Eltrombopag 12.5mg tablets
Requires a prescription from a doctor or prescriber
Eltrombopag is used to treat low blood platelet counts in adults with chronic immune (idiopathic) thrombocytopenia (ITP), when certain other medicines, or surgery to remove the spleen, have not worked well enough.
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Yellow Card reports
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1 branded products available
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(5)
Eltrombopag for treating chronic immune thrombocytopenia (TA293)
Eltrombopag for treating severe aplastic anaemia refractory to immunosuppressive therapy (terminated appraisal) (TA382)
Avatrombopag for treating primary chronic immune thrombocytopenia (TA853)
Immune (idiopathic) thrombocytopenic purpura: rituximab (ESUOM35)
Fostamatinib for treating refractory chronic immune thrombocytopenia (TA835)
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. 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: 24 · Randomised trials: 12 · 2017–2026
Showing the 50 most relevant studies, sorted by most relevant.
E. Olíva, C. Alati, V. Santini, et al.
The Lancet. Haematology, 2017
Xiaofang Zhang, Yuan Zhao, Minghang Yang, et al.
Frontiers in Immunology, 2025
Senlin Zhang, Qingwei Wang, K. Cui, et al.
Clinical Drug Investigation, 2023
Sadia Afrin, Md. Shanzid Hasan, Md. Rezwan Ahmed Mahedi, et al.
Research Journal of Pharmacy and Technology, 2024
Lai Y, Pan Q, Wang S, et al.
2025
ObjectiveThe objective of this study was to compare and rank the efficacy and safety of different thrombopoietin receptor agonists (TPO-RAs) in the treatment of chemotherapy-induced thrombocytopenia (CIT) among patients with solid tumors.MethodsPubMed, Cochrane Library, Embase, MEDLINE, Web of Science, ClinicalTrials.gov, CNKI, Wanfang Database, VIP Database, SinoMed, and China Drug Trials (www.chinadrugtrials.org.cn) were searched for randomized controlled trials (RCTs) of TPO-RAs for CIT in solid tumors from the inception to 31 December 2024. The Cochrane Risk of Bias Assessment Tool 2 was used for assessing the risk of bias. We performed a random-effects network meta-analysis using STATA 14.0 software. Treatments were ranked according to the surface under the cumulative ranking curve. Confidence of the evidence was assessed using Confidence in Network Meta-Analysis. The study protocol was registered with PROSPERO (number CRD42024612536).ResultsA total of eight studies (568 patients) were included. Most RCTs (7/8) showed a low risk of bias. The confidence in evidence was often low or very low. Our network meta-analysis indicates that when compared with placebo, hetrombopag (summary RR 0.45, 95% confidence interval 0.28-0.73) and eltrombopag (0.57, 0.41-0.81) significantly reduced the incidence of chemotherapy dose reduction or delay due to thrombocytopenia. Hetrombopag (0.29, 0.13-0.68) also significantly reduced the platelet transfusions. Eltrombopag had the lowest risk for bleeding event (0.41, 0.13-1.23) and mortality (0.83, 0.48-1.44). There were no significant differences in the risk of adverse events (AEs) between interventions. Hetrombopag (0.37, 0.02-8.68) showed the least risk of thrombosis. According to rankograms, hetrombopag was ranked as the best for reducing the incidence of chemotherapy dose reduction or delay, and platelet transfusions, with the least risk of serious AEs and thrombosis. Eltrombopag carried the least risk of bleeding events and mortality.ConclusionOur network meta-analysis suggested that based on the limited indirect data, hetrombopag may represent the preferred therapy for avoiding chemotherapy dose reductions or delays and platelet transfusion. Eltrombopag may be considered the preferred therapeutic option for avoiding bleeding events and mortality. Both compounds have acceptable safety profiles. However, larger head-to-head trials are needed to confirm these findings.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD42024612536, identfier CRD42024612536.
Abstract licence: CC BY
Mahsa Dabir, Maryam Kamrani Mousavi, Shervin Manteghi, et al.
Health Science Reports, 2025
Kumar A, Singh A, Reljic T, et al.
2026
- Thrombocytopenia
- Benzoates
- Hydrazines
Tan S, Shang M, Guo Y, et al.
2025
Zhang H, Hu J, Jiang Y, et al.
2026
BackgroundThe comparative efficacy of pharmacological treatments for lower-risk myelodysplastic syndromes (LR-MDS) remains uncertain because head-to-head randomised evidence is limited.MethodsWe performed a systematic review and network meta-analysis of randomised controlled trials evaluating pharmacological treatments for LR-MDS. Outcomes of interest were haematological improvement-erythroid (HI-E), red blood cell transfusion independence (RBC-TI), haematological improvement-platelet (HI-P), and adverse events (AEs).ResultsWe included 20 trials (2,877 participants), of which 17 trials (2,670 participants) contributed to connected treatment networks. For HI-E, luspatercept and ESA-based regimens were associated with higher rates. Lenalidomide-containing regimens showed favourable RBC-TI outcomes, including lenalidomide plus ESA, lenalidomide with or without ESA and/or G-CSF, and lenalidomide monotherapy. For HI-P, eltrombopag and romiplostim showed potential benefits. Safety profiles differed across treatments: CC-486 and imetelstat were associated with higher odds of neutropenia and gastrointestinal toxicity, whereas luspatercept was associated with increased fatigue and AEs.ConclusionComparative treatment benefit in LR-MDS differs by clinical endpoint. These findings support an individualised, goal-directed treatment approach rather than a single universally superior therapy.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420251184384.
Abstract licence: CC BY
Tan S, Shang M, Guo Y, et al.
2026
BackgroundAplastic anemia (AA) is a bone marrow failure syndrome. Whether the combination of TPO-RAs and IST is superior to IST alone is an ongoing debate. This meta-analysis compares the efficacy of EPAG+IST versus IST alone, and assesses the initiation timing and treatment duration of eltrombopag (EPAG) across different age groups of AA patients.MethodsThe literature was retrieved from Chinese and English databases up to October 1, 2025. The analysis was conducted using RevMan 5.4 software, employing a fixed-effects model to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for the outcomes. The I² statistic was used to assess heterogeneity among included studies.Results21 studies involving 2,239 patients were included. The overall response rate in the EPAG+IST group was higher at 3 months (OR = 2.13, 95% CI 1.65 - 2.74, P ConclusionThe addition of EPAG to IST may improve early hematological responses at 3 and 6 months in patients with AA, with no significant difference at 12 months. Concurrent initiation (within 7 days) was associated with earlier responses in adults.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42024604778.
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
None known
Half-life
21-32 hours
Mechanism
Eltrombopag is an orally bioavailable, small-molecule TPO-receptor agonist that…
Food interactions
2 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2-6 hours
Half-life
21-32 hours
About 26-35 hours in patients with idiopathic thrombocytopenic purpura.
Protein binding
99%
Volume of distribution
50%
Metabolism
Elimination
59%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 753 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
About 26-35 hours in patients with idiopathic thrombocytopenic purpura.
Proteins and enzymes this drug interacts with in the body
PMID:15899890 PMID:37633268
In turn, These signaling cascades lead to the proliferation, survival, and differentiation of megakaryocytes, ultimately leading to increased platelet production
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:10358072 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (dehydroepiandrosterone 3-sulfate, 17-beta-glucuronosyl estradiol, and estrone 3-sulfate), as well as eicosanoids (prostaglandin E2, thromboxane B2, leukotriene C4, and leukotriene E4), and thyroid hormones (T4/L-thyroxine, and T3/3,3',5'-triiodo-L-thyronine) .
PMID:10358072 PMID:10601278 PMID:10873595 PMID:11159893 PMID:12196548 PMID:12568656 PMID:15159445 PMID:15970799 PMID:16627748 PMID:17412826 PMID:19129463 PMID:26979622
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
Involved in the clearance of endogenous and exogenous substrates from the liver .
PMID:10358072 PMID:10601278
Transports coproporphyrin I and III, by-products of heme synthesis, and may be involved in their hepatic disposition .
PMID:26383540
May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable). Can transport HMG-CoA reductase inhibitors (also known as statins), such as pravastatin and pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:10601278 PMID:15159445 PMID:15970799
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drug methotrexate .
PMID:23243220
May also transport antihypertension agents, such as the angiotensin-converting enzyme (ACE) inhibitor prodrug enalapril, and the highly selective angiotensin II AT1-receptor antagonist valsartan, in the liver .
PMID:16624871 PMID:16627748
Shows a pH-sensitive substrate specificity towards prostaglandin E2 and T4 which may be ascribed to the protonation state of the binding site and leads to a stimulation of substrate transport in an acidic microenvironment .
PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions PMID:19129463
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
ATC B02BX05
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)
Eltrombopag
Additional database identifiers
Drugs Product Database (DPD)
20661
ChemSpider
19879943
ZINC
ZINC000011679756
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7217
GenAtlas
MPL
GeneCards
MPL
GenBank Gene Database
M90102
Guide to Pharmacology
1722
UniProt Accession
TPOR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12535
GeneCards
UGT1A3
GenBank Gene Database
M84127
GenBank Protein Database
340135
UniProt Accession
UD13_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10959
GenAtlas
SLCO1B1
GeneCards
SLCO1B1
GenBank Gene Database
AF060500
GenBank Protein Database
5051630
Guide to Pharmacology
1220
UniProt Accession
SO1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72