IC1870 西尼地平 跨膜转运/离子通道 索莱宝

IC1870 西尼地平 跨膜转运/离子通道 索莱宝

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  • ¥208 - 1290
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  • 北京
  • IC1870
  • 2025年12月23日
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    • 详细信息
    • 技术资料
    • 保存条件

      Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year

    • 保质期

      Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year

    • 英文名

      Cilnidipine

    • 库存

      现询

    • 供应商

      北京索莱宝科技有限公司

    • CAS号

      132203-70-4

    • 规格

      5mg/100mg/50mg/10mg

    规格:5mg产品价格:¥208.0
    规格:100mg产品价格:¥1290.0
    规格:50mg产品价格:¥790.0
    规格:10mg产品价格:¥340.0

    是L型和N型钙离子阻断剂。

    基本信息
    CASNo.132203-70-4
    中文名称西尼地平
    英文名称Cilnidipine
    别名西尼地平;FRC8653
    分子式C27H28N2O7
    分子量492.52
    溶解性Soluble in DMSO
    纯度HPLC≥98%
    外观(性状)Light yellow to green yellow Solid
    储存条件Powder:2-8℃,2 years;Insolvent(母液):-20℃,6 months;-80℃,1 year
    ECEINECS 634-350-6
    MDLMFCD00865853
    SMILESO=C(C1=C(C)NC(C)=C(C(OC/C=C/C2=CC=CC=C2)=O)C1C3=CC=CC([N+]([O-])=O)=C3)OCCOC
    靶点Calcium Channel
    通路Membrane Transporter&Ion Channel;Neuronal Signaling
    背景说明是L型和N型钙离子阻断剂。
    In VitroFollowing H(2)O(2)exposure,the viability of nPC12 cells decreased significantly; however,treatment with cilnidipine increased the viability of H(2)O(2)-injured nPC12 cells in a concentration-dependent manner. Treatment with H(2)O(2)resulted in a concentration-dependent increase in free radical levels in nPC12 cells,and cilnidipine treatment reduced free radical levels in H(2)O(2)-injured nPC12 cells in a dose-dependent manner. Cilnidipine treatment increased the expression of p85aPI3K(phosphatidylinositol 3-kinase)phosphorylated Akt,phosphorylated glycogen synthase kinase-3(pGSK-3beta),and heat shock transcription factor(HSTF-1)which are proteins related to neuronal cell survival,and decreased levels of cytosolic cytochrome c,activated caspase 3,and cleaved poly(ADP-ribose)polymerase(PARP),which are associated with neuronal cell death,in H(2)O(2)-injured nPC12 cells. These results indicate that cilnidipine mediates its neuroprotective effects by reducing oxidative stress,enhancing survival signals(e.g.,PI3K,phosphorylated Akt,pGSK-3beta,and HSTF-1),and inhibiting death signals from cytochrome c release,caspase 3 activation,and PARP cleavage.[2]
    细胞实验Administration of cilnidipine(10 mg/kg),an L and N-type dual calcium channel blocker,significantly attenuated the immobilized stress-induced behavioral changes and restored memory deficits along with normalization of the corticosterone levels. Cilnidipine mediated attenuation of corticosterone release by blockage of calcium channels(both L and N-type)on the HPA-axis is responsible for beneficial effects in restoration of behavioral alterations and memory deficits in immobilization-induced acute stress in mice.[1]
    细胞实验To evaluate the effect of cilnidipine on viability,nPC12 cells were treated with several concentrations of this drug before performing viability assays. Cell viability was not affected by low concentrations of cilnidipine up to 150 microM,but it was slightly decreased at 200 microM cilnidipine. [2]
    数据来源文献[1]. Naresh Kumar, et al. Anti-stress effects of cilnidipine and nimodipine in immobilization subjected mice. Physiol Behav. 2012 Mar 20;105(5):1148-55.
    [2]. Young Joo Lee, et al. Cilnidipine mediates a neuroprotective effect by scavenging free radicals and activating the phosphatidylinositol 3-kinase pathway. J Neurochem. 2009 Oct;111(1):90-100.
    单位

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