Nifedipine

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

硝苯地平（Adalat），一种具有钙拮抗作用的强效血管扩张剂。

Nifedipine(Adalat), a potent vasodilator agent with calcium antagonistic action.(In Vitro):Nifedipine (BAY-a-1040) (100 μM) significantly lowers the viability of the WKPT-0293 Cl.2 Cells, and treatment of nifedipine (10 or 100 μM) plus FAC induces a significant reduction in cell viability, but there are no significant differences in viability between the control cells and the cells treated with 100 μM of FAC or 1 and 10 μM of nifedipine.Nifedipine (BAY-a-1040) (1, 10, or 100 μM) significantly increases iron level in WKPT-0293 Cl.2 cells. Nifedipine treatment also increases expression of TfR1, DMT1+IRE and DMT1-IRE in WKPT-0293 Cl.2 cells. In addition, co-treatment with nifedipine (100 μM) and FAC (100 μM) increases TfR1, DMT1+IRE and DMT1-IRE expression in WKPT-0293 Cl.2 cells. Nifedipine plus ritodrine produces a significantly greater inhibition of contractility than each drug alone in the midrange of concentrations. The combination of nifedipine plus nitroglycerin or nifedipine plus atosiban produces a significantly greater inhibition than nitroglycerin or atosiban alone but not greater than nifedipine. The combination of nifedipine plus NS-1619 (Ca2+-activated K+ [BKCa] channel opener) reduces the inhibitory effect of each drug. Nifedipine (BAY-a-1040) (2 μM) significantly inhibits P. capsici mycelial growth and sporulation. Nifedipine (BAY-a-1040)-induced inhibition of mycelial growth is calcium-dependent. Nifedipine (0.5 μM) increases P. capsici sensitivity to H2O2 in a calcium-dependent manner. Nifedipine inhibition of P. capsici virulence and expression of genes involved in pathogenicity.(In Vivo):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.

Nifedipine (BAY-a-1040) (100 μM) significantly lowers the viability of the WKPT-0293 Cl.2 Cells, and treatment of nifedipine (10 or 100 μM) plus FAC induces a significant reduction in cell viability, but there are no significant differences in viability between the control cells and the cells treated with 100 μM of FAC or 1 and 10 μM of nifedipine.Nifedipine (BAY-a-1040) (1, 10, or 100 μM) significantly increases iron level in WKPT-0293 Cl.2 cells. Nifedipine treatment also increases expression of TfR1, DMT1+IRE and DMT1-IRE in WKPT-0293 Cl.2 cells. In addition, co-treatment with nifedipine (100 μM) and FAC (100 μM) increases TfR1, DMT1+IRE and DMT1-IRE expression in WKPT-0293 Cl.2 cells. Nifedipine plus ritodrine produces a significantly greater inhibition of contractility than each drug alone in the midrange of concentrations. The combination of nifedipine plus nitroglycerin or nifedipine plus atosiban produces a significantly greater inhibition than nitroglycerin or atosiban alone but not greater than nifedipine. The combination of nifedipine plus NS-1619 (Ca2+-activated K+ [BKCa] channel opener) reduces the inhibitory effect of each drug. Nifedipine (BAY-a-1040) (2 μM) significantly inhibits P. capsici mycelial growth and sporulation. Nifedipine (BAY-a-1040)-induced inhibition of mycelial growth is calcium-dependent. Nifedipine (0.5 μM) increases P. capsici sensitivity to H2O2 in a calcium-dependent manner.

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.

BAY 1040

GPCR/G Protein

Calcium Channel

Calcium Channel| CAM| Potassium Channel

Cardiovascular Disease

——

21829-25-4

346.34

C17H18N2O6

>98% (HPLC)

Ethanol: 15 mg/mL (43.31 mM); DMSO: 69 mg/mL (199.23 mM)

O=C(C1=C(C)NC(C)=C(C(OC)=O)C1C2=CC=CC=C2[N+]([O-])=O)OC

dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate

(-20℃)

With Ice Pack

≥ 2 years