Vasopressor · septic shock
Giapreza is the synthetic human form of angiotensin II, an eight-amino-acid hormone (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) that sits at the end of the body's renin-angiotensin-aldosterone cascade1. The body uses it to tighten blood vessels; as a drug it runs as an intravenous infusion for adults in septic or other distributive shock whose blood pressure needs raising1.
Angiotensin II is the main active product of the renin-angiotensin system. Its pressure-raising role was worked out through kidney research that began in 1898 and advanced in the 1930s, and the name angiotensin was agreed in 19584. According to the FDA label, it binds the angiotensin II type 1 (AT1) receptor on the smooth muscle of blood vessel walls, triggering calcium-calmodulin signaling that contracts the muscle and narrows the vessels; it also increases release of aldosterone, a hormone that promotes salt and water retention1.
In distributive shock, such as from severe infection, blood vessels dilate so much that pressure stays low despite fluids and standard vasopressors such as norepinephrine. Angiotensin II offers a different receptor pathway for raising pressure in that setting.
The pivotal ATHOS-3 trial enrolled adults with vasodilatory shock who stayed hypotensive despite high-dose vasopressors. Of 321 treated patients, 70% on angiotensin II reached the blood-pressure target at hour 3 versus 23% on placebo, and cardiovascular organ-failure scores improved more by 48 hours. Death by day 28 occurred in 46% versus 54%, a difference that was not statistically significant2.
A post hoc analysis of 105 ATHOS-3 patients with acute kidney injury who were on renal replacement therapy (dialysis-type kidney support) when the study drug started reported higher 28-day survival (53% versus 30%) and more patients coming off dialysis by day 7 with angiotensin II; because this was a subgroup analysis after the fact, it raises a hypothesis rather than settling the question3.
Giapreza gained FDA approval in December 2017 as a vasoconstrictor for adults with septic or other distributive shock1. A generic version (ANDA 216966) was approved in June 20255.
Thrombosis is the label's headline warning. In ATHOS-3, arterial or venous clots occurred in 13% of patients given angiotensin II and 5% given placebo, most of the gap being deep vein thrombosis, and the label directs that venous-thromboembolism prophylaxis be given at the same time1. Its adverse-reaction table, which lists events seen in at least 4% of treated patients and at least 1.5 points more often than with placebo, adds thrombocytopenia (low platelets; 9.8% vs 7.0%), tachycardia (8.6% vs 5.7%), fungal infection (6.1% vs 1.3%), delirium and acidosis (5.5% vs 0.6% each), and hyperglycemia and peripheral ischemia (4.3% vs 2.5% each)1.
This page is educational reference material about compounds studied in research settings. It is not medical advice, and nothing here is a recommendation to buy, possess, or use any compound. Research findings described are from published literature; individual compounds may not be approved for human use. Talk to a licensed clinician about anything that affects your health.
Brand names on this page belong to their owners and are used only to identify a product. goodtides is not affiliated with those companies.