Cilnidipine NEW
| Price | $41 | $81 | $134 |
| Package | 10mg | 50mg | 100mg |
| Supply Ability: | 10g |
| Update Time: | 2025-04-27 |
Product Details
| Product Name: Cilnidipine | CAS No.: 132203-70-4 |
| Purity: 100% | Supply Ability: 10g |
| Release date: 2025/04/27 |
Product Introduction
Bioactivity
| Name | Cilnidipine |
| Description | Cilnidipine (FRC-8653)(FRC8653) is a dual L- and N-type calcium channel blocker and displays antihypertensive, sympatholytic and neuroprotective activity. |
| In vitro | Cilnidipine inhibits the rise in blood urea nitrogen and the decline in creatinine clearance, as well as the progression of glomerulosclerosis. It prevents the increased content of renal angiotensin II, the expression of NADPH oxidase, and the augmented membrane translocation of dihydroethidium in SHR/ND rats. Administering 30 mg/kg of Cilnidipine daily to Dahl salt-sensitive rats effectively treated the elevation of systolic blood pressure. Compared to control-treated Dahl S rats, Cilnidipine reduced plasma norepinephrine levels and plasma renin activity. In spinal cord destruction rats, it suppressed the pressor responses induced by sympathetic nerve stimulation and angiotensin II. In anesthetized rats, Cilnidipine, or omega-conotoxin MVIIA, lowered mean arterial blood pressure with a slight increase in heart rate. At antihypertensive doses in rats, Cilnidipine affected sympathetic nerve N-type calcium channels (Ca(2+)), besides vascular L-type channels. Following NMDA receptor activation, Cilnidipine reduced Ca(2+) influx through N-type channels, and in rats in vivo, it protected neurons from ischemic reperfusion injury in the retina. Compared to amlodipine-treated spontaneously hypertensive rats/ND mcr-cp (SHR/ND), Cilnidipine significantly prevented the increase in fibrillary protein staining and restored the expression of podocin and nephrin in the glomeruli. |
| In vivo | Cilnidipine at 10 mM can inhibit the increase in the ratio induced by 40 mM potassium chloride, and is also effective in inhibition when treated with omega-conotoxin GVIA. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | DMSO : 45 mg/mL (91.37 mM), Sonication is recommended. Ethanol : 4.9 mg/mL (9.95 mM), Sonication is recommended. |
| Keywords | long-acting | Inhibitor | inhibit | FRC8653 | FRC 8653 | Dual L-and N-type calcium channel | dihydropyridine Ca | Cilnidipine | channel | CalciumChannel | Calcium Channel | Ca2+ channels | Ca channels | Antihypertensive |
| Inhibitors Related | Nisoldipine | Diltiazem hydrochloride | Levetiracetam | L-Ascorbic acid | L-Phenylalanine | D-Menthol | Ethyl cinnamate | L-Ascorbic acid sodium salt | 1-Octanol | 2-Nitrobenzoic acid | Nifedipine | Otilonium bromide |
| Related Compound Libraries | Bioactive Compound Library | Pain-Related Compound Library | Neuronal Signaling Compound Library | Membrane Protein-targeted Compound Library | Anti-Cancer Clinical Compound Library | Drug Repurposing Compound Library | Neuroprotective Compound Library | Inhibitor Library | Anti-Cancer Approved Drug Library | Bioactive Compounds Library Max | Ion Channel Targeted Library | Anti-Cancer Drug Library |
Company Profile Introduction
TargetMol Chemicals Inc. is headquartered in Boston, MA, and specializes in products and services that serve the research needs of chemical and biological scientists worldwide. With a client base in 40+ countries, TargetMol has evolved into one of the biggest global research suppliers for compound libraries and small molecule compounds.
170+ Compound Libraries， 10000+ Noval Small Molecucles，16000+ Nature Compounds
TargetMol diligently updates and offers over 170 types of compound libraries and a wide range of high-quality research chemicals, including inhibitors, activators, natural products, peptides, antibodies , and novel life-science kits for laboratory and scientific use. In addition, our lab allows us to conduct CADD (computer-aided drug design) and chemical synthesis to meet the customization needs of our clients.
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