Evidence Grade A — Regulatory approved. 37801 published studies. 218 registered clinical trials.
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Vasopressin (sold as Vasostrict) is a synthetic version of the body's natural antidiuretic hormone, used in intensive care to raise dangerously low blood pressure during septic shock and other forms of circulatory collapse. It works through a completely different mechanism than the standard blood-pressure drugs used in ICUs, making it useful when conventional treatments alone are not enough.
Vasopressin is also known by these brand and alternate names:
37,801 published studies: 14981 human, 19954 animal, 2813 in-vitro, 4873 reviews
Vasopressin is marketed as Vasostrict (approved 2014) for vasodilatory shock. It was previously included in advanced cardiac life support protocols for cardiac arrest but was removed from guidelines in 2020 after failing to show superiority over adrenaline.
Vasopressin gained public attention for dramatic price increases — the cost rose from approximately $4 per vial to over $300 following regulatory changes requiring approved formulations in critical care. This became a prominent case study in pharmaceutical pricing debates. Clinically, vasopressin remains a standard second-line vasopressor in septic shock alongside noradrenaline, and its non-catecholamine mechanism provides a complementary approach to blood pressure support.
Vasopressin works through three different receptor types. In blood vessels, it causes powerful constriction, raising blood pressure — which is its primary use in shock. In the kidneys, it tells the collecting ducts to reabsorb water rather than excrete it, concentrating the urine and maintaining blood volume. A third receptor type in the pituitary gland mediates the release of ACTH (a stress hormone). In critical care, its blood pressure-raising effect operates through a different pathway than standard vasopressors like noradrenaline, making it useful when conventional treatments alone are insufficient.
Vasopressin is a standard second-line blood pressure support in septic shock, used alongside noradrenaline. Clinical trials (VANISH, VASST) provided mixed evidence for a direct mortality benefit but supported its role as a catecholamine-sparing agent — meaning it helps maintain blood pressure while reducing the dose of other drugs that can stress the heart. Vasopressin was previously part of cardiac arrest protocols but was removed in 2020 after failing to show superiority over adrenaline. The drug gained public attention for dramatic price increases — from approximately $4 to over $300 per vial — which became a prominent case study in pharmaceutical pricing debates. Research into more selective vasopressin-like drugs (targeting only the blood vessel receptors without the kidney and hormonal effects) continues.
PeptideTrace tracks 218 registered clinical trials for Vasopressin sourced from ClinicalTrials.gov.
Effect of Vasopressin Versus Norepinephrine on Post-operative Mean Pulmonary Arterial Pressure Following Pulmonary Endarterectomy Surgery,
Efficacy of Early Argipressin in the Management of Intensive Care Patients With Norepinephrine-refractory Vasoplegic Shock
Tranexamic Acid vs Vasopressin in Placenta Previa Trial
Inhibition of Aggressive Behavior in Participants With Fragile X Syndrome
Echocardiography-guided Cirrhosis and Liver Failure-Intensive Care Protocol Sepsis
Health Canada Market Authorisation
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Vasopressin (antidiuretic hormone, ADH) is a 9-amino-acid cyclic neuropeptide structurally related to oxytocin, differing at only 2 of 9 positions: position 3 (Ile→Phe) and position 8 (Leu→Arg). It is synthesized in the hypothalamus and released from the posterior pituitary in response to plasma osmolality changes and hypovolemia.
Vasopressin acts through three receptor subtypes: V1a (vascular smooth muscle → Gq/PLC → vasoconstriction; also expressed in hepatocytes and platelets), V2 (renal collecting duct → Gs/cAMP → aquaporin-2 insertion into apical membrane → water reabsorption), and V1b/V3 (anterior pituitary → Gq → ACTH release). The vasoconstrictive (V1a) and antidiuretic (V2) effects are the basis for its therapeutic uses.
Vasopressin is marketed as Vasostrict (approved April 17, 2014 for vasodilatory shock). It was previously included in the AHA ACLS algorithm for cardiac arrest but was removed in 2020 guidelines (no superiority over epinephrine demonstrated). The drug gained notoriety for a dramatic price increase—from approximately $4.50 per vial in 2010 to over $150 per vial by 2020 (a >5,400% increase by Endo/Par Pharmaceutical). A generic vasopressin injection was approved in December 2021.
Linaclotide is marketed as Linzess (approved August 2012). It is taken as a daily oral capsule on an empty stomach, at least 30 minutes before the first meal. The recommended dose is 290 mcg for IBS-C and 72 or 145 mcg for chronic constipation. In clinical trials, approximately 34% of IBS-C patients met the composite improvement endpoint compared to 17% on placebo. Diarrhoea is the most common side effect (approximately 20%) and the leading reason for discontinuation. Linaclotide has a boxed warning against use in children under 6 years due to deaths in young mice, though no such events have been reported in humans. It competes with plecanatide (which targets the same pathway) and other IBS-C treatments.
Elamipretide (Forzinity) was approved by the FDA for Barth syndrome based on the TAZPOWER trial. The randomised crossover phase (12 patients) did not meet its primary endpoints, but the open-label extension (168 weeks) demonstrated durable improvements in walking distance and muscle strength that formed the basis for approval. Barth syndrome affects approximately 1 in 300,000–400,000 births. A larger Phase III trial in primary mitochondrial myopathy (218 patients, MMPOWER-3) did not meet its primary endpoint, and the drug was not approved for that broader indication. Elamipretide remains approved exclusively for Barth syndrome. See also SS-31 (#158) for the research compound context.
Palopegteriparatide is marketed as Yorvipath (Ascendis Pharma, approved August 2024). It is the first FDA-approved PTH replacement therapy for hypoparathyroidism, a condition that previously had no approved hormone replacement and was managed only with high doses of calcium supplements and active vitamin D — an approach that does not fully normalise calcium metabolism. In the PaTHway trial, 79% of patients achieved independence from calcium and active vitamin D supplements while maintaining normal blood calcium levels, compared to 5% on placebo. This represents a fundamental shift in managing hypoparathyroidism — from supplementation to actual hormone replacement. Patients also showed improvements in kidney function markers and bone metabolism parameters.
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