Terlipressin 1mg/5ml solution for injection vials
Requires a prescription from a doctor or prescriber
Terlipressin is a synthetic analogue of vasopressin, which is an endogenous neurohormone that acts as a vasoconstrictor.[A2601] It is a prodrug of [lypressin], or lysine vasopressin.
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Suspected adverse reactions reported for Terlipressin
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Suspected adverse reactions reported for Terlipressin
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Terlipressin 1mg/5ml solution for injection vials
WHO defined daily dose (DDD)
12 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 25 · Randomised trials: 19 · 1993–2026
Showing the 50 most relevant studies, sorted by most relevant.
A. Sanyal, T. Boyer, R. Frederick, et al.
Alimentary Pharmacology & Therapeutics, 2017
Jody C. Olson, Ram Subramanian
PLOS ONE, 2024
Xinmiao Zhou, D. Tripathi, Tingxue Song, et al.
Medicine, 2018
Mona Hassan, Nooraldin Merza, Yusuf Nawras, et al.
Annals of Medicine and Surgery, 2023
Adnan Malik, M. Malik, Shahbaz Qureshi, et al.
Annals of hepatology, 2024
Shang Y, Wang C, Lu H, et al.
2024
- Liver Cirrhosis
- Vasoconstrictor Agents
- Terlipressin
Yue-Meng Wan, Song-Quan Huang, Hua-Mei Wu, et al.
Frontiers in Pharmacology, 2024
McDonald R, Burns M, Wong A, et al.
2025
- Shock, Septic
- Vasoconstrictor Agents
- Acute Kidney Injury
BackgroundPatients with septic shock are high risk for developing acute kidney injury (AKI), with its associated morbidity. This systematic review assessed the evidence for an effect on renal outcomes from choice of vasopressor.MethodsSearches were conducted on Medline, Embase, Cochrane Central, congress abstracts and trial registries. The search strategy included septic shock, vasopressor agents and renal impairment. Inclusion criteria were non-crossover randomised controlled trials of adult septic shock comparing individual or combinations of vasopressors and placebo controlled trials. Primary outcome was the incidence of AKI in study participants. Secondary outcomes were AKI duration, renal replacement therapy (RRT) rate, RRT duration, renal failure free days, requirement for long term RRT and Major Adverse Kidney Events (MAKE) at 30 and 90 days.ResultsA total of 4259 patients, from 17 studies, were included. Vasopressin and terlipressin studies predominated. In 8 studies reporting AKI rate, no effect was seen relating to vasopressor choice. RRT rate was the most reported secondary outcome. Of five studies that investigated the role of vasopressin, only one showed significant benefit. Alongside limited reporting, no conclusive benefit was demonstrated in other secondary outcomes. No studies reported requirement for long term RRT, MAKE 30 or 90.ConclusionsThis is the first systematic review focussed on renal outcomes with differential vasopressor therapy in septic shock. It illustrates the paucity of evidence supporting a particular vasopressor. Also highlighted are problems of population and study heterogeneity, as well as the focus on RRT as a proxy for renal outcomes. Standardised renal outcome reporting, large and appropriately powered trials and focussed sub-population studies are required to further inform renal focussed vasopressor research and practice.Trial registrationThis systematic review was prospectively registered on PROSPERO (CRD42023481778).
Abstract licence: CC BY
Fengkai Mao, D. Liang, Zewen Tang, et al.
Shock, 2023
Moses John Wesley, Anjali Avula, Hafsa Tehniyat, et al.
Cureus, 2025
This systematic review evaluates and compares the clinical effectiveness of terlipressin and octreotide in the management of acute gastroesophageal variceal bleeding among cirrhotic patients. A comprehensive literature search was conducted across PubMed, Google Scholar, and clinical trial registries, identifying five randomized controlled trials that met predefined inclusion criteria. These studies assessed key outcomes, including bleeding control, mortality, hepatic venous pressure gradient (HVPG) reduction, hemodynamic stability, and safety profiles. The findings demonstrated that both agents are effective in controlling variceal bleeding, with no major differences in short-term mortality. However, terlipressin was associated with sustained HVPG reduction, more durable hemodynamic effects, and, in some cases, shorter hospital stays. In alcoholic cirrhosis subgroups, terlipressin showed a superior portal pressure response. Risk of bias assessments indicated generally low-to-moderate concerns across studies, supporting the reliability of findings. This review highlights terlipressin’s potential advantages in specific clinical contexts and underscores the need for further large-scale trials to refine therapy selection and optimize patient outcomes.
Abstract licence: CC BY
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
0.9 hours
Mechanism
Endogenous vasopressin, also referred to as antidiuretic hormone (ADH) or argini…
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 mg
Half-life
0.9 hours
[L43217]
Volume of distribution
6.3 L
[L43217]
Metabolism
Elimination
1%
[L43217]
Clearance
27.4 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L43217]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 396 interactions
[L43217]
Vasopressin is considered a stress hormone as it is released into the bloodstream in response to various volume and pressure stimuli, such as pain, surgery, syncope and shock.[A2601][A2605][A252677] Shock conditions such as hypovolemia initially cause an increase in the release of vasopressin to maintain organ perfusion; however, as the shock state progresses, plasma vasopressin concentrations decrease due to several causes such as depleted stores of vasopressin in refractory shock and a central inhibitory effect of initially elevated vasopressin levels on further vasopressin release.[A2605]
Terlipressin is a synthetic vasopressin analogue that can cause sustained increases in blood pressure in patients with shock conditions.[A2605] It exhibits twice the selectivity for vasopressin V1 receptors versus V2 receptors. Terlipressin is pharmacologically active but acts as a prodrug for [lypressin] (also known as lysine vasopressin), a vasoconstrictor and antidiuretic agent. The exact mechanism of action of terlipressin is not fully understood; however, terlipressin works to cause vasoconstriction in shock and other conditions associated with vasodilation. Hepatorenal syndrome (HRS) is caused by splanchnic and systemic arterial vasodilation along with a reduced mean arterial pressure (MAP) and cardiac output, resulting in a marked decrease in effective circulating volume.[A252672] Terlipressin is thought to increase renal blood flow in patients with HRS-1 by reducing portal hypertension and blood circulation in portal vessels and increasing effective arterial volume and mean arterial pressure (MAP).[L43217]
Terlipressin increases arterial pressure (diastolic, systolic, and mean) and decreases heart rate in patients with hepatorenal syndrome type 1 (HRS-1). After the administration of a single 0.85 mg dose of terlipressin in patients with HRS-1, cardiovascular effects were observed within five minutes after dosing and were maintained for at least six hours after dosing. The maximum change in blood pressure and heart rate occurred at 1.2 to two hours post-dose.[L43217]
How the body processes this drug — absorption, distribution, metabolism, and elimination
Plasma concentrations of terlipressin demonstrate proportional increases with the dose administered.
[L43217]
[L43217]
[L43217]
Due to the ubiquitous nature of peptidases in body tissues, it is unlikely that the metabolism of terlipressin will be affected by disease state or other drugs.
[L43217]
[L43217]
[L43217]
Proteins and enzymes this drug interacts with in the body
ATC H01BA04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Terlipressin
Additional database identifiers
ChemSpider
65067
HUGO Gene Nomenclature Committee (HGNC)
HGNC:895
GenAtlas
AVPR1A
GeneCards
AVPR1A
GenBank Gene Database
L25615
GenBank Protein Database
667068
Guide to Pharmacology
366
UniProt Accession
V1AR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:896
GenAtlas
AVPR1B
GeneCards
AVPR1B
GenBank Gene Database
D31833
GenBank Protein Database
563982
Guide to Pharmacology
367
UniProt Accession
V1BR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:897
GenAtlas
AVPR2
GeneCards
AVPR2
GenBank Gene Database
U04357
GenBank Protein Database
28418
Guide to Pharmacology
368
UniProt Accession
V2R_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q324147), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.