Angiotensin II is an endogenous 8-amino-acid peptide (sequence: Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, MW ~1046.2 g/mol) that serves as the primary effector of the renin-angiotensin-aldosterone system (RAAS). A synthetic form (Giapreza, La Jolla Pharmaceutical) was FDA-approved in December 2017 for the treatment of vasodilatory shock in adults. It is the only exogenous angiotensin II product approved as a vasopressor.
Category: Cardiovascular / Vasoactive. Evidence rating: A (strong human clinical data).
Clinical status: FDA-approved (Giapreza, December 2017) for vasodilatory shock in adults
Angiotensin II binds to AT1 receptors on vascular smooth muscle cells, activating Gq-coupled signaling that increases intracellular calcium via phospholipase C and IP3, producing potent vasoconstriction. It stimulates aldosterone release from the adrenal zona glomerulosa, promoting sodium and…
Safety considerations: Thromboembolic events: DVT and arterial thrombosis reported more frequently with angiotensin II vs placebo in ATHOS-3 (12.9% vs 5.1%); concurrent VTE prophylaxis recommended; Tachyarrhythmias reported in clinical trials; Peripheral ischemia, including digital ischemia, has been reported.
Reviewed by the PeptideAtlas Editorial Team.
| Amino-acid sequence | Asp-Arg-Val-Tyr-Ile-His-Pro-Phe (DRVYIHPF) |
|---|---|
| Molecular weight | ~1046.2 g/mol |
| CAS number | 4474-91-3 |
| Half-life | ~1-2 minutes (circulating) |
| Production method | synthetic |
| Anti-doping status | not-listed |
| US regulatory status | FDA-approved (Giapreza, December 2017) for treatment of hypotension in adults with septic or other distributive shock. |
Related peptides: Angiotensin 1-7, Bradykinin, Endothelin-1.
Angiotensin II (Giapreza) is used as a vasopressor in adults with vasodilatory (distributive) shock who remain hypotensive despite adequate volume resuscitation and first-line vasopressor therapy (norepinephrine, vasopressin). It is typically a third- or fourth-line agent in refractory shock.
Angiotensin II works through the RAAS pathway (AT1 receptors) rather than adrenergic or vasopressin receptors, providing an alternative mechanism when catecholamine-based vasopressors are insufficient. The ATHOS-3 trial demonstrated efficacy when added to high-dose catecholamines.
The primary ATHOS-3 trial was not powered for mortality. Day-28 mortality was 46% vs 54% (angiotensin II vs placebo, p=0.12). Post-hoc analyses suggested survival benefit in specific subgroups (high renin, RRT patients), but these require prospective validation.
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