Moexipril (莫艾普利)是一种口服有效的血管紧张素转换酶 (ACE) 抑制剂。Moexipril 可以轻易穿透脂质膜，从而靶向血浆和组织ACE。Moexipril 可改善内皮功能障碍，发挥神经保护作用。Moexipril 可用于心血管疾病研究。

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].

Moexipril shows inhibitory activity against purified ACE from rabbit lung and ACE in rat plasma, with IC 50 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 Fe 2+/3+ -induced neurotoxicity [3]. Moexipril dose not cause significant changes in the percentage of apoptotic neurons [3].

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 mm 3 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.

103775-10-6

C27H34N2O7

498.57

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years