Moexipril HCl

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Moexipril HCl 是一种有效的口服活性非巯基血管紧张素转换酶 (ACE) 抑制剂，用于治疗高血压和充血性心力衰竭。

Moexipril HCl is a potent orally active nonsulfhydrylangiotensin converting enzyme (ACE)inhibitor, used for the treatment of hypertension and congestive heart failure.(In Vitro):Moexipril hydrochloride is devoid of anti-inflammatory properties and has no effect on platelet function.Moexipril hydrochloride hydrolyzes to Moexiprilat, and Moexiprilat inhibits ACE in guinea pig serum as well as on purified ACE from rabbit lung with IC50s of 2.6 and 4.9 nM, respectively.Moexipril hydrochloride (0.01 nM-0.1 mM) exhibits high potency against both plasma ACE and purified ACE from rabbit lung, with IC50s of 2.7 mM and 0.165 mM, respectively.Moexipril hydrochloride (0-100 μM, 24 h) significantly reduced the percentage of damaged neurons in a dose-dependent manner.Moexipril hydrochloride (0-100 μM, 24 h) significantly attenuates Fe2+/3+-induced neurotoxicity.Moexipril hydrochloride dose not cause significant changes in the percentage of apoptotic neurons.(In Vivo):Moexipril hydrochloride can not cross the blood-brain barrier.Moexipril hydrochloride (3 mg/kg, 30 mg/kg and 10 mg/kg, respectively; p.o.; once daily; 5 days) exhibits the a dose-dependent and antihypertensive effects in renal hypertensive rats, spontaneously hypertensive rats and perinephritic hypertensive dogs, respectively.Moexipril hydrochloride (0.3 mg/kg, i.p.) significantly reduces the infarct area on the mouse brain surface in NMRI mice.Moexipril hydrochloride (0.1 mg/kg, i.p.) significantly attenuates the cortical infarct volume in Long-Evans rats.

Moexipril hydrochloride is devoid of anti-inflammatory properties and has no effect on platelet function.Moexipril hydrochloride hydrolyzes to Moexiprilat, and Moexiprilat inhibits ACE in guinea pig serum as well as on purified ACE from rabbit lung with IC50s of 2.6 and 4.9 nM, respectively.Moexipril hydrochloride (0.01 nM-0.1 mM) exhibits high potency against both plasma ACE and purified ACE from rabbit lung, with IC50s of 2.7 mM and 0.165 mM, respectively.Moexipril hydrochloride (0-100 μM, 24 h) significantly reduced the percentage of damaged neurons in a dose-dependent manner.Moexipril hydrochloride (0-100 μM, 24 h) significantly attenuates Fe2+/3+-induced neurotoxicity.Moexipril hydrochloride dose not cause significant changes in the percentage of apoptotic neurons.

Moexipril hydrochloride can not cross the blood-brain barrier.Moexipril hydrochloride (3 mg/kg, 30 mg/kg and 10 mg/kg, respectively; p.o.; once daily; 5 days) exhibits the a dose-dependent and antihypertensive effects in renal hypertensive rats, spontaneously hypertensive rats and perinephritic hypertensive dogs, respectively.Moexipril hydrochloride (0.3 mg/kg, i.p.) significantly reduces the infarct area on the mouse brain surface in NMRI mice.Moexipril hydrochloride (0.1 mg/kg, i.p.) significantly attenuates the cortical infarct volume in Long-Evans rats. Animal Model:Spontaneously hypertensive rats Dosage:30 mg/kg Administration:Oral gavage; once daily; 5 days Result:Caused a progressive lowering of mean blood pressure from pretreatment values of 180 +/- 7 mmHg to a trough on day 4 of 127 +/- 4 mmHg.Dose-dependently decreased arterial blood pressure, and inhibited plasma and tissue ACE activity.Animal Model:Renal hypertensive rats Dosage:0.03-10 mg/kg Administration:Oral gavage; once daily; 5 days Result:Caused a dose-dependent decrease in blood pressure with a threshold dose of 0.3 mg/kg. Lowered mean blood pressure by about 70 mmHg of 3 mg/kg.Animal Model:Perinephritic hypertensive dogs Dosage:10 mg/kg Administration:Oral gavage; once daily; 5 days Result:Caused a drop of mean blood pressure by 25 mmHg from pre-treatment control, which persisted for 24 h, by a rapid onset and a long duration of action.Animal Model:NMRI mice (male, Permanent focal ischemia) Dosage:0, 0.03, 0.3, and 3 mg/kg Administration:Intraperitoneal injection (1 h before middle cerebral artery occlusion)Result:Significantly reduced the infarct area on the mouse brain surface with a dose of 0.3 mg/kg, and other doses were not effective.Animal Model:Long-Evans rats (male, Permanent focal ischemia)Dosage:0, 0.01, 0.1 mg/kg Administration:Intraperitoneal injection (1 h before middle cerebral artery occlusion)Result:Significantly attenuated the cortical infarct volume from 114.4 to 98.2 mm as compared to non-treated animals in a dose of 0.01 mg/kg, without reducing the infarct volume of the rat brain at dosages >0.01 mg/kg.

RS-10085

Others

Other Targets

ACE

Cardiovascular Disease

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82586-52-5

535.03

C27H34N2O7·HCl

>98% (HPLC)

DMSO : ≥ 100 mg/mL; 186.91 mM

Cl.CCOC(=O)[C@H](CCC1=CC=CC=C1)N[C@@H](C)C(=O)N1CC2=CC(OC)=C(OC)C=C2C[C@H]1C(O)=O

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(-20℃)

With Ice Pack

≥ 2 years