Cilnidipine

Catalog No.S1293 Batch:S129301

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Technical Data

Formula

C27H28N2O7

Molecular Weight 492.52 CAS No. 132203-70-4
Solubility (25°C)* In vitro DMSO 99 mg/mL (201.0 mM)
Ethanol 15 mg/mL (30.45 mM)
Water Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Cilnidipine is a unique L-type and N-type calcium channel blocker, used for high blood pressure treatment.
Targets
Calcium channel [1]
In vitro 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.[1]
In vivo 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. [2] 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. [3] 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. [4] 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. [5]

Protocol (from reference)

Selleck's Cilnidipine has been cited by 7 publications

Calcium channel blocker amlodipine besylate therapy is associated with reduced case fatality rate of COVID-19 patients with hypertension [ Cell Discov, 2020, 6(1):96] PubMed: 33349633
A Patient-Derived Cell Atlas Informs Precision Targeting of Glioblastoma [ Cell Rep, 2020, 32(2):107897] PubMed: 32668248
High-Throughput Screening of an FDA-Approved Drug Library Identifies Inhibitors against Arenaviruses and SARS-CoV-2 [ ACS Infect Dis, 2020, acsinfecdis.0c00486] PubMed: 33183004
A high throughput screen for TMPRSS2 expression identifies FDA-approved and clinically advanced compounds that can limit SARS-CoV-2 entry [ Res Sq, 2020, rs.3.rs-48659] PubMed: 32818215
The Effect of Promiscuous Aggregation on in Vitro Drug Metabolism Assays [ Pharm Res, 2019, 36(12):170] PubMed: 31654151
Activation of the Anti-Aging and Cognition-Enhancing Gene Klotho by CRISPR-dCas9 Transcriptional Effector Complex [Chen CD, et al. J Mol Neurosci, 2018, 64(2):175-184] PubMed: 29352444
Quantitative High-Throughput Screening Using a Coincidence Reporter Biocircuit. [ Curr Protoc Neurosci, 2017, 79:5] PubMed: 28398644

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.