Alamandine TFA , a member of the renin-angiotensin system (RAS), a vasoactive peptide, is an endogenous ligand of the G protein-coupled receptor MrgD. Alamandine TFA targets to protect the kidney and heart through anti-hypertensive actions[1][2].

Alamandine TFA is generated by catalysis of Ang A via ACE2 or directly from Angiotensin 1-7 (Ang-(1-7)). Derived from angiotensin II (Ang II) by Ang II-converting enzyme 2 (ACE2), it shows vasodilating (thus protective) properties. Ang (1-7) can be decarboxylated to a peptide called Alamandine TFA. Alamandine TFA is also an endogenous peptide identified in human blood[1]. Alamandine TFA elevates cAMP concentration in primary endothelial and mesangial cells, also suggesting Gs coupling[2]. Alamandine TFA decreases secretion, expression, and blood levels of leptin. Alamandine TFA induced expression of iNOS and plasminogen activator inhibitor-1 (PAI-1) in adipose tissue and isolated adipocytes[2].

Alamandine TFA (0.15 ?μL/h; administered by mini-osmotic pumps; for 6 weeks) treatment ameliorates hypertension and impaires left ventricle (LV) function in SHRs. Also decreases the mass gains of heart and lung in SHRs, suppresses cardiomyocyte cross-sectional area expansion, and inhibits the mRNA levels of atrial natriuretic peptide and brain natriuretic peptide[3]. heart and lung in SHRs, suppresses cardiomyocyte cross-sectional area expansion, and inhibits the mRNA levels of atrial natriuretic peptide and brain natriuretic peptide[3].