Angiotensin II 2.5mg/1ml solution for infusion vials
Requires a prescription from a doctor or prescriber
Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure.
Safety information for pregnancy and breastfeeding
Pregnancy
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
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Suspected adverse reactions reported for Angiotensin II
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1 branded products available
MHRA licensed products
View all licensed products for Angiotensin II on the MHRA register
Giapreza 2.5mg/1ml concentrate for solution for infusion vials
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(10)
Angiotensin II for treating vasosuppressor-resistant hypotension caused by septic or distributive shock (terminated appraisal) (TA859)
Chronic heart failure in adults: diagnosis and management (NG106)
Hypertension in adults: diagnosis and management (NG136)
Sacubitril valsartan for treating symptomatic chronic heart failure with reduced ejection fraction (TA388)
Heart valve disease presenting in adults: investigation and management (NG208)
Hypertension in pregnancy: diagnosis and management (NG133)
Hypertension in pregnancy (QS35)
Acute kidney injury: prevention, detection and management (NG148)
Chronic heart failure in adults (QS9)
Acute kidney injury (QS76)
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: 38 · Randomised trials: 2 · 1993–2026
Showing the 50 most relevant studies, sorted by most relevant.
J. Cohn, G. Tognoni
The New England journal of medicine, 2001
K. Dickstein, J. Kjekshus
Lancet, 2002
Steven J. Forrester, George W. Booz, Curt D. Sigmund, et al.
Physiological Reviews, 2018
- Signal Transduction
- Angiotensin II
- Blood Vessels
R. Santos, W. Sampaio, A. Alzamora, et al.
Physiological Reviews, 2017
W. Ni, Xiuwen Yang, Deqing Yang, et al.
Critical Care, 2020
Vaibhav B. Patel, J. Zhong, M. Grant, et al.
Circulation research, 2016
Seema Patel, A. Rauf, H. Khan, et al.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2017
María Paz Ocaranza, Jaime A Riquelme, Lorena García, et al.
Nature Reviews. Cardiology, 2019
X. Li, Jianfeng Zhang, J. Zhuo
Pharmacological research, 2017
Eric L. Barker, Lauren B. Arendse, A. H. J. Danser, et al.
Pharmacological Reviews, 2019
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
Not available
Mechanism
As part of the renin-angiotensin-aldosterone-system (RAAS), angiotensin II raise…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
3 hours
Half-life
Volume of distribution
Metabolism
40%
Elimination
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
As of December 21, 2017 the FDA approved La Jolla Pharmaceutical's Giapreza (angiotensin II) Injection for Intravenouse Infusion for the indication of acting as a vasoconstrictor to increase blood pressure in adults with septic or other distributive shock. The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help maintain body blood pressure.
Shock is the inability to maintain blood flow to vital tissues and the potential resultant organ failure and death within hours, no matter young or o ld. As distributive shock is the most common type of shock in the inpatient setting and affects up to one third of patients in the intensive care unit, the FDA determined that there is a need for treatment options for critically ill hypotensive patients who do not adequately respond to currently available therapies.
Known interactions with other medications. Always consult a healthcare professional.
Showing 11 of 11 interactions
In the ATHOS-3 clinical study there was a higher incidence of arterial and venous thrombotic and thromboembolic events in patients who received angiotensin II compared to placebo treated patients. The major imbalance was in deep venous thromboses - which prompts the potential need to use concurrent venous thromboembolism (VTE) prohphylaxis [FDA Label].
Adverse effects of noticeable potential (>= 10%) include thromboembolic events (ie. like deep vein thrombosis) including arterial and venous thrombotic events, thrombocytopenia, tachycardia, and fungal infection.
Effects whose potential are < 10% include delirium, acidosis, hyperglycemia, peripheral ischemia [FDA Label].
Concomitant use of angiotensin converting enzymes (ACE) inhibitors may increase the response of angiotensin II [FDA Label].
Concomitant use of angiotensin II blockers (ARBs) may decrease the response to angiotensin II [FDA Label].
There are no formal data regarding the safe use of angiotensin II in pregnant women. However, septic or other distributive shock is a medical emergency that can be fatal if left untreated. Delaying treatment in pregnant women with hypotension associated with septic or otherdistributive shock is likely to increase the risk of maternal and fetal morbidity and mortality [FDA Label].
There is no formal data regarding whether or not angiotensin II may become present in human milk and there is no data available on the effects of angiotensin II on the breastfed child or the effects on milk production [FDA Label].
The safety and efficacy of angiotensin II in pediatric patients has not yet been established [FDA Label].
There is no difference in the safety or efficacy between patients less than 65 years old and those 65 years or older when treated with angiotensin II [FDA Label].
There is no difference in pharmacokinetics between male and female patients [FDA Label].
The pharmacokinetics of angiotensin II are not expected to be influenced by renal impairment or hepatic impairment [FDA Label].
The direct action of angiotensin II on surrounding vessel walls is facilitated by binding to the G-protein-coupled angiotensin II receptor type 1 (AT-1) on vascular smooth muscle cells, which stimulates Ca2+/calmodulin-dependent phosphorylation of myosin and causes smooth muscle contraction that results in vasoconstriction [FDA Label, A31494].
The RAAS is ultimately regulated by a negative feedback effect of angiotensin II on renin production by the juxtaglomerular cells of the renal afferent arteriole. Unresuscitated septic shock associated with marked hypovolemia, extracellular fluid volume depletion, decreased cardiac output, low arterial blood pressure and decreased systemic vascular resistance causes an increase in renin secretion by the juxtaglomerular cells, resulting in elevated angiotensin II plasma levels and an increased secretion of aldosterone from the adrenal cortex. Angiotensin II binding to AT-1 receptors causes dose-dependent vasoconstriction of both afferent and efferent glomerular arterioles. The most pronounced effect of angiotensin II results on efferent arterioles, resulting in reduced renal blood flow and increased glomerular filtration pressure. [A31494]
In the RAAS, juxtaglomerular cells of the renal afferent arteriole synthesize the proteolytic enzyme renin. Although stored in an inactive form called pro-renin, decreases in arterial blood pressure or extracellular fluid volume depletion can cause various enzymatic reactions to release active renin into the systemic circulation and surrounding tissues. Such renin release allows for the production of the alpha-2-globulin angiotensinogen predominantly in the liver and to some extent, the kidneys and other organs. [A31494]
Angiotensin I, itself a decapeptide with weak biological activity, is produced from angiotensinogen and then quickly converted to angiotensin II by angiotensin converting enzymes (ACE). Consequently, angiotensin II demonstrates its strong vasopressor activity when it is rapidly degraded by aminopeptidases A and M into further entities like angiotensin III and angiotensin IV, respectively. Such species like angiotensin III can then bind and interact with specific G protein coupled receptors like angiotensin receptor 1, or AT-1 [A31494] where strong vasoconstricson can occur. [A31494]
Furthermore, in the ATHOS-3 clinical trial, for the 114 (70%) patient subjects in the angiotensin II arm who reached the target mean arterial pressure (MAP) at Hour 3, the median time to reach the target MAP endpoint was approximately 5 minutes. The angiotensin II was titrated to effect for each individual patient. [FDA Label].
How the body processes this drug — absorption, distribution, metabolism, and elimination
Nevertheless, the official prescribing information also notes that no formal studies have been conducted that examine the metabolism of angiotensin II [FDA Label].
Proteins and enzymes this drug interacts with in the body
PMID:28379944 PMID:29967536 PMID:31899086 PMID:8185599
Signals primarily via a non-canonical G-protein- and beta-arrestin independent pathways .
PMID:28379944
Cooperates with MTUS1 to inhibit ERK2 activation and cell proliferation PMID:15123706
PMID:15611106 PMID:1567413 PMID:25913193 PMID:26420482 PMID:30639100 PMID:32079768 PMID:8987975
The activated receptor in turn couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C PMID:15611106
ATC C01CX09
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)
Angiotensin II
Additional database identifiers
ChemSpider
150504
BindingDB
50228195
ZINC
ZINC000169676920
HUGO Gene Nomenclature Committee (HGNC)
HGNC:338
GenAtlas
AGTR2
GeneCards
AGTR2
GenBank Gene Database
U20860
Guide to Pharmacology
35
UniProt Accession
AGTR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:336
GenAtlas
AGTR1
GeneCards
AGTR1
GenBank Gene Database
M91464
GenBank Protein Database
179122
Guide to Pharmacology
34
UniProt Accession
AGTR1_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q412999), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.