Eptifibatide 20mg/10ml solution for injection vials
Requires a prescription from a doctor or prescriber
Synthetic cyclic hexapeptide that binds to platelet receptor glycoprotein and inhibits platelet aggregation.
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Eptifibatide 20mg/10ml solution for injection vials
WHO defined daily dose (DDD)
200 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(2)
Guidance on the use of glycoprotein IIb/IIIa inhibitors in the treatment of acute coronary syndromes (TA47)
ClearWay RX for drug delivery to coronary artery thrombotic lesions (MIB55)
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
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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 all 27 studies.
Reviews & meta-analyses: 4 · Randomised trials: 2 · 2021–2026
Showing all 27 studies, sorted by most relevant.
Ali H, Shehzad R, Ahmed U, et al.
2026
- Tirofiban
- Eptifibatide
- Ischemic Stroke
Jingting Liu, Yihong Yang, Hongbo Liu
Journal of Thrombosis and Thrombolysis, 2021
- Ischemic Stroke
- Brain Ischemia
- Stroke
Rines I, Adeoye O, Barreto AD, et al.
2025
M. Mousavi, Fatemeh Sehati, A. Tayebi, et al.
Cardiovascular revascularization medicine : including molecular interventions, 2023
- ST Elevation Myocardial Infarction
- Eptifibatide
- Ecchymosis
Gašper Tonin, Jasna Klen
International Journal of Molecular Sciences, 2023
- Pharmacology, Clinical
- Angioplasty, Balloon, Coronary
- Eptifibatide
Therapeutic peptides are oligomers or short polymers of amino acids used for various medical purposes. Peptide-based treatments have evolved considerably due to new technologies, stimulating new research interests. They have been shown to be beneficial in a variety of therapeutic applications, notably in the treatment of cardiovascular disorders such as acute coronary syndrome (ACS). ACS is characterized by coronary artery wall damage and consequent formation of an intraluminal thrombus obstructing one or more coronary arteries, leading to unstable angina, non-ST elevated myocardial infarction, and ST-elevated myocardial infarction. One of the promising peptide drugs in the treatment of these pathologies is eptifibatide, a synthetic heptapeptide derived from rattlesnake venom. Eptifibatide is a glycoprotein IIb/IIIa inhibitor that blocks different pathways in platelet activation and aggregation. In this narrative review, we summarized the current evidence on the mechanism of action, clinical pharmacology, and applications of eptifibatide in cardiology. Additionally, we illustrated its possible broader usage with new indications, including ischemic stroke, carotid stenting, intracranial aneurysm stenting, and septic shock. Further research is, however, required to fully evaluate the role of eptifibatide in these pathologies, independently and in comparison to other medications.
Abstract licence: CC BY
M. Safi, Roozbeh Nazari, Nahid Senobari, et al.
Clinical Case Reports, 2024
Eptifibatide, a GPIIb/IIIa receptor inhibitor, has shown its efficacy and safety in patients with high clot burden in their coronary vessels. It is widely used in patients with this condition. However, this medication use is accompanied by complications in some cases. Thrombocytopenia which is a relatively common condition in patients admitted to the hospital, especially in the acute setting, can be caused by medications. This condition can occur as an antibody or non-antibody-mediated process, caused by medications, such as heparin, clopidogrel, and eptifibatide. In this case, we present a woman with acute coronary syndrome and a complex lesion with a clot in her coronary vessel who was treated with eptifibatide. It led to asymptomatic thrombocytopenia. Once detected in laboratory data, the infusion was held, and the platelet count recovered in less than 5 days without additional treatment for this adverse effect. Eptifibatide is a medication used to treat acute coronary syndrome patients with a large thrombus in their coronary vessels. The mechanism of inducing thrombocytopenia by eptifibatide has not been proven yet, but it might be related to IgG antibodies. The severity of the disease can vary significantly, and the treatment is based on this factor. However, the main pillar of the treatment is the cessation of eptifibatide as soon as possible. This case draws the attention of physicians to one of the infrequent adverse effects of a commonly used medication in cardiology patients. Thrombocytopenia and its manifestations should be investigated and considered in patients who receive eptifibatide.
Abstract licence: CC BY
O. Adeoye, Joseph P Broderick, C. P. Derdeyn, et al.
The New England journal of medicine, 2024
- Eptifibatide
- Ischemic Stroke
Paul-Adrian Călburean, P. Grebenișan, Ioana-Andreea Nistor, et al.
Frontiers in Pharmacology, 2024
Background: Current guidelines recommend that glycoprotein IIb/IIIa inhibitor (GPI) and manual aspiration thrombectomy should not be routinely used in patients with ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (pPCI), although there is a lack of dedicated studies. The aim of this study was to examine the impact of combined usage of a potent P2Y12 inhibitor, GPI, and manual aspiration thrombectomy on long-term survival after STEMI. Methods: All STEMI patients treated by pPCI in a tertiary center who have been included prospectively in the local PCI registry between January 2016 and December 2022 were analyzed in this study. Patients were excluded if they required oral anticoagulation or bridging between clopidogrel or ticagrelor during hospitalization. Results: A total of 1,210 patients were included in the present study, with a median follow-up of 2.78 (1.00–4.88) years. Ticagrelor significantly reduced all-cause and cardiovascular-cause mortality [HR = 0.27 (0.21–0.34), p < 0.0001 and HR = 0.23 (0.17–0.30), p < 0.0001, respectively]. Eptifibatide significantly reduced all-cause and cardiovascular-cause mortality [HR = 0.72 (0.57–0.92), p = 0.002, and HR = 0.68 (0.52–0.89), p = 0.001, respectively]. Manual thrombus aspiration had no significant effect on both all-cause and cardiovascular-cause mortality. In multivariate Cox regression, all-cause mortality was reduced by ticagrelor, while eptifibatide or manual thrombus aspiration had no significant effect. However, cardiovascular-cause mortality was reduced by both ticagrelor and eptifibatide, while manual thrombus aspiration had no significant effect. Conclusion: Ticagrelor consistently reduced cardiovascular and all-cause mortality, while eptifibatide reduced only cardiovascular mortality. Manual thrombus aspiration provided no long-term benefit. Our findings support the current guideline recommendation that GPI and manual aspiration thrombectomy should not be routinely used in treatment of STEMI with pPCI.
Abstract licence: CC BY
P. Latacz, Tadeusz J. Popiela, P. Brzegowy, et al.
Neurology International, 2024
OBJECTIVES: The optimal treatment strategy for ischemic stroke in patients presenting with tandem occlusions of the internal carotid artery remains controversial. Several studies have demonstrated better clinical outcomes after eptifibatide, which is a short half-life antiplatelet agent. This retrospective analysis focused on the safety and efficacy of low-dose eptifibatide administration in stroke patients with tandem lesions. METHODS: We evaluated the results of endovascular treatment in 148 stroke patients with tandem lesions. Patients in whom balloon angioplasty alone resulted in satisfactory cerebral flow did not receive eptifibatide (33 patients); others received this drug together with stent implantation (115 patients). Eptifibatide was given as an intravenous bolus of 180 μg/kg and then in a modified low dose of 1 μg/kg/min for 24 hours. RESULTS: There were no statistically significant differences between both groups regarding 30-day mortality, frequency of thrombotic events, or hemorrhagic complications. An analysis of clinical status at 30-day follow-up revealed that the administration of eptifibatide was associated with a statistically significant better outcome: a higher rate of either no neurological symptoms or only mild symptoms (4 NIHSS points maximally). CONCLUSIONS: The administration of eptifibatide in stroke patients presenting with tandem lesions is relatively safe. Moreover, treatment with this drug can improve clinical outcomes in these challenging patients.
Abstract licence: CC BY
Travis R. Huffman, Evan Gleaves, Glee Lenoir, et al.
American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists, 2023
- Thrombocytopenia
- Eptifibatide
- Heparin
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
44 found
Half-life
2.5 hours
Mechanism
Eptifibatide inhibits platelet aggregation by reversibly binding to the platelet…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
2.5 hours
Protein binding
25%
Metabolism
Clearance
55 mL
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 419 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
Integrin alpha-IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain (By similarity). Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen .
PMID:9111081
This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. Fibrinogen binding enhances SELP expression in activated platelets (By similarity).
ITGAV:ITGB3 binds to fractalkine (CX3CL1) and acts as its coreceptor in CX3CR1-dependent fractalkine signaling .
PMID:23125415 PMID:24789099
ITGAV:ITGB3 binds to NRG1 (via EGF domain) and this binding is essential for NRG1-ERBB signaling .
PMID:20682778
ITGAV:ITGB3 binds to FGF1 and this binding is essential for FGF1 signaling .
PMID:18441324
ITGAV:ITGB3 binds to FGF2 and this binding is essential for FGF2 signaling .
PMID:28302677
ITGAV:ITGB3 binds to IGF1 and this binding is essential for IGF1 signaling .
PMID:19578119
ITGAV:ITGB3 binds to IGF2 and this binding is essential for IGF2 signaling .
PMID:28873464
ITGAV:ITGB3 binds to IL1B and this binding is essential for IL1B signaling .
PMID:29030430
ITGAV:ITGB3 binds to PLA2G2A via a site (site 2) which is distinct from the classical ligand-binding site (site 1) and this induces integrin conformational changes and enhanced ligand binding to site 1 .
PMID:18635536 PMID:25398877
ITGAV:ITGB3 acts as a receptor for fibrillin-1 (FBN1) and mediates R-G-D-dependent cell adhesion to FBN1 .
PMID:12807887
In brain, plays a role in synaptic transmission and plasticity. Involved in the regulation of the serotonin neurotransmission, is required to localize to specific compartments within the synapse the serotonin receptor SLC6A4 and for an appropriate reuptake of serotonin. Controls excitatory synaptic strength by regulating GRIA2-containing AMPAR endocytosis, which affects AMPAR abundance and composition (By similarity).
ITGAV:ITGB3 act as a receptor for CD40LG .
PMID:31331973
ITGAV:ITGB3 acts as a receptor for IBSP and promotes cell adhesion and migration to IBSP PMID:10640428
Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen .
PMID:9111081
This step leads to rapid platelet aggregation which physically plugs ruptured endothelial cell surface (By similarity)
They are involved in pain signaling .
PMID:25296916
Calcium channels containing alpha-1B subunit may play a role in directed migration of immature neurons. Mediates Ca(2+) release probability at hippocampal neuronal soma and synaptic terminals (By similarity)
ATC B01AC16
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)
Eptifibatide
Additional database identifiers
Drugs Product Database (DPD)
11891
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6156
GenAtlas
ITGB3
GeneCards
ITGB3
GenBank Gene Database
J02703
GenBank Protein Database
306786
Guide to Pharmacology
2457
UniProt Accession
ITB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6138
GenAtlas
ITGA2B
GeneCards
ITGA2B
GenBank Gene Database
J02764
GenBank Protein Database
190068
Guide to Pharmacology
2441
UniProt Accession
ITA2B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1399
GenAtlas
CACNA2D1
GeneCards
CACNA2D1
GenBank Gene Database
M76559
GenBank Protein Database
179762
UniProt Accession
CA2D1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1400
GenAtlas
CACNA2D2
GeneCards
CACNA2D2
GenBank Gene Database
AJ251368
UniProt Accession
CA2D2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1389
GenAtlas
CACNA1B
GeneCards
CACNA1B
GenBank Gene Database
M94172
GenBank Protein Database
179758
Guide to Pharmacology
533
UniProt Accession
CAC1B_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q2295855), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.