Terlipressin

Terlivaz, Glypressin, Variquel, Remestyp, triglycyl-lysine vasopressin, TGLVP, terlipressin acetate

Cardiovascular & circulation

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Note on this profile. Terlipressin is an approved hospital medicine in the US (since 2022), EU, UK, Australia and many other countries, given intravenously under intensive monitoring. It is not a research-only compound and has no outpatient or self-directed use. This page explains the published science.

Summary

Class: Synthetic 12-amino-acid prodrug: lysine-vasopressin with three glycine residues added at the N-terminus
Mechanism: Slowly cleaved in the body to lysine-vasopressin, which constricts splanchnic (gut) arteries via V1 receptors, lowering portal pressure and redirecting blood to the kidneys
Routes studied: Intravenous bolus (every 4–6 hours) and continuous infusion
Half-life: ~50 minutes for the prodrug; the active lysine-vasopressin is released over 4–6 hours, giving a far longer effect than vasopressin itself
Storage: Lyophilised powder (US) refrigerated; solution (EU) refrigerated, protect from light; reconstituted vials used promptly per label
Regulatory status: Approved medicine (US 2022; EU national approvals since the 1990s; UK; AU; ZA †)

Doses are as reported in studies or by the community — never recommendations.

1What it is

Terlipressin is a vasopressin analogue designed as a prodrug: three extra glycines on the front of lysine-vasopressin are trimmed off by tissue enzymes over several hours, releasing the active hormone gradually. That design converts a hormone with a few minutes of action into a drug that can be given every 4–6 hours as a bolus, with fewer of the sudden peaks that make vasopressin itself hard to use. It has been a mainstay of European hepatology since the 1990s for bleeding oesophageal varices and for hepatorenal syndrome — the acute kidney failure that complicates advanced cirrhosis because the gut circulation steals blood from the kidneys.

In the US it was repeatedly rejected (2009, 2020) before approval in September 2022 for hepatorenal syndrome with rapid worsening of kidney function; the delay reflected concerns about respiratory failure. Vasopressin and desmopressin are covered under profile #107; oxytocin, a related nonapeptide, under #48.

2How it's thought to work

V1 receptor agonism. on vascular smooth muscle constricts splanchnic arterioles, reducing portal venous inflow and pressure (variceal bleeding) and raising systemic arterial pressure, which improves kidney perfusion and switches off the renin–angiotensin and sympathetic overdrive of hepatorenal syndrome.

Modest V2 activity. causes water retention, which contributes to fluid overload.

Usually combined with intravenous albumin, which expands circulating volume and may bind vasodilators.

A prodrug converted slowly to lysine-vasopressin, used for the opposite reason: the vessel-narrowing arm, to raise pressure in the splanchnic circulation in variceal bleeding and hepatorenal syndrome.Schematic — not to scale

3What the research shows

Hepatorenal syndrome (HRS-AKI)

CONFIRM, the pivotal US phase 3 trial, randomised 300 patients with cirrhosis and HRS type 1 to terlipressin or placebo, both with albumin. Verified HRS reversal (two creatinine values ≤1.5 mg/dL at least 2 hours apart while alive without renal replacement for 10 days) occurred in 32% vs 17%; 90-day mortality was not different (51% vs 45%); respiratory failure occurred in 14% vs 5% of patients (Wong 2021, NEJM). Earlier trials — OT-0401 (Sanyal 2008, Gastroenterology) and REVERSE (Boyer 2016, Gastroenterology) — showed improved creatinine and HRS reversal in subsets without a mortality benefit. A Cochrane review found reduced mortality in pooled analysis, with low certainty (Allegretti 2017, Cochrane Database Syst Rev †). [1][2][3]

Acute variceal bleeding

Randomised trials and meta-analyses show terlipressin controls bleeding and reduces mortality compared with placebo, and is roughly equivalent to octreotide and somatostatin when combined with endoscopic therapy (Ioannou 2003, Cochrane Database Syst Rev; Seo 2014, Hepatology — three-way comparison in 780 patients). Pre-hospital administration has been studied in Europe. [5][6]

Graded A (small)

Continuous infusion versus bolus in HRS

A randomised trial of 78 patients found continuous infusion as effective as bolus dosing with fewer adverse events at a lower total dose (Cavallin 2016, Hepatology). [4]

Septic shock, paracentesis-induced circulatory dysfunction

Small trials as an adjunct vasopressor in catecholamine-resistant septic shock and to prevent circulatory dysfunction after large-volume paracentesis; neither is a licensed indication.

4Reported side effects and interactions

Literature-reported

abdominal pain and cramps, diarrhoea, nausea, headache, pallor, bradycardia, hypertension and peripheral vasoconstriction (cold or cyanosed extremities, skin necrosis at the extremities or injection site, scrotal or abdominal skin ischaemia); myocardial and mesenteric ischaemia; hyponatraemia (especially in patients with preserved liver function); fluid overload and pulmonary oedema. The US label carries a boxed warning for serious or fatal respiratory failure, particularly in patients with volume overload or ACLF grade 3, and advises against use when serum creatinine is ≥5 mg/dL. Risk of ischaemic complications is higher in patients with established coronary, cerebral or peripheral vascular disease.

Community-reported

essentially none documented.

Theoretical. reduced intestinal perfusion could worsen bacterial translocation; uterine contraction (contraindicated in pregnancy).

Interactions. additive bradycardia with beta-blockers (commonly prescribed in cirrhosis); additive QT prolongation with other QT-prolonging drugs; caution with other vasoconstrictors.

Markers researchers commonly monitor

Taken from the label and critical-care practice:

Marker	Why it's watched
Serum creatinine and urine output	the treatment target in HRS; response is judged over days.
Serum sodium	hyponatraemia is common, especially with high doses or preserved liver function.
Oxygen saturation, respiratory rate, chest examination, fluid balance	the boxed-warning risk is respiratory failure from fluid overload.
ECG and troponin	ischaemia and bradycardia; continuous telemetry in most units.
Blood pressure and heart rate	mean arterial pressure rise is both the mechanism and the hazard.
Peripheral and skin perfusion checks	early signs of ischaemic necrosis.
Lactate	mesenteric ischaemia signal.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

A hospital product. In the US it is supplied as a 0.85 mg vial with 5 mL sodium chloride for slow IV push over 2 minutes. European solution-for-injection products (1 mg/8.5 mL or similar) are ready to use. Given with telemetry, oxygen-saturation and fluid-balance monitoring. The calculator is not applicable.

6Commonly studied alongside

Intravenous albumin (nearly always co-administered), octreotide and somatostatin (variceal bleeding comparators), noradrenaline (an alternative vasopressor for HRS in intensive care), vasopressin and desmopressin (#107), oxytocin (#48), midodrine.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	FDA-approved September 2022 (Terlivaz) to improve kidney function in adults with hepatorenal syndrome with rapid reduction in kidney function; boxed warning for respiratory failure; hospital use only
European Union	Nationally authorised in most member states (Glypressin, Variquel, generics) for bleeding oesophageal varices; HRS indication in several countries
United Kingdom	MHRA-licensed (Glypressin, Variquel and generics) for bleeding oesophageal varices; used for HRS per national guidelines
Australia	TGA-registered (Glypressin) for variceal bleeding and HRS †
South Africa	SAHPRA registration †
Sport (WADA)	Not prohibited

8Open questions

Why consistent improvement in kidney function has not translated into a survival benefit in HRS trials.
Whether continuous infusion should replace bolus dosing as standard.
How to select patients at low risk of respiratory failure (volume status, ACLF grade).

9References

1Wong F et al. (2021). Terlipressin plus albumin for the treatment of type 1 hepatorenal syndrome (CONFIRM). NEJM. PubMed · DOI
2Boyer TD et al. (2016). Terlipressin plus albumin is more effective than albumin alone in improving renal function in patients with cirrhosis and hepatorenal syndrome type 1 (REVERSE). Gastroenterology. PubMed · DOI
3Sanyal AJ et al. (2008). A randomized, prospective, double-blind, placebo-controlled trial of terlipressin for type 1 hepatorenal syndrome. Gastroenterology. PubMed · DOI
4Cavallin M et al. (2016). Terlipressin given by continuous intravenous infusion versus intravenous boluses in the treatment of hepatorenal syndrome: a randomized controlled study. Hepatology. PubMed · DOI
5Seo YS et al. (2014). Lack of difference among terlipressin, somatostatin, and octreotide in the control of acute gastroesophageal variceal hemorrhage. Hepatology. PubMed · DOI
6Ioannou GN, Doust J, Rockey DC (2003). Terlipressin for acute esophageal variceal hemorrhage. Cochrane Database Syst Rev. PubMed · DOI
7Terlivaz (terlipressin) US prescribing information (current label). PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

31 Oct 2026Profile published — awaiting medical review

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