilnidipine at lower concentration of 10(-6) M blocks both L-and N-type HVA I(Ca) in the hippocampal neurons.
