Apremilast 10mg tablets
Requires a prescription from a doctor or prescriber
Apremilast, also known as Otezla, is a phosphodiesterase 4 (PDE4) inhibitor used to treat various types of symptoms resulting from certain inflammatory autoimmune diseases.
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Suspected adverse reactions reported for Apremilast
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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 Apremilast
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5 branded products available
MHRA licensed products
View all licensed products for Apremilast on the MHRA register
Otezla 10mg tablets
Apremilast 10mg tablets
Apremilast 10mg tablets
Apremilast 10mg tablets
Apremilast 10mg tablets
WHO defined daily dose (DDD)
60 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.
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(12)
Apremilast for treating active psoriatic arthritis (TA433)
Apremilast for treating moderate to severe plaque psoriasis (TA419)
Dimethyl fumarate for treating moderate to severe plaque psoriasis (TA475)
Deucravacitinib for treating moderate to severe plaque psoriasis (TA907)
Brodalumab for treating moderate to severe plaque psoriasis (TA511)
Tofacitinib for treating active psoriatic arthritis after inadequate response to DMARDs (TA543)
Certolizumab pegol and secukinumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA445)
Tildrakizumab for treating moderate to severe plaque psoriasis (TA575)
Certolizumab pegol for treating moderate to severe plaque psoriasis (TA574)
Upadacitinib for treating active psoriatic arthritis after inadequate response to DMARDs (TA768)
Ixekizumab for treating active psoriatic arthritis after inadequate response to DMARDs (TA537)
Spondyloarthritis in over 16s: diagnosis and management (NG65)
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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Supply & safety information
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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
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: 24 · Randomised trials: 21 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
A. Armstrong, M. Gooderham, R. Warren, et al.
Journal of the American Academy of Dermatology, 2022
A. Vossen, M. V. van Doorn, H. H. van der Zee, et al.
Journal of the American Academy of Dermatology, 2019
R. Spencer, K. Elhage, Joy Q. Jin, et al.
Dermatology and Therapy, 2023
R. Alharthy, Joud M. Alharthy, R. Bawazir, et al.
Cureus, 2024
Roudin H. Alhasawi, Esraa A. Shaheen, Noura Mohammed Alshabanat, et al.
Dermatology Reports, 2025
Pemphigus is a severe autoimmune blistering disorder that significantly affects patients’ quality of life. While corticosteroids and immunosuppressive agents are commonly used, they have substantial side effects, highlighting the need for safer alternatives. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, has shown efficacy in treating other autoimmune diseases and may offer promise for pemphigus. This systematic review evaluated the clinical outcomes, safety, and potential role of apremilast in the treatment of pemphigus by synthesizing available case reports and series. A literature search was conducted across multiple databases (PubMed, EMBASE, Cochrane, Web of Science, ScienceDirect, and Google Scholar) for case reports and series involving apremilast in pemphigus. Inclusion criteria were a confirmed pemphigus diagnosis and apremilast treatment. Five studies (four case reports and one case series) involving 7 patients were included. Apremilast led to significant clinical improvement in 4 patients, with reductions in disease activity, lesion severity, and symptom scores (Pemphigus Disease Area Index [PDAI], Autoimmune Bullous Skin Disorder Intensity Score [ABSIS], Visual Analog Scale [VAS], and Numerical Rating Score [NRS]). Increases in regulatory T cells and decreases in anti-desmoglein antibodies were observed. No serious adverse events were reported, although one study noted treatment failure, possibly due to short follow-up or concurrent infections. Apremilast appears to be a promising treatment for therapy-resistant or corticosteroid-intolerant pemphigus patients. Although the evidence is limited, it supports apremilast’s efficacy and favorable safety profile. Further research with larger sample sizes and randomized controlled trials is necessary to confirm these findings.
Abstract licence: CC BY-NC
Vedashree Mahajan, Bhakti Patil
Indian Dermatology Online Journal, 2025
Chiara Rizzo, Silvia Grazzini, Edoardo Conticini, et al.
Reumatismo, 2025
Jafarzadeh A, Darvishi MA, Khosravi M, et al.
2026
Background and aimsThe latest advances in the treatment of vitiligo involve the introduction of Janus kinase inhibitors (JAKI) and small molecule inhibitors (SMI). These modern treatment modalities target specific inflammatory pathways that can improve outcomes for vitiligo in adults, adolescents, and children.MethodsWe did a literature search among PubMed, Scopus, and Web of Science, utilizing PRISMA guidelines. Articles included in the study were those reporting systemic medications using JAKI and SMI for vitiligo, categorized into subgroups of children (2-12), adolescents (12-18), and adults (over 18). We extracted information based on patient demographics, treatment regimens, efficacy outcomes, adverse effects, and follow-up data.ResultsAfter screening 987 studies, a total of 25 articles met the inclusion criteria and were included. The analysis demonstrated that JAKI, as well as the phosphodiesterase-4 Inhibitor (PDE4 Inhibitor), apremilast, showed notable efficacy in the treatment of vitiligo across various age groups. Among these, ritlecitinib was the most extensively studied, showing significant improvements in both Facial-VASI and Total-VASI scores, especially when combined with NB-UVB phototherapy. Tofacitinib demonstrated up to 75% repigmentation, particularly in sun-exposed areas and pediatric populations, with higher efficacy noted when used alongside phototherapy. Upadacitinib showed ≥ 35% improvement in Facial-VASI scores, though higher doses were associated with increased adverse events, including a serious nonfatal ischemic stroke. Baricitinib led to > 50% VASI improvement in 70.6% of patients when combined with NB-UVB. Apremilast showed partial disease control and up to 61.5% repigmentation, though it was generally less effective than corticosteroids in halting progression.ConclusionsJAKI and SMIs appear to be promising treatment options for vitiligo in adults, adolescents, and children, offering better efficacy than traditional treatments. However, some treatments like Apremilast had conflicting results about efficacy in vitiligo. Although these are notable findings, further research is required to establish their long-term safety, particularly in children and adolescents.
Abstract licence: CC BY
E. Simpson, S. Imafuku, Y. Poulin, et al.
The Journal of investigative dermatology, 2019
Gupta AK, Bamimore MA, Wang T, et al.
2026
- Scalp Dermatoses
- Psoriasis
- Immunomodulating Agents
BackgroundRecently, the literature has expanded with peer-reviewed studies on immunomodulatory agents' efficacy on scalp psoriasis-which, in turn, widened knowledge gaps regarding these agents' relative effectiveness. We determined the relative efficacy of immunomodulatory monotherapies for scalp psoriasis.MethodsWe ran Bayesian network meta-analyses (NMAs) using outcomes related to Psoriasis Scalp Severity Index (PSSI) and scalp-specific Physician's Global Assessment of clear (0) or almost clear (1) (Sc-PGA 0/1).ResultsWe estimated the relative efficacy of 22 interventions (including placebo), and analyzed 9 outcomes, namely: proportion of participants who attained Sc-PGA 0/1, proportion of participants who achieved 100% improvement in PSSI (PSSI-100), and proportion of participants who achieved 90% improvement in PSSI (PSSI-90) at 8, 12, and 16 weeks.ConclusionsWe are the first to provide comparative evidence on the efficacy of newly investigated agents such as deucravacitinib, tildrakizumab, roflumilast and icotrokinra. In general, the IL-17 inhibitors (bimekizumab, ixekizumab, secukinumab, brodalumab) and IL-23 inhibitors (icotrokinra, guselkumab, tildrakizumab) were effective depending upon the outcome and time-point being considered. At 16 weeks, for PSSI-100, ixekizumab 150 mg at weeks 0, 2, 4, 8, and 12 ranked highest; at 16 weeks, for Sc-PGA 0/1 bimekizumab 320 mg every 4 weeks ranked highest; at 8 weeks, for PSSI-100 ixekizumab 80 mg every 2 weeks ranked highest; at 8 weeks, for Sc-PGA 0/1 secukinumab 300 mg at weeks 1, 2, 3 and then every 4 weeks ranked highest. Small-molecule therapies (apremilast, deucravacitinib, roflumilast) improved scalp psoriasis modestly. Our work would guide the design of future studies and clinical decision-making.
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
6-9 hours
Mechanism
The full mechanism of action of this drug is not fully established, however, it…
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
73%
Half-life
6-9 hours
[A181226][L7501]
Protein binding
68%
[L7498]
Volume of distribution
87 L
[L7498]
Metabolism
45%
Elimination
3%
[L7498]…
Clearance
10 L/h
[L7498]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L7501]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1651 interactions
[L7505]
Overdose information
In healthy subjects receiving a maximum dose of 100 mg (given as 50 mg twice daily) for about 5 days, no significant toxicity was observed. In cases of an overdose, supportive and symptomatic treatment should be administered. Contact the local poison control center for the most recent overdose management for apremilast.
[L7502]
Apremilast may cause unwanted weight loss and worsen depression, leading to suicidal thoughts or actions. It is advisable to monitor for symptoms of depression and seek medical attention if they occur, especially in patients with pre-existing depression. The need for apremilast should be carefully assessed along with the risk of worsening depression and suicide. If weight loss occurs, the degree of weight loss should be evaluated, and consideration should be made for the possible discontinuation of apremilast.[L7501]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A181229]
Food intake does not appear to affect apremilast absorption.
[L7501]
[A181226][L7501]
[L7498]
[L7498]
[A3737]
The CYP3A4 primarily mediates the oxidative metabolism of this drug, with smaller contributions from CYP1A2 and CYP2A6 enzymes.
[L7498]
The main metabolite of apremilast, M12, is an inactive glucuronide conjugate form of the O-demethylated drug.
[L7498]
Some other major metabolites, M14 and M16, are significantly less active in the inhibition of PDE4 and inflammatory mediators than their parent drug, apremilast. After an oral dose, unchanged apremilast (45%) and the inactive metabolite, O-desmethyl apremilast glucuronide (39%) are found in the plasma.
[A181235]
Minor metabolites M7 and M17 are active, but are only present in about 2% or less of apremilast concentrations, and likely not significant contributors to the actions of apremilast.
[A181235]
[L7498]
[L7498]
Proteins and enzymes this drug interacts with in the body
Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex
Involved in initiation and maintenance of cell cycle exit during cell differentiation; prevents cell proliferation and negatively regulates cell differentiation, but is required for the proliferation of specific cell types (e.g. erythroid and hematopoietic cells). Essential for cell proliferation within the dentate gyrus of the hippocampus and the subventricular zone of the lateral ventricles. Required during thymocyte development.
Promotes the production of newborn neurons, probably by modulating G1 length. Promotes, at least in astrocytes, changes in patterns of gene expression, changes in the actin cytoskeleton including loss of stress fibers, and enhanced motility during cell differentiation. Prevents myeloid differentiation by interfering with RUNX1 and reducing its transcription transactivation activity, but promotes proliferation of normal myeloid progenitors.
Delays senescence. Promotes the proliferation of beta-cells in pancreatic islets of Langerhans. May play a role in the centrosome organization during the cell cycle phases PMID:23918663
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
ATC L04AA32
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)
Apremilast
Additional database identifiers
Drugs Product Database (DPD)
22541
ChemSpider
9736448
BindingDB
50248919
PDB
A9L
ZINC
ZINC000030691736
UniProt Accession
Q86V67_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1773
GenAtlas
CDK4
GeneCards
CDK4
GenBank Gene Database
M14505
GenBank Protein Database
456427
Guide to Pharmacology
1976
UniProt Accession
CDK4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1777
GenAtlas
CDK6
GeneCards
CDK6
GenBank Gene Database
X66365
GenBank Protein Database
36623
Guide to Pharmacology
1978
UniProt Accession
CDK6_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:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_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: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 (Q2858961), 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.