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    Ramipril (HOE-498)
    Ramipril (HOE-498)

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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 #: V1783
    CAS #: 87333-19-5 Purity ≥98%

    Description: Ramipril (HOE-498; Altace; Carasel; Ramace; Zabien; Tritace; Ramace; Triatec; Tritace; Vesdil) is a potent angiotensin-converting enzyme (ACE) inhibitor with anti-hypertensive effects. It inhibits ACE with an IC50 of 5 nM and has been approved for hypertension treatment. Ramipril is a produg that has to be activated by hydrolysis to the active metabolite Ramiprilat. Studies indicate that Ramipril is a more potent inhibitor in comparison to Zofenopril (sc-208496). Acute coronary syndrome investigations demonstrate that Ramipril increases IL-10, and decreases the levels of MCP-1 and IL-18.

    References: Circ Res. 2004 Jan 9;94(1):60-7; Cardiovasc Drugs Ther. 2007 Dec;21(6):423-9. 

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    Molecular Weight (MW)416.51 
    FormulaC23H32N2O5 
    CAS No.87333-19-5 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 83 mg/mL (199.3 mM)
    Water: <1 mg/mL
    Ethanol: 83 mg/mL (199.3 mM)
    Solubility (In vivo)30% PEG400+0.5% Tween80+5% Propylene glycol: 30 mg/mL  
    SynonymsHOE-498; Altace; Carasel; HOE498; Ramace; Zabien; HOE 498; Tritace; Ramace; Triatec; Tritace; Vesdil;


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    In Vitro

    In vitro activity: Ramipril is an angiotensin-converting enzyme (ACE) inhibitor with IC50 of 5 nM. Ramipril enhances the activity of ACE-associated CK2 and the phosphorylation of ACE Ser1270 in cultured endothelial cells, but is unable to activate JNK or stimulate the nuclear accumulation of c-Jun in endothelial cells expressing a S1270A ACE mutant or in ACE-deficient cells. Prolonged Ramipril treatment increases ACE expression in primary cultures of human endothelial cells and in vivo (mouse lung), which can be prevented by pretreatment with the JNK inhibitor SP600125. Ramipril displays little enhanced effect on the rate of in vitro endothelial apoptosis induced by the serum deprivation method.


    Cell Assay: The HUVECs are pretreated with the active metabolites of Ramipril for 24 hours. A serum deprivation method is used to induce apoptosis in the presence of Ramipril for an additional 24 hours. The rate of apoptosis is then determined using flow cytometry with two makers annexinV fluorescein isothiocyanate (FITC+) and propidium iodide (PI). 

    In VivoChronic in vivo administration of Ramipril to rats at a dosage that has similar hypotensive effects in vitro HUVECs significantly reduces the rate of LPS-induced apoptosis compared to the other ACE inhibitors, which contrasts with the apoptosis effect in vitro. Ramipril inhibits systolic blood pressure (SBP) with IC50 of 1.97 mg/kg in spontaneously hypertensive rats (SHR). When in combination with AT1-receptor blockade by candesartan-cilexetil increases SBP reduction synergistically rather than additively. Administration of Ramipril to spontaneously hypertensive rats (SHR) produces significant inhibition of aorta ACE and lung ACE with IC50 ~5 mg/kg, but shows little effect for brain ACE ex vivo. Ramipril prevents beta cell dysfunction in osteoprotegerin treated mice through decreasing islet monocyte/macrophage infiltration, fibrosis and apoptosis involving decreasing RAS, growth factor genes and inflammatory molecules expressions.
    Animal modelMale spontaneously hypertensive rats
    Formulation & DosageDissolved in distilled water by using gum arabic (10% w/v); 0.03-10 mg/kg; Oral gavage 
    References

    Circ Res. 2004 Jan 9;94(1):60-7; Cardiovasc Drugs Ther. 2007 Dec;21(6):423-9.  


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

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