Merck
CN

N7634

Sigma-Aldrich

硝苯地平

≥98% (HPLC), powder

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别名:
1,4-二氢-2,6-二甲基-4-(2-硝基苯基)-3,5-吡啶二甲酸二甲酯
经验公式(希尔记法):
C17H18N2O6
CAS号:
分子量:
346.33
EC 号:
MDL编号:
PubChem化学物质编号:
NACRES:
NA.77

质量水平

检测方案

≥98% (HPLC)

形式

powder

颜色

yellow

溶解性

DMSO: soluble
ethanol: soluble

创始人

Bayer

储存温度

2-8°C

SMILES string

COC(=O)C1=C(C)NC(C)=C(C1c2ccccc2[N+]([O-])=O)C(=O)OC

InChI

1S/C17H18N2O6/c1-9-13(16(20)24-3)15(14(10(2)18-9)17(21)25-4)11-7-5-6-8-12(11)19(22)23/h5-8,15,18H,1-4H3

InChI key

HYIMSNHJOBLJNT-UHFFFAOYSA-N

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应用

硝苯地平被用于:
  • 评估其对豚鼠小肠R-型钙通道中肌间神经元钙电流的影响
  • 评估L型钙通道阻滞剂对胆碱能和多巴胺能神经元的神经保护作用
  • 确定硝苯地平(抗高血压药物)与降糖药共同给药对人脐静脉细胞(HUVEC)的影响

生化/生理作用

硝苯地平是一种L型Ca2+ 通道阻滞剂; 可诱导人成胶质细胞瘤细胞凋亡。硝苯地平具有神经保护作用,可保护黑质。硝苯地平具有抗氧化作用。硝苯地平可下调炎性细胞因子,如巨噬细胞炎症蛋白-2(MIP-2)、肿瘤坏死因子-α(TNF-α)。硝苯地平具有抗高血压作用。硝苯地平可抑制腺苷A2a受体(ADORA2A)基因的胞外区。

特点和优势

该化合物在受体分类和信号转导手册的 钙通道环核苷酸门控(CNG)和超极化激活的环核苷酸门控(HCN)通道 页面上有详细描述。如需浏览其他手册页面,请点击此处
该化合物是ADME Tox和环核苷酸研究的特色产品。发现更多 ADME Tox环核苷酸 的特色产品。了解更多有关用于其他研究领域的生物活性小分子的信息,请访问sigma.com/discover-bsm
该化合物由 Bayer开发。想浏览其他制药公司开发的化合物和已批准药物/候选药物目录, 请单击此处

象形图

Exclamation mark

警示用语:

Warning

危险声明

危险分类

Acute Tox. 4 Oral

储存分类代码

11 - Combustible Solids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

dust mask type N95 (US), Eyeshields, Gloves


分析证书(COA)

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  1. Which document(s) contains shelf-life or expiration date information for a given product?

    If available for a given product, the recommended re-test date or the expiration date can be found on the Certificate of Analysis.

  2. How do I get lot-specific information or a Certificate of Analysis?

    The lot specific COA document can be found by entering the lot number above under the "Documents" section.

  3. How do I find price and availability?

    There are several ways to find pricing and availability for our products. Once you log onto our website, you will find the price and availability displayed on the product detail page. You can contact any of our Customer Sales and Service offices to receive a quote.  USA customers:  1-800-325-3010 or view local office numbers.

  4. What is the Department of Transportation shipping information for this product?

    Transportation information can be found in Section 14 of the product's (M)SDS.To access the shipping information for this material, use the link on the product detail page for the product. 

  5. What is the solubility of Product N7634, Nifidipine?

    Nifedipine can be dissolved in DMSO at 50 mg/ml1. It is sparingly soluble in absolute ethanol2. Herembert, T. et al., dissolved nifedipine in absolute ethanol (no concentration reported); the maximum ethanol concentration in cultures was 0.2% without any effect of solvent on the cells3. Nifedipine is soluble (g/L, at 20°C) in the following solvents: acetone, 250; methylene chloride, 160; chloroform, 140; ethyl acetate, 50; methanol, 26; ethanol, 17.4 It is practically insoluble in water. The solubilities at 37°C in buffer solutions of different pH values are: pH 4, 0.0058 g/L; pH 7, 0.0056 g/L; pH 9.0, 0.0078 g/L; pH 13, 0.006 g/L1. References:  1.  Ali, S.L., Analytical Profiles of Drug Substances, 18, 221, (1989).   2.  Martindale, The Extra Pharmacopoeia, 30th ed., 374, (1993).  and 3.  Herembert, T. et al. Brit. J. Pharmacol., 114, 1703, (1995).

  6. Are there any recommended dosages for Product N7634, Nifidipine, in vivo and in vitro?

    Nifedipine is reported to inhibit Ca2+-sensitive K+ channels at 100 μM1. Doses for different animals have been reported2,3. In randomly growing cultures of aortic cells of rats, nifedipine at 10 μM inhibited cell proliferation. References:  1.  Thomas-Young, R.J. et al. Biochim. Biophys. Acta, 1146, 81, (1993).      2.  Drug Dosages In Laboratory Animals: A Handbook, 3rd ed., Telford Press.  and 3.  Borchard, R.E. et al. Drug Dosage in Laboratory Animals, A Handbook, Third Edition, p. 315, The Telford Press, (1990).

  7. What is the half life of Product N7634, Nifidipine, in vivo?

    After administration by the mouth, the half-life is 2 to 5 hours 1. In plasma, about 92-98% binds to plasma proteins.  Nifedipine is completely metabolized. About 70% of a dose is excreted in the urine in 24 hours as metabolites including 5-methoxycarbonyl-2,6-dimethyl-4-(2-nitrophenyl) pyridine-3-carboxylic acid; dimethyl 2,6-dimethyl-4-(2-nitrophenyl pyridine-3,5-dicarboxylate and 2-hydroxymethyl-5-methoxycarbonyl-6-methyl-4-(2-nitrophenyl) pyridine-3-carboxylic acid and its lactone derivative. Up to 15% of a dose is eliminated in the feces as metabolites in 4 days 2. References:  1.  Martindale, 29th ed., pgs. 1509-1513.  2.  Clarke's Isolation and Identification of Drugs., 2nd ed., p. 811.

  8. Are there any recommended conditions that Product N7634, Nifidipine, should be used in?

    When exposed to daylight and certain wavelengths of artificial light, nifedipine readily converts to a nitrosophenylpyridine derivative. Exposure to ultra-violet light leads to the formation of a nitrophenylpyridine derivative. Therefore, USP recommends that assays be performed in the dark or under golden fluorescent or other low actinic light. Low actinic glassware should be used1.

  9. My question is not addressed here, how can I contact Technical Service for assistance?

    Ask a Scientist here.

Combination therapy with cisplatin and nifedipine induces apoptosis in cisplatin-sensitive and cisplatin-resistant human glioblastoma cells
Kondo S, et al.
British Journal of Cancer, 71(2), 282-282 (1995)
R-type calcium channels in myenteric neurons of guinea pig small intestine
Bian X, et al.
American Journal of Physiology: Gastrointestinal and Liver Physiology, 287(1), G134-G142 (2004)
Cell-type-specific interrogation of CeA Drd2 neurons to identify targets for pharmacological modulation of fear extinction
McCullough KM, et al.
Translational Psychiatry, 8(1), 164-164 (2018)
Combination therapy of nifedipine and sulphonyl ureas exhibits a mutual antagonistic effect on the endothelial cell dysfunction induced by hyperglycemia linked to vascular disease
Wang LP, et al.
Cellular Physiology and Biochemistry, 38(6), 2337-2347 (2016)
An Liu et al.
Neurochemical research, 44(3), 683-691 (2017-10-21)
Abnormal processing of amyloid precursor protein (APP) and aggregation of the Aβ peptide are known to play a key role in the pathogenesis of Alzheimer disease, but the function of endogenous APP under normal physiological conditions remains poorly understood. In

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Cyclic nucleotides, including cyclic AMP (cAMP), cyclic GMP (cGMP) and cyclic ADP-ribose, have been extensively studied as second messengers of intracellular events initiated by activation of GPCRs. cAMP modifies cell function in all eukaryotic cells, principally through the activation of cAMP-dependent protein kinase (PKA), but also through cAMP-gated ion channels and guanine nucleotide exchange factors directly activated by cAMP.

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