RAAS inhibitor
Moexipril HCl is a potent orally active nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, used for the treatment of hypertension and congestive heart failure.
Moexipril HCl 10 mM (1mL in DMSO)
£120.00
Target: angiotensin converting enzyme (ACE)
Chemical name: (3S)- 2-[(2S)-2-[[(1S)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]-1,2,3,4-tetrahydro-6,7-dimethoxy-3-isoquinolinecarboxylic acid,hydrochloride (1:1)
Formula: C27H34N2O7.HCl
Molecular weight: 535.03
Purity: 99.73 %
Solubility: 20 mg/mL (DMSO)
Size: 10 mM (1mL in DMSO)
Storage: 3 years -20°C powder, 2 years -80°C in solvent
In vitro:
Moexipril dose-dependently reduces the percentage of damaged neurons, as well as mitochondrial reactive oxygen species generation induced by glutamate, staurosporine or Fe2+/3+. Moexipril and enalapril attenuates staurosporine-induced neuronal apoptosis as determined by nuclear staining with Hoechst 33258. [1]
In vivo:
Moexipril (0.3 mg/kg) significantly reduces brain damage after focal ischemia as compared to control mice. Moexipril (0.01 mg/kg) is able to reduce the infarct volume in the rat model after focal cerebral ischemia. [1] Moexipril reduces blood pressure after the first week of treatment but it has no apparent effect on either the proximal tibial metaphysis or the tibial shaft in ovariectomized (OVX) spontaneously hypertensive rats (SHR). Moexipril combined with hydrochlorothiazide (HCTZ) exhibits a much more potent hypotensive effect and has the same effect on bone mass and dynamic end-points as HCTZ alone. [2] Moexiprilat exhibits a higher inhibitory potency than enalaprilat against both plasma ACE and purified ACE from rabbit lung. Moexipril (0.1-30 mg/kg/day) lowers blood pressure and differentially inhibits ACE activity in plasma, lung, aorta, heart and kidney in a dose-dependent fashion. Moexipril (10 mg/kg/day) leads to comparable decreases in blood pressure, inhibition of plasma ACE and reduction of plasma angiotensinogen and to a similar attenuation of the pressor responses to angiotensin I and potentiation of the depressor responses to bradykinin. [3]
References:
[1] Ravati A, et al. Eur J Pharmacol,?999, 373(1), 21-33.
[2] Ma YF, et al. J Endocrinol,?997, 154(3), 467-474.
[3] Edling O, et al. J Pharmacol Exp Ther,?995, 275(2), 854-863.