| Identification | Back Directory | [Name]
(D-ALA7)-ANGIOTENSIN I/II (1-7) | [CAS]
159432-28-7 | [Synonyms]
A-779
DRVYIHA
A 779(3TFA)
A 779?, >98%
ASP-ARG-VAL-TYR-ILE-HIS-D-ALA
(D-ALA7)-ANGIOTENSIN I/II (1-7)
Asp-Arg-Val-Tyr-Ile-His-D-Ala-OH
H-ASP-ARG-VAL-TYR-ILE-HIS-D-ALA-OH
(D-Ala7)-Angiotensin I/II (1-7)
A-779
5-L-Isoleucine-7-D-Alanine-1-7-Angiotensin II
1-7-Angiotensin II, 5-L-isoleucine-7-D-alanine-
A 779,Asp-Arg-Val-Tyr-Ile-His-d-Ala,DRVYIHd-ALA, >98% | [Molecular Formula]
C39H60N12O11 | [MDL Number]
MFCD00672447 | [MOL File]
159432-28-7.mol | [Molecular Weight]
872.97 |
| Chemical Properties | Back Directory | [density ]
1.45±0.1 g/cm3(Predicted) | [storage temp. ]
-15°C | [form ]
lyophilized powder | [pka]
3.29±0.10(Predicted) | [color ]
white to off-white | [Water Solubility ]
≥ 29.1mg/mL in Water with gentle warming |
| Hazard Information | Back Directory | [Uses]
A 779 is an angiotensin heptapeptide analog antagonist. | [Biochem/physiol Actions]
A-779 (D-Ala7-Ang-(1-7)) is a potent and selective antagonist of angiotensin (1-7), an endogenous peptide that acts through activation of a non-AT1, non-AT2 receptor, Mas, and opposes the activity of angiotensin. A-779 has an IC50 of 0.3 nM for Mas with negligible affinity for either AT1R or AT2R. | [Enzyme inhibitor]
This peptidomimetic Mas antagonist (FW = 872.98 g/mol; CAS 159432-
28-7; Sequence: Asp-Arg-Val-Tyr-Ile-His-D-Ala (or DRVYIH-D-A);
Solubility: 1 mg/mL H2O) targets the Mas receptor, or Ang- (1-7) Receptor,
the Class I seven-transmembrane G-protein-coupled angiotensin- (1-7)
receptor that preferentially couples to the Gq protein, thereby activating the
phospholipase C signaling pathway, with roles in hypotension, smooth
muscle relaxation and cardio-protection by mediating the effects of
angiotensin- (1-7). A-779 exhibits no significant affinity for AT1 or AT2
receptors at a concentration of 1 μM. It also inhibits antidiuretic effect of
Ang- (1-7) in water-loaded rats. A779 attenuates monocrotaline-induced
pulmonary fibrosis in rats. | [in vivo]
Infusion of Ang(1-7) and A-779 (400 ng/kg/min, s.c.) alone or combined for 6 weeks does not prevent uterus atrophy or inhibit the body weight gain of OVX rats. A-779 markedly elevates serum bone specific alkaline phosphatase (BALP), telopeptides of collagen type I (CTX), tartarate resistant acid phosphatase (TRAcP 5b), osteocalcin (OC) and urinary deoxypyridinoline (DPD). Infusion of Ang(1-7) and/or A-779 does not significantly change serum minerals concentrations in sham or OVX groups. A-779 in the OVX animals does not change AngII, Ang(1-7), AT1R, AT2R, ACE, ACE-2, Mas receptor, RANKL and OPG proteins expressions in relation to OVX group, while AngII (P < 0.05), AT1R (P < 0.05), ACE (P < 0.01) and RANKL (P < 0.01) expressions are significantly higher and Ang(1-7), AT2R, ACE-2, MasR and OPG are significantly (P < 0.01) lower than sham group. Blocking of the G-protein coupled receptor (Mas) by A-779 markedly abolishes Ang(1-7) favorable effects on bone health suggesting the vital role of Mas receptor in mediating Ang(1-7) osteo-protective effects[1]. Inhibition of Ang1-7 cascade by A-779 (400 ng/kg/min) significantly eradicates captopril protective effects on bone metabolism, mineralization and micro-structure. A-779 also restores OVX effects on RANKL expression and ACE-1/AngII/AT1R cascade and down-regulates OPG expression and ACE-2/Ang1-7/Mas pathway[2]. | [IC 50]
AT2 Receptor; AT1 Receptor | [storage]
Store at -20°C |
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