Selexipag 800microgram tablets
Requires a prescription from a doctor or prescriber
Selexipag was approved by the United States FDA on December 22, 2015 for the treatment of pulmonary arterial hypertension (PAH) to delay disease progression and reduce risk of hospitalization.
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Selexipag
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Selexipag
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Selexipag on the MHRA register
Uptravi 800microgram tablets
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.
Check stock at pharmacies and supply information
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Supply & safety information
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
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: 21 · Randomised trials: 6 · 2012–2026
Showing the 50 most relevant studies, sorted by most relevant.
Shang Wang, Yi Yan, Jian Zhang, et al.
Animal Models and Experimental Medicine, 2023
- Pulmonary Arterial Hypertension
- Hypertension, Pulmonary
- Acetamides
Meng Li, Lin Liu, Cong Liu, et al.
Clinical Therapeutics, 2023
- Hypertension, Pulmonary
- Acetamides
- Antihypertensive Agents
Patsiou V, Grantza T, Chrysochoidis-Trantas T, et al.
2025
Ji-Eun An, Jahyun Cho, Min Ju Kim, et al.
Reviews in Cardiovascular Medicine, 2026
Alowami M, Ch'ng BX, Babasola RO, et al.
2026
Qin J, Wang G, Han D
2025
De-Gang Mo, Hong-Yan Dai, Jun Guan
2023
Suresh SB, Noor K, Hyun J, et al.
2025
Abstract Background Inoperable or residual chronic thromboembolic pulmonary hypertension treatment modalities remain challenging due to limited comparison of alternatives between BPA and pharmacological agents. Objective To compare the relative efficacy and safety of BPA and pharmacological treatments in patients with inoperable or residual CTEPH. By integrating both direct and indirect comparisons, the study aims to provide a hierarchised, evidence-based framework to inform personalised treatment selection and guideline development for this high-risk population. Methods A systematic search of major databases through November 2024 identified randomized trials evaluating BPA, Riociguat, endothelin receptor antagonists (Bosentan, Ambrisentan, Macitentan), PDE-5 inhibitors (Sildenafil), and prostacyclin analogs (Selexipag). Outcomes included pulmonary vascular resistance (PVR), mean pulmonary artery pressure (mPAP), cardiac index (CI), 6-minute walk distance (6MWD), NT-proBNP, and Borg Dyspnea Index (BDI). A frequentist random-effects model was applied using the netmeta R package. Results Nine studies with 839 participants were analyzed. BPA showed the greatest reduction in PVR (MD -444.02 dyn·s·cm⁻⁵, 95% CI -606.99 to -281.05) and mPAP (MD -16.17 mmHg), with the highest SUCRA scores across outcomes. Riociguat ranked second overall, improving PVR, 6MWD, and CI. Macitentan and selexipag significantly improved CI, while bosentan reduced NT-proBNP. Ambrisentan and sildenafil did not demonstrate significant benefits over placebo. High heterogeneity was observed for PVR and BDI outcomes. Conclusions Ballon Pulmonary Angioplasty (BPA) demonstrates the most robust and consistent improvements in hemodynamics as evidenced by PVR, mPAP and mRAP measurements as well in functional and biomarker improvements (6MWD and NT-proBNP) in patients with inoperable CTEPH while Riociguat remains the most effective pharmacologic agent, offering significant benefits across multiple domains including PVR, 6MWD, mPAP and CI. Macitentan and Selexipag showed promising improvements in cardiac output while Bosentan provided NT-proBNP and pVR benefit. Ambrisentan and Sildenafil did not demonstrate significant advantages over placebo in this population. These findings support BPA as the most effective intervention for inoperable CTEPH, with Riociguat as the preferred pharmacologic therapy. However, limited direct comparisons and heterogeneity in some endpoints warrant long-term outcome studies to refine treatment sequencing, combination strategies and the consideration for future head-to-head trials between advanced oral therapies and BPA.
Abstract licence: CC BY
Jinlv Qin, Guizuo Wang, Dong Han
Current Problems in Cardiology, 2022
- Pulmonary Arterial Hypertension
- Hypertension, Pulmonary
- Acetamides
Minshan Chen, Yuanqiang Lai, Riken Chen, et al.
Pulmonary Pharmacology & Therapeutics, 2021
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
7 found
Half-life
0.8-2.5 hours
Mechanism
Selexipag is a selective prostacyclin (IP, also called PGI2) receptor agonist.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
3-4 hours
Half-life
0.8-2.5 hours
Protein binding
99%
Metabolism
3%
Elimination
93%
Clearance
35 L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1070 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Other than active metabolite, other metabolites in circulation do not exceed 3% of the total drug-related material.
Proteins and enzymes this drug interacts with in the body
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:10779507 PMID:15159445 PMID:17412826
Shows broad substrate specificity, can transport both organic anions such as bile acid taurocholate (cholyltaurine) and conjugated steroids (17-beta-glucuronosyl estradiol, dehydroepiandrosterone sulfate (DHEAS), and estrone 3-sulfate), as well as eicosanoid leukotriene C4, prostaglandin E2 and L-thyroxine (T4) .
PMID:10779507 PMID:11159893 PMID:12568656 PMID:15159445 PMID:17412826 PMID:19129463
Hydrogencarbonate/HCO3(-) acts as the probable counteranion that exchanges for organic anions .
PMID:19129463
Shows a pH-sensitive substrate specificity towards sulfated steroids, taurocholate 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
Involved in the clearance of bile acids and organic anions from the liver .
PMID:22232210
Can take up bilirubin glucuronides from plasma into the liver, contributing to the detoxification-enhancing liver-blood shuttling loop .
PMID:22232210
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 pitavastatin, a clinically important class of hypolipidemic drugs .
PMID:15159445
May play an important role in plasma and tissue distribution of the structurally diverse chemotherapeutic drugs methotrexate and paclitaxel .
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
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC B01AC27
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)
Selexipag
Additional database identifiers
Drugs Product Database (DPD)
22681
ChemSpider
8089417
BindingDB
50235383
ZINC
ZINC000003990451
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9602
GenAtlas
PTGIR
GeneCards
PTGIR
GenBank Gene Database
L29016
GenBank Protein Database
495043
Guide to Pharmacology
345
UniProt Accession
PI2R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1863
GenAtlas
CES1
GeneCards
CES1
GenBank Gene Database
M73499
Guide to Pharmacology
2592
UniProt Accession
EST1_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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:10961
GeneCards
SLCO1B3
GenBank Gene Database
AJ251506
GenBank Protein Database
9187497
Guide to Pharmacology
1221
UniProt Accession
SO1B3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_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 (Q15424759), 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.