Selumetinib 25mg capsules
Requires a prescription from a doctor or prescriber
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Safety monitoring data
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Suspected adverse reactions reported for Selumetinib
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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.
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Suspected adverse reactions reported for Selumetinib
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1 branded products available
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Koselugo 25mg capsules
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)
Selumetinib for treating symptomatic and inoperable plexiform neurofibromas associated with type 1 neurofibromatosis in children aged 3 and over (HST20)
Sotorasib for previously treated KRAS G12C mutation-positive advanced non-small-cell lung cancer (TA781)
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. 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: 14 · Randomised trials: 4 · 2015–2026
Showing the 50 most relevant studies, sorted by most relevant.
P. Jänne, Michel M. van den Heuvel, F. Barlesi, et al.
JAMA, 2017
R. Carvajal, S. Piperno-Neumann, E. Kapiteijn, et al.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2018
Lanzafame K, Blanco G, Paratore S, et al.
2026
Background/Objectives: The primary objective of this systematic review is to synthesize the available evidence regarding the safety of the various treatment options for advanced uveal melanoma. A thorough understanding of a drug's safety profile enables early identification and management of adverse reactions, thereby preventing clinical deterioration and minimizing the need for dose reduction, treatment delays, or therapy discontinuation. Methods: In accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) and AMSTAR (Assessing the Methodological Quality of Systematic Reviews) guidelines, this review included all clinical studies that examined the most common adverse events associated with all available systemic treatments for metastatic uveal melanoma. Following the study selection process, nine studies were considered eligible and were included in the review. Results: Treatment with the bispecific antibody was associated with a favorable toxicity profile. The most severe adverse event observed was limited to cutaneous toxicity. Analysis of treatment-related adverse events (TRAEs) of grade ≥3 showed that patient cohorts receiving trametinib, selumetinib, and darovasertib experienced the lowest incidence of severe events (with the exception of creatine phosphokinase elevation observed with selumetinib), suggesting a comparatively more favorable safety profile for these agents. At present, the most robust efficacy data in the metastatic uveal melanoma setting are available for tebentafusp and darovasertib. Conclusions: This study provides the most comprehensive analysis of TRAEs in randomized trials of UM, delineating the toxicity and safety profiles of current therapies to guide personalized treatment decisions.
Abstract licence: CC BY
Jisun Hwang, H. Yoon, B. Lee, et al.
Neurology, 2022
A. Gross, P. Wolters, E. Dombi, et al.
The New England journal of medicine, 2020
G. Oxnard, J.C. Yang, H. Yu, et al.
Annals of oncology : official journal of the European Society for Medical Oncology, 2020
E. Dombi, A. Baldwin, L. Marcus, et al.
The New England journal of medicine, 2016
J. Fangusaro, A. Onar-Thomas, T. Young Poussaint, et al.
The Lancet. Oncology, 2019
A. Banerjee, R. Jakacki, A. Onar-Thomas, et al.
Neuro-Oncology, 2017
A. Ho, M. Dedecjus, L. Wirth, et al.
Journal of Clinical Oncology, 2022
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
6.2 hours
Mechanism
The Ras-Raf-MEK-ERK signaling cascade is known to be activated in several types…
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1- 1.5 hours
Half-life
25 mg/m
[A193536]
The elimination half-life associated with a dose of 25 mg/m2 in pediatric patients is 6.2…
Protein binding
96%
[L12852]
Overall, approximately 98.4% of selumetinib is plasma protein bound.
[L12852]
Volume of distribution
78 L
[L12852]
…
Metabolism
10%
Hydrolysis of selumetinib’s amide…
Elimination
59%
[A193422][L12852]
Clearance
8.8 L/h
[L12852]
…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Results from clinical trials investigating earlier developed MEK inhibitors were underwhelming.[A193611] However, selumetinib demonstrated impressive efficacy and tolerability in Phase I trials, leading to its continued investigation for the treatment of various types of tumours in Phase II trials.[A193611]
"The novel MEK 1/2 inhibitor, selumetinib, was initially approved solely for the treatment of pediatric patients with Neurofibromatosis type 1 (NF-1) and symptomatic, inoperable plexiform neurofibromas (PN). NF-1 is considered rare, with an estimated incidence of 1/3000 individuals.[A193608] It is a genetic, autosomal dominant condition resulting from mutations of the NF1 gene, which can lead to various complications, including the development of multiple tumours in the nervous system.[A193533][A193608] While some patients with this disorder develop PNs, this is considered relatively uncommon compared to other variants of NF-1.[A193608] Use of selumetinib in this population has shown efficacy in shrinking associated tumours and is linked to other positive clinical outcomes.[A193533] Following its initial FDA approval on April 10, 2020,[L49991] and Health Canada approval on August 23, 2022,[L49986] the regulatory landscape has evolved. Most recently, on November 20, 2025, the FDA expanded this indication to include adults [L53881]
[A193611][L12852][L12969][L49986][L53881]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1014 interactions
[A193713][L12852]
Ras as well as several kinases and phosphatases are responsible for regulating the Raf-MEK-ERK pathway.[A193614] Often in cancers, Ras (a G-protein coupled receptor) is deregulated, allowing downstream signalling to proceed unchecked.[A193614] Through several complex steps, Raf phosphorylates and activates MEK, which then phosphorylates and activates ERK.[A193602][A193614] ERK is then able to exert its effects on several downstream targets.[A193602][A193614]
As such, therapies inhibiting upstream components of this pathway have become attractive targets for cancer treatment.[A193602] Selumetinib exerts its effects by selectively inhibiting MEK1 and MEK2 which can effectively blunt the pleiotropic effects of the Ras-Raf-MEK-ERK cascade.[A193533][A193620] By inhibiting this oncogenic pathway, selumetinib reduces cell proliferation, and promotes pro-apoptotic signal transduction.[A193602][A193602][A193632]
Selumetinib has minimal off-target activity, contributing to its impressive safety profile.[A193638]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A193536][A193422][L12852]
In healthy adults, the mean absolute oral bioavailability was reported to be 62%.
[L12852]
Selumetinib should be administered on an empty stomach since food significantly decreases serum concentrations of the drug.
[L12852]
[A193536]
The elimination half-life associated with a dose of 25 mg/m2 in pediatric patients is 6.2 hours.
[L12852]
In a study observing the pharmacokinetic effects of various selumetinib regimens in select Japanese patients, the half-life ranged from 9.2- 10.6 hours.
[A193536]
In other studies where selumetinib 75 mg is administered twice daily, the half-life is reported to be approximately 13 hours.
[A193422]
[L12852]
Overall, approximately 98.4% of selumetinib is plasma protein bound.
[L12852]
[L12852]
A study in healthy adult males found a mean apparent volume of distribution of 146 L.
[A193422]
Another study observing the pharmacokinetic effects of various selumetinib doses and regimens in select Japanese patients found that the apparent volume of distribution values at steady-state ranged from 73.2 - 148.1 L.
[A193536]
Hydrolysis of selumetinib’s amide functional group produces M15 (AZ13326637), which contains a carboxylic acid.
[A193422]
Elimination of the ethanediol moiety from the parent compound results in the formation of the primary amide M14 (AZ12791138) metabolite.
[A193422]
Amide hydrolysis transforms M14 into M15, glucuronidation and further oxidation of M14 leads to M2, M6 and M1, and N-demethylation of M14 produces M12.
[A193422]
The amide glucuronide (M2) is thought to be the major circulating metabolite.
[A193422]
Demethylation of selumetinib produces the pharmacologically active M8 (AZ12442942), and further oxidation of M8 leads to M11.
[A193422]
Glucuronidation of M8 produces M3 or M5, and elimination of the ethanediol moiety from M8 results in a primary amide, producing M12.
[A193422]
Although the N-demethylated metabolite (M8) accounts for <10% of the circulating metabolites, it is responsible for approximately 21-35% of any observed pharmacological activity.
[A193422][L12852]
Ribose conjugation transforms M12 into M9, while oxidation of M12 leads to M10 and M13 metabolites.
[A193422]
Glucuronidation of M10 produces M1.
[A193422]
Direct glucuronidation of selumetinib produces M4 or M7, which can both eventually transform into M3 and M5 metabolites.
[A193422]
[A193422][L12852]
[L12852]
A study in healthy adult males found a clearance value of 15.7 L/hr.
[A193422]
Another study observing the pharmacokinetic effects of various selumetinib doses and regimens in select Japanese patients found clearance values that ranged from 9.2 - 15.9 L/hr.
[A193536]
Proteins and enzymes this drug interacts with in the body
Both MAP2K1/MEK1 and MAP2K2/MEK2 function specifically in the MAPK/ERK cascade, and catalyze the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in the extracellular signal-regulated kinases MAPK3/ERK1 and MAPK1/ERK2, leading to their activation and further transduction of the signal within the MAPK/ERK cascade. Activates BRAF in a KSR1 or KSR2-dependent manner; by binding to KSR1 or KSR2 releases the inhibitory intramolecular interaction between KSR1 or KSR2 protein kinase and N-terminal domains which promotes KSR1 or KSR2-BRAF dimerization and BRAF activation .
PMID:29433126
Depending on the cellular context, this pathway mediates diverse biological functions such as cell growth, adhesion, survival and differentiation, predominantly through the regulation of transcription, metabolism and cytoskeletal rearrangements. One target of the MAPK/ERK cascade is peroxisome proliferator-activated receptor gamma (PPARG), a nuclear receptor that promotes differentiation and apoptosis.
MAP2K1/MEK1 has been shown to export PPARG from the nucleus. The MAPK/ERK cascade is also involved in the regulation of endosomal dynamics, including lysosome processing and endosome cycling through the perinuclear recycling compartment (PNRC), as well as in the fragmentation of the Golgi apparatus during mitosis
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
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
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
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC L01EE04
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)
Selumetinib
Additional database identifiers
Drugs Product Database (DPD)
23774
ChemSpider
8303141
BindingDB
50355497
PDB
3EW
ZINC
ZINC000031773258
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6840
GenAtlas
MAP2K1
GeneCards
MAP2K1
GenBank Gene Database
L05624
GenBank Protein Database
188569
Guide to Pharmacology
2062
UniProt Accession
MP2K1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6842
GeneCards
MAP2K2
Guide to Pharmacology
2063
UniProt Accession
MP2K2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_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:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_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:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_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
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