103775-10-6

103775-10-6 structure

Name: Moexipril
Chemical Name: (3S)-2-[(2S)-2-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-6,7-dimethoxy-3,4-dihydro-1H-isoquinoline-3-carboxylic acid
CAS Number: 103775-10-6
Molecular Formula: C₂₇H₃₄N₂O₇
Molecular Weight: 498.57
Catalog: API Circulatory system medication Antihypertensive drug
Create Date: 2018-08-31 10:09:29
Modify Date: 2024-01-05 13:03:55
Moexipril is an orally active and potent angiotensin-converting enzyme (ACE) inhibitor. Moexipril can readily penetrate lipid membranes and thus target plasma and tissue ACE. Moexipril may improve endothelial dysfunction and exert neuroprotective effects. Moexipril can used for cardiovascular disease research[1][2].

Name	(3S)-2-[(2S)-2-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-6,7-dimethoxy-3,4-dihydro-1H-isoquinoline-3-carboxylic acid
Synonyms	Moexiprilum (3S)-2-(N-{(1S)-1-[(ethyloxy)carbonyl]-3-phenylpropyl}-L-alanyl)-6,7-bis(methyloxy)-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid Univasc [3S-[2[R(R)],3R*]]-2-[2-[[1-(Ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]-1,2,3,4-tetrahydro-6,7-dimethoxy-3-isoquinolinecarboxylic Acid (3S)-2-((2S)-N-((1S)-1-Carboxy-3-phenylpropyl)alanyl)-1,2,3,4-tetrahydro-6,7-dimethoxy-3-isoquinolinecarboxylic acid 2-ethyl ester 3-Isoquinolinecarboxylic acid, 2-[(2S)-2-[[(1S)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]-1,2,3,4-tetrahydro-6,7-dimethoxy-, (3S)- UNII-WT87C52TJZ Moexipril Moexipril (INN) Moexipril [INN:BAN] Moexiprilum [INN-Latin] (3S)-2-{N-[(1S)-1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl}-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (3S)-2-{N-[(2S)-1-Ethoxy-1-oxo-4-phenyl-2-butanyl]-L-alanyl}-6,7-dimethoxy-1,2,3,4-tetrahydro-3-isoquinolinecarboxylic acid (3S)-2-{N-[(2S)-1-Ethoxy-1-oxo-4-phenylbutan-2-yl]-L-alanyl}-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid MFCD00865878 Uniretic

Description	Moexipril is an orally active and potent angiotensin-converting enzyme (ACE) inhibitor. Moexipril can readily penetrate lipid membranes and thus target plasma and tissue ACE. Moexipril may improve endothelial dysfunction and exert neuroprotective effects. Moexipril can used for cardiovascular disease research[1][2].
Related Catalog	Research Areas >> Cardiovascular Disease Signaling Pathways >> Metabolic Enzyme/Protease >> Angiotensin-converting Enzyme (ACE) Research Areas >> Neurological Disease
Target	IC50: 2.1 nM (purified ACE from rabbit lung), 1.75 nM (ACE in rat plasma)[1]
In Vitro	Moexipril shows inhibitory activity against purified ACE from rabbit lung and ACE in rat plasma, with IC50 values of 2.1 nM and 1.75 nM, respectively[1]. Moexipril (0-100 μM, 24 h) significantly reduced the percentage of damaged neurons in a dose-dependent manner[3]. Moexipril (0-100 μM, 24 h) significantly attenuates Fe2+/3+-induced neurotoxicity[3]. Moexipril dose not cause significant changes in the percentage of apoptotic neurons[3].
In Vivo	Moexipril (SHR, 10 mg/kg, Orally, once a day for 3 days) completely blocks plasma ACE activity 1 h after dosage and still inhibits 56% plasma ACE activity 24 h afterward[1]. Moexipril (SHR, 0-30 mg/kg, Orally, once a day for 4 weeks) dose-dependently decreases arterial blood pressure, and inhibits plasma and tissue ACE activity[1]. Moexipril (NMRI mice, 0.3 mg/kg, IP, once) significantly reduces the infarct area on the mouse brain surface[3]. Moexipril (Long-Evans rats, 0.1 mg/kg, IP, once) significantly attenuates the cortical infarct volume[3]. Animal Model: SHR (spontaneously hypertensive rats, n=10)[1] Dosage: 10 mg/kg Administration: Orally, once daily for 3 days Result: Completely blocked plasma ACE activity 1 h after dosage and still inhibited 56% plasma ACE activity 24 h afterward, decreased the concentration of ANG Ⅱ and increased the concentration of ANG Ⅰ 1 h after dosage and recovered to control levels 24 h after dosage. Animal Model: SHR (n = 8 to 10 per group)[1] Dosage: 0, 0.1, 1, 3, 10, 30 mg/kg Administration: Orally, once daily for 4 weeks Result: Decreased arterial blood pressure, and inhibited plasma and tissue (lung, aorta, heart and kidney) ACE activity in a dose-dependent manner. Animal Model: NMRI mice (male, Permanent focal ischemia)[3] Dosage: 0, 0.03, 0.3, and 3 mg/kg Administration: IP, once (injected 1 h before middle cerebral artery occlusion) Result: Significantly reduced the infarct area on the mouse brain surface (at 0.3 mg/kg), and other doses were not effective. Animal Model: Long-Evans rats (male, Permanent focal ischemia)[3] Dosage: 0, 0.01, 0.1 mg/kg Administration: IP, once (injected 1 h before middle cerebral artery occlusion) Result: Significantly attenuated the cortical infarct volume from 114.4 to 98.2 mm3 as compared to non-treated animals (at 0.01 mg/kg), did not reduce the infarct volume of the rat brain at dosages higher than 0.01 mg/kg.
References	[1]. [1] Edling O, et al. Moexipril, a new angiotensin-converting enzyme (ACE) inhibitor: pharmacological characterization and comparison with enalapril. J Pharmacol Exp Ther. 1995 Nov;275(2):854-63. [2]. [2] Pines A, Fisman EZ. ACE Inhibition with moexipril: a review of potential effects beyond blood pressure control. Am J Cardiovasc Drugs. 2003;3(5):351-60. [3]. [3] Ravati A, et al. Enalapril and moexipril protect from free radical-induced neuronal damage in vitro and reduce ischemic brain injury in mice and rats. Eur J Pharmacol. 1999 May 28;373(1):21-33.

Density	1.2±0.1 g/cm3
Boiling Point	709.3±60.0 °C at 760 mmHg
Molecular Formula	C₂₇H₃₄N₂O₇
Molecular Weight	498.57
Flash Point	382.8±32.9 °C
Exact Mass	498.236603
PSA	114.40000
LogP	4.05
Vapour Pressure	0.0±2.4 mmHg at 25°C
Index of Refraction	1.565

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