SSAA09E1 is an inhibitor of severe acute respiratory syndrome coronavirus (SARS-CoV) viral entry.1It reduces infection of HEK293T cells transiently transfected with angiotensin-convertingenzyme 2 (ACE2) by an HIV-based virus system pseudotyped with SARS-CoV surface glycoprotein (EC50= 6.7 μM). SSAA09E1 also inhibits the proteolytic activity of cathepsin L (IC50= 5.33 μM) but not cathepsin B when used at a concentration of 20 μM. 1.()
Angiotensin I II (1-6) TFA is a chemical compound comprising amino acids 1-6. It is derived from the Angiotensin I II peptide, which is formed by the cleavage of the precursor angiotensinogen by renin. The resulting Angiotensin I is then hydrolyzed by angiotensin-convertingenzyme (ACE) to produce biologically active Angiotensin II. Angiotensin II has been extensively studied for its potential applications in the treatment of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy[1][2][3].
Pueroside B may can treat coronary heart disease, it can interact with two or more targets[peroxisome proliferator activated receptor γ (PPAR-γ), angiotensin-convertingenzyme (ACE), hydroxymethylglutaryl coenzyme A receptor (HMGR), cyclooxygenase-2 (COX2
Pentoprilat is a member of a series of l-glutarylindoline-2(S)-carboxylic acid derivatives. Pentopril was evaluated as an inhibitor of a cell-free preparation of angiotensin-convertingenzyme (ACE) isolated from rabbit lung. Intravenous administration of incremental doses of pentopril to anesthetized normotensive rats produced a dose-related inhibition of angiotensin I (AI) pressor responses. The onset of inhibition of the A1 pressor response was rapid, and substantial inhibition occurred at 5 min after administration of the ACE inhibitors. Pentopril hydrolyzed in vivo to the biologically active free-acid form of CGS 13934. It was well tolerated in normal volunteers and hypertensive patients. Pentopril was developed for the treatment of both hypertension and congestive heart failure. Pentopril produced little clinical improvement and no biochemical improvement in a patients with rheumatoid arthritis.