您好,欢迎来到试剂仪器网! [登录] [免费注册]
试剂仪器网
位置:首页 > 产品库 > Nifedipine
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
Nifedipine
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Nifedipine图片
CAS NO:21829-25-4
包装与价格:
包装价格(元)
10mM (in 1mL DMSO)电议
1g电议
5g电议
10g电议

产品介绍

化学性质

StorageStore at -20°C
M.Wt346.33
Cas No.21829-25-4
FormulaC17H18N2O6
Solubilityinsoluble in H2O; ≥15.75 mg/mL in DMSO; ≥7.14 mg/mL in EtOH with ultrasonic
Chemical Namedimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
Canonical SMILESCC1=C(C(C(=C(N1)C)C(=O)OC)C2=CC=CC=C2[N+](=O)[O-])C(=O)OC
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

Nifedipine (BAY-a-1040) is an efficient calcium channel blocker which blocked L-type calcium current with an IC50 of 0.3 μM[1]. In the heart, it is also a drug of choice for cardiac insufficiency.

Nifedipine (BAY-a-1040) is wildly used as a dihydropyridine derivative. It forms a stable complex with the binding site of L-type calcium receptors. Nifedipine preferentially blocks various cell types’ Ca2+ channels and reduces cytosolic Ca2+ concentrations to prevent Ca2+ influx into the cells[2]. Nifedipine can decrease heart muscle sensitively during activation of beta 1-adrenergic receptors[3].

Nifedipine (BAY-a-1040) (100 μM) strongly reduce the viability of the WKPT-0293 Cl.2 Cells, and cell viability is significantly reduced when treated with nifedipine (10 or 100 μM) plus FAC, but there are no obvious differences in viability between the control cells and the cells treated with 100 μM of FAC or 1 and 10 μM of nifedipine. Iron level is considerably increased by treatment of Nifedipine (BAY-a-1040) (1, 10, or 100 μM) in WKPT-0293 Cl.2 cells. Nifedipine treatment also increases TfR1, DMT1+IRE and DMT1-IRE expression in WKPT-0293 Cl.2 cells. In addition, co-treatment with nifedipine (100 μM) and FAC (100 μM) increases expression of TfR1, DMT1+IRE and DMT1-IRE in WKPT-0293 Cl.2 cells[4]. Nifedipine plus ritodrine produces a significantly greater inhibition of contractility comparing with each drug alone in the midrange of concentrations. Nifedipine plus NS-1619 (Ca2+-activated K+ [BKCa] channel opener) combination decreases the inhibitory effect of each drug[5]. Nifedipine (BAY-a-1040) (2 μM) strongly inhibits the growth and sporulation of P. capsici mycelial. Nifedipine (BAY-a-1040)-induced mycelial growth inhibition is calcium-dependent[6].

In Nifedipine (BAY-a-1040) (50 mg/kg)- and CsA-treated rats, the BL dimensions (BLi and BLk), MD dimensions (MDk) and vertical dimensions (VHi and VHk) are significantly increased (P < 0.05) at the end of the 4th week[7].

References:

[1]. Jian-Bing Shen, Bin Jiang and Achilles J. Pappano. Comparison of L-Type Calcium Channel Blockade by Nifedipine and/or Cadmium in Guinea Pig Ventricular Myocytes. Journal of Pharmacology and Experimental Therapeutics August 2000, 294 (2) 562-570;

[2]. Nguemo F., Fleischmann B. K., Gupta M. K., Saric T., Malan D., Liang H., et al. (2013). The L-type Ca 2+ channels blocker nifedipine represses mesodermal fate determination in murine embryonic stem cells. PLoS One. 2013;8(1):e53407.

[3]. Legssyer AK, Hove-Madsen L, Hoerter J, Fischmeister R. Sympathetic modulation of the effect of nifedipine on myocardial contraction and Ca current in the rat. J Mol Cell Cardiol. 1997 Feb;29(2):579-91.

[4]. Yu SS, et al. Nifedipine Increases Iron Content in WKPT-0293 Cl.2 Cells via Up-Regulating Iron Influx Proteins. Front Pharmacol. 2017 Feb 13;8:60

[5]. Carvajal JA, et al. The Synergic In Vitro Tocolytic Effect of Nifedipine Plus Ritodrine on Human Myometrial Contractility. Reprod Sci. 2017 Apr;24(4):635- 640.

[6]. Liu P, et al. The L-type Ca2+Channel Blocker Nifedipine Inhibits Mycelial Growth, Sporulation, and Virulence of Phytophthora capsici. Front Microbiol. 2016 Aug 4;7:1236.

[7]. Ratre MS, et al. Effect of azithromycin on gingival overgrowth induced by cyclosporine A + nifedipine combination therapy: A morphometric analysis in rats. J Indian Soc Periodontol. 2016 Jul-Aug;20(4):396-401.