High impact information on Zofenoprilat

• On the other hand, fosinoprilat is excreted both in urine and bile (as with temocaprilat, zofenoprilat and spiraprilat), and thus an adjustment of dosage and/or administration interval may be unnecessary in patients with moderate to severe renal dysfunction, as impaired renal function influences little of the pharmacokinetics of fosinoprilat [1].
• The overexpression of eNOS/FGF-2 produced, at the functional level, enhanced cell proliferation and migration, the latter effect being dose-dependent and maximal at 0.1 muM zofenoprilat [2].
• The direct effects of the angiotensin-converting enzyme inhibitors, zofenoprilat and enalaprilat, on isolated human pancreatic islets [3].
• The presence of either of the ACE inhibitors counteracted several of the deleterious effects of high glucose exposure, including reduction of insulin secretion and increased oxidative stress; zofenoprilat showed significantly more marked effects [3].
• In contrast, zofenoprilat levels in kidney and non-infarcted left ventricle were markedly increased by hydrochlorothiazide, whereas plasma concentrations were unchanged [4].

Biological context of Zofenoprilat

• Coronary vasodilation induced by captopril and zofenoprilat: evidence for a prostaglandin-independent mechanism [5].
• Zofenopril is a pro-drug designed to undergo metabolic hydrolysis yielding the active free sulfhydryl compound zofenoprilat, which is an angiotensin converting enzyme (ACE) inhibitor, endowed also with a marked cardioprotective activity [6].

Gene context of Zofenoprilat

• Ox-LDL and TNF-alpha increased the activation of NF-kappaB and the preincubation of HUVECs with zofenoprilat, but not with enalaprilat, dose dependently reduced its activation (P <.001) [7].
• Indeed, the S-thiolation of ALR2 by ZSSG occurred exclusively through the insertion of the Zofenoprilat moiety of ZSSG on the enzyme [8].
• Zofenoprilat, an antioxidant thiol compound, mimics the effect of GSH [9].

References