82586-52-5 Moexipril hydrochloride AKSci G636
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  G636    AKSci Reference Standard
Moexipril hydrochloride
, 98% (HPLC)

CAS Number:82586-52-5
MDL Number:MFCD00940481
Min. Purity Spec:98% (HPLC)
Physical Form (at 20°C):Solid
Melting Point:141-161°C
Flash Point:382.8°C
Optical Rotation:+34.2° (c=1.1, in ethanol)
Long-Term Storage:Store long-term at 2-8°C
Not hazardous material

Solubility:H2O: soluble 32 mg/mL
Application(s):Enzyme (ACE) inhibitor
Form:HCl salt


 Moexipril is a prodrug for moexiprilat, which inhibits ACE in humans and animals. The mechanism through which moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Moexiprilat is about 1000 times as potent as moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration (mean increases of about 0.25 mEq/L were seen when moexipril was used alone). Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of moexipril remains to be elucidated. Although the principal mechanism of moexipril in blood pressure reduction is believed to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in apparent low-renin hypertension.

[1]Asmar R, Sayegh F, Tracz W, Hlawaty M, Olszowska M, Jourde M, Vincent M, Goujoun B, Maldonado J: Reversal of left ventricular hypertrophy with the ACE inhibitor moexipril in patients with essential hypertension. Acta Cardiol. 2002 Feb;57(1):31-2.
[2] Blacher J, Raison J, Amah G, Schiemann AL, Stimpel M, Safar ME: Increased arterial distensibility in postmenopausal hypertensive women with and without hormone replacement therapy after acute administration of the ACE inhibitor moexipril. Cardiovasc Drugs Ther. 1998 Sep;12(4):409-14.
[3] Brogden RN, Wiseman LR: Moexipril. A review of its use in the management of essential hypertension. Drugs. 1998 Jun;55(6):845-60.
[4] Cawello W, Boekens H, Waitzinger J, Miller U: Moexipril shows a long duration of action related to an extended pharmacokinetic half-life and prolonged ACE inhibition. Int J Clin Pharmacol Ther. 2002 Jan;40(1):9-17.



Signal Word

Hazard Statements

Precautionary Statements
P273; P391; P501

G636Moexipril hydrochloride

Current as of May 21, 2024

AKSci Reference Standards are high-purity, low-impurity compounds suitable for use as standards.

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 APIs and Bioactives > ACE Inhibitors