Moexipril (hydrochloride)

Moexipril hydrochloride (RS-10085) is an orally active inhibitor of angiotensin-converting enzyme (ACE), and becomes effective by being hydrolyzed to moexiprila (hydrochloride). Moexipril hydrochloride exhibits antihypertensive and neuroprotective effects^[1]-[4]. IC50 & Target: IC50: 2.1 nM (purified ACE from rabbit lung), 1.75 nM (ACE in rat plasma)^[3] In Vitro: Moexipril hydrochloride is devoid of anti-inflammatory properties and has no effect on platelet function^[2].
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^[2].
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^[3].
Moexipril hydrochloride (0-100 μM, 24 h) significantly reduced the percentage of damaged neurons in a dose-dependent manner^[4].
Moexipril hydrochloride (0-100 μM, 24 h) significantly attenuates Fe^2+/3+-induced neurotoxicity^[4].
Moexipril hydrochloride dose not cause significant changes in the percentage of apoptotic neurons^[4]. In Vivo: Moexipril hydrochloride can not cross the blood-brain barrier^[1].
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^[3].
Moexipril hydrochloride (0.3 mg/kg, i.p.) significantly reduces the infarct area on the mouse brain surface in NMRI mice^[4].
Moexipril hydrochloride (0.1 mg/kg, i.p.) significantly attenuates the cortical infarct volume in Long-Evans rats^[4].