Angiotensin II
The eight-amino-acid effector hormone of the renin-angiotensin system, marketed as Giapreza, an intravenous vasopressor approved in 2017 to raise blood pressure in adults with septic or other distributive shock that resists conventional vasopressors.
Also referenced as: Giapreza, LJPC-501, Angiotensin II acetate, Ang II
Also appears in: Hormone
Public product evidence No certificate records are bound to a tracked Angiotensin II product page A record counts here only when a vendor publishes a certificate against one of its own tracked Angiotensin II product pages. Other certificates naming this compound may still exist — search the wider certificate database.This compound maps to at least one regulated medical product or label context in the United States.
Primary research area: Cardiovascular. Also surfaces under Hormone for browsing and discovery.
Where the compound acts, as a browse axis. It is an editorial grouping for discovery, not a claim about labeled indications.
Giapreza, LJPC-501, Angiotensin II acetate, Ang II
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Angiotensin II is an FDA-approved medicine with substantial published trial evidence. Note that research-market products sold under this name are not the approved medicine and are not held to the same manufacturing or labeling standards.
Angiotensin II has 6 name-matched clinical trials (highest phase: Phase 4) and 19 PubMed-indexed publications and holds an FDA drug label. 2 trials have posted results.
Re-checked nightly against the registries — tracked since 2026-11-03. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-11-03 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is Angiotensin II?
Angiotensin II is the octapeptide effector hormone of the renin-angiotensin system, with the sequence Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, molecular formula C50H71N13O12 and an average molecular weight of about 1,046 Da as the free base. The pharmaceutical version is synthetic human angiotensin II supplied as a non-stoichiometric acetate salt, developed by La Jolla Pharmaceutical Company under the code LJPC-501 and marketed as Giapreza.
Unlike most peptides with a research following, this one reaches people almost exclusively as a hospital pressor: it is a prescription intravenous drug for adults whose blood pressure will not come up on conventional vasopressors, and it has little if any presence in the research-peptide market. ACE2 clips the C-terminal phenylalanine off this molecule to produce angiotensin-(1-7), a counter-regulatory heptapeptide that signals through a different receptor and pushes in the opposite direction.
How it works
- AT1 receptor agonism. Angiotensin II binds the Gq-coupled AT1 receptor on vascular smooth muscle, activating phospholipase C, inositol trisphosphate release and a rise in intracellular calcium that produces direct vasoconstriction; the same receptor drives NADPH oxidase activity, growth signaling and fibrosis on longer timescales (Forrester et al., Physiological Reviews, 2018;98(3):1627–1738).
- Endocrine arm. AT1 signaling in the adrenal zona glomerulosa stimulates aldosterone synthesis, and central AT1 receptors promote vasopressin release and thirst, so the pressor effect is layered on sodium and water retention rather than being purely a vascular squeeze (Forrester et al., Physiological Reviews, 2018).
- Replacing a failed conversion step. In catecholamine-resistant vasodilatory shock, renin is markedly elevated and the angiotensin I/II ratio is high, a pattern consistent with impaired conversion of angiotensin I to angiotensin II; infusing the octapeptide cut renin concentrations by a median 54.3% at three hours against 14.1% with placebo, restoring the negative feedback loop (Bellomo et al., American Journal of Respiratory and Critical Care Medicine, 2020;202(9):1253–1261; Bellomo et al., Critical Care, 2020;24(1):43).
- Catecholamine sparing. Because the pressor effect runs through a receptor system separate from the adrenergic one, blood pressure can be supported while background vasopressor requirements fall. That observation drove the program from its 20-patient pilot onward (Chawla et al., Critical Care, 2014;18(5):534).
Research status
The pivotal evidence is a single randomized trial. ATHOS-3 (NCT02338843) enrolled adults with vasodilatory shock receiving more than 0.2 µg/kg/min of norepinephrine or an equivalent, randomized 344 patients and analyzed 321 (163 angiotensin II, 158 placebo) across 75 ICUs in nine countries. The primary endpoint, a mean arterial pressure response at hour 3 without an increase in background vasopressors, was met by 69.9% on angiotensin II versus 23.4% on placebo (odds ratio 7.95; 95% CI 4.76–13.3; P<0.001). Cardiovascular SOFA improvement at 48 hours favored treatment (−1.75 versus −1.28; P=0.01). Death by day 28 occurred in 46% versus 54% (hazard ratio 0.78; 95% CI 0.57–1.07; P=0.12), a difference the trial was not designed or powered to resolve (Khanna et al., New England Journal of Medicine, 2017;377(5):419–430).
The mortality signals that circulate about the drug come from post hoc subgroups of that one trial. Among the 105 patients already on renal replacement therapy at study drug initiation, 28-day survival was 53% versus 30% (P=0.012) and liberation from renal replacement therapy by day 7 was 38% versus 15% (P=0.007). That is a hypothesis-generating analysis in a small slice of the cohort (Tumlin et al., Critical Care Medicine, 2018;46(6):949–957). In patients with baseline renin above the study median, 28-day mortality was 50.9% versus 69.9% (hazard ratio 0.56; 95% CI 0.35–0.88; interaction P=0.048), which is the basis for the renin-guided-treatment hypothesis (Bellomo et al., 2020). Neither subgroup finding has been replicated in a prospective trial.
Postmarketing experience is observational. A retrospective cohort of 270 patients at five US centers found that 67% showed a hemodynamic response; responsiveness was associated with lower 30-day mortality (hazard ratio 0.50; 95% CI 0.35–0.71), lower lactate and concurrent vasopressin predicted response, arrhythmias occurred in 10% and venous thromboembolism was identified in four patients (Wieruszewski et al., Chest, 2021;159(2):596–605). Synthesis work has been consistently cautious: a meta-analysis of adjunctive vasopressors in septic shock rated the pooled mortality evidence low certainty (Bauer et al., Shock, 2025;63(5):668–676), and an overview of six systematic reviews found their methodological quality mostly low, with a reproducible effect on mean arterial pressure and background vasopressor requirements but subgroup-limited mortality findings that the authors declined to generalize. The authors give those limited and inconsistent data as the reason the drug has not entered treatment guidelines (Desfosses and Røislien, BMC Anesthesiology, 2026;26(1):257).
Two registered studies were active on November 3, 2026. A multicenter phase 3 trial in Chinese adults with refractory distributive shock (NCT06351150, Chia Tai Tianqing, 214 patients, primary completion June 2027) is the first randomized replication attempt, again with a three-hour blood pressure response as the primary endpoint rather than survival. A small open-label single-arm phase 4 study in children with refractory hypotension, run across two Northwell Health pediatric sites, began enrolling on October 28, 2025 (NCT07212686, 30 patients planned); the approved indication remains adults only.
Common dosage forms
Giapreza is supplied as an injection for intravenous infusion in two concentrations, 0.5 mg/mL and 2.5 mg/mL angiotensin II, in 1 mL single-dose vials; an earlier 2 mL vial of the 2.5 mg/mL strength has been discontinued. The European product authorized as Giapreza is the same concentrate for solution for infusion. There is no oral, subcutaneous, retail or self-administered presentation.
Key considerations
- Regulatory status. The FDA Approved status reflects Giapreza (NDA 209360), approved December 21, 2017 under Priority Review to increase blood pressure in adults with septic or other distributive shock. The European Union authorized it on August 23, 2019.
- Thrombosis. The US label’s only Warnings and Precautions entry is risk of thrombosis: arterial and venous thrombotic and thromboembolic events occurred in 13% of ATHOS-3 patients on angiotensin II versus 5% on placebo, driven mainly by deep vein thrombosis, and the label recommends concurrent prophylaxis against venous thromboembolism. Thromboembolic events are also listed among the most common adverse reactions in the European assessment. The only randomized estimate of that risk comes from ATHOS-3 and is too imprecise to size reliably (Bauer et al., Shock, 2025).
- Efficacy evidence. The efficacy case is a blood pressure case. One adequately powered trial demonstrated a pressor and catecholamine-sparing effect; no trial has demonstrated a survival benefit, and the mortality results most often quoted are post hoc subgroups of that same trial. Whether renin concentration can prospectively select responders is still an open question.
- Naming. The endogenous hormone and the drug product share a name, so literature on angiotensin II physiology or on angiotensin II as a disease driver in hypertension and heart failure is not evidence about the infused product. The angiotensin II receptor blockers used in cardiology antagonize the receptor this drug activates. Angiotensin-(1-7) is a different, shorter peptide acting at a different receptor with broadly opposing effects.