Nifedipine

Catalog No.S1808 Batch:S180801

Print

Technical Data

Formula

C17H18N2O6
Molecular Weight 346.33 CAS No. 21829-25-4
Solubility (25°C)* In vitro DMSO 69 mg/mL (199.23 mM)
Ethanol 15 mg/mL (43.31 mM)
Water Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
4.0mg/ml Taking the 1 mL working solution as an example, add 50 μL of 80 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
Clear solution
5% DMSO 95% Corn oil
4.0mg/ml Taking the 1 mL working solution as an example, add 50 μL of 80 mg/ml clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results. 
* <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 Nifedipine is a dihydropyridine calcium channel blocker, used to lower hypertension and to treat angina.
Targets
calcium channel [1]
In vitro Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. [1] Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family. [2] Nifedipine dose-dependently decreases the values of [(3)H]-thymidine incorporation and total cellular protein content as well as the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) 1/2, mitogen-activated protein kinase kinase (MEK) 1/2, and even the phosphorylation of Pyk2, in vascular smooth muscle cells (VSMC). Nifedipine suppresses the levels of proliferative cell nuclear antigen (PCNA) dose-dependently in both VSMC and balloon-injured thoracic aortae in VSMC. [3]
In vivo Nifedipine (3 mg/kg) slightly lowers the level of systolic and/or diastolic blood pressure or increased the heart rate in rats. [3] Nifedipine (1 μm) produces a maximal inhibition of the store-operated pathway in choroidal arteriolar smooth muscle. [4] Nifedipine (20 and 40 mg/kg) markedly prevents the HCl plus ethanol-induced gastric mucosal injury and the increase in the content of thiobarbituric acid-reactive substances in the injured mucosa in rats. Nifedipine (20 and 40 mg/kg) dose-dependently promotes the ulcer healing and inhibites the increase in the content of thiobarbituric acid-reactive substances in the ulcerated mucosa in rats. [5]

Protocol (from reference)

Customer Product Validation

Data from [Data independently produced by , , Sci Rep, 2017, 7(1):3156]

Data from [Data independently produced by , , Biochem Biophys Res Commun, 2019, 509(1):76-81]

Selleck's Nifedipine has been cited by 13 publications

Electrical stimulation of cochlear implant promotes activation of macrophages and fibroblasts under inflammation [ Laryngoscope Investig Otolaryngol, 2023, 8(5):1390-1400] PubMed: 37899874
Repurposing screen identifies Amlodipine as an inducer of PD-L1 degradation and antitumor immunity [ Oncogene, 2021, 40(6):1128-1146] PubMed: 33323966
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
YiQiFuMai Powder Injection Attenuates Coronary Artery Ligation-Induced Heart Failure Through Improving Mitochondrial Function via Regulating ROS Generation and CaMKII Signaling Pathways. [ Front Pharmacol, 2019, 10:381] PubMed: 31031629
SAD-A, a downstream mediator of GLP-1 signaling, promotes the phosphorylation of Bad S155 to regulate in vitro β-cell functions [Wang K Biochem Biophys Res Commun, 2019, 509(1):76-81] PubMed: 30573363
Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER-mitochondrial dynamics [ Cell Death Dis, 2018, 9(10):966] PubMed: 30237514
Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER-mitochondrial dynamics [ Cell Death Dis, 2018, 9(10):966] PubMed: 30237514
Long-term presence of angiotensin II type 1 receptor autoantibody reduces aldosterone production by triggering Ca2+ overload in H295R cells [Lei J Immunol Res, 2018, 66(1):44-51] PubMed: 29147891
Dual effects of fructose on ChREBP and FoxO1/3α are responsible for AldoB up-regulation and vascular remodelling [ Clin Sci (Lond), 2017, 131(4):309-325] PubMed: 28007970
Modeling Congenital Hyperinsulinism with ABCC8-Deficient Human Embryonic Stem Cells Generated by CRISPR/Cas9. [Guo D, et al. Sci Rep, 2017, 7(1):3156] PubMed: 28600547

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

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.