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    Cilnidipine (FRC8653)
    Cilnidipine (FRC8653)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1650
    CAS #: 132203-70-4Purity ≥98%

    Description: Cilnidipine (formerly also known as FRC-8653; FRC8653; Atelec; Cinalong; Siscard) is a novel, potent and unique dual L-type and N-type calcium channel blocker (CCB) that was approved as an anti-hypertensive drug in 1995 for high blood pressure treatment. Cilnidipine lowers mean blood pressure and reduces the size of cerebral infarction in the rat model of focal brain ischemia. Cilnidipine has displayed renal and vascular protective effects and improved baroreflex sensitivity in patients with hypertension. It has also demonstrated neuroprotective effects in a rat focal brain ischemia model by removing free radicals and activating the phosphatidylinositol 3-kinase pathway.

    References: Hypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43.

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    Molecular Weight (MW)492.52 
    CAS No.132203-70-4 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 99 mg/mL (201.0 mM) 
    Water: <1 mg/mL
    Ethanol: 15 mg/mL (30.5 mM) 
    Solubility (In vivo)5% DMSO+Corn oil: 7 mg/mL  
    SynonymsFRC-8653; Cilnidipine; Atelec; Cinalong; Siscard; FRC 8653; FRC8653.

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    In Vitro

    In vitro activity: Cilnidipine (10 mM) suppresses the elevation of the ratio induced by 40 mM KCl, and this suppression is effectively inhibited after the treatment with omega-conotoxin GVIA.

    In VivoCilnidipine reduces Ca(2+) influx via N-type Ca(2+) channels after NMDA receptors activation and then protects neurons against ischemia-reperfusion injury in the rat retina in vivo. Cilnidipine significantly prevents the increase in desmin staining and restores the glomerular podocin and nephrin expression compared with amlodipine in spontaneously hypertensive rat/ND mcr-cp (SHR/ND). Cilnidipine also prevents the increase in renal angiotensin II content, the expression and membrane translocation of NADPH oxidase subunits and dihydroethidium staining in SHR/ND. Cilnidipine (30 mg/kg/d as food admix) treatment suppresses the increase in systolic blood pressure in Dahl salt-sensitive rats. Cilnidipine inhibits the increase in blood urea nitrogen and decrease in creatinine clearance as well as progression of glomerular sclerosis. Cilnidipine reduces plasma norepinephrine level and plasma rennin activity compared with vehicle-treated Dahl S rats. Cilnidipine suppresses the pressor response induced by sympathetic nerve stimulation and angiotensin II in pithed rats. Cilnidipine or omega-conotoxin MVIIA decreases mean blood pressure, but slightly increases heart rate in anesthetized rats. Cilnidipine can affect sympathetic N-type Ca(2+) channels in addition to vascular L-type Ca(2+) channels in antihypertensive doses in the rat in vivo.
    Animal modelRats
    Formulation & Dosage30 mg/kg/d as food admix
    ReferencesHypertens Res. 2003 Sep;26(9):743-7; J Hypertens. 2010 May;28(5):1034-43. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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