Afamelanotide 16mg implant
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Afamelanotide
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Afamelanotide
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Afamelanotide
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
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 Afamelanotide on the MHRA register
Scenesse 16mg implant
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
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
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. 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: 5 · Randomised trials: 2 · Trials: 3 · 2013–2026
Showing the 50 most relevant studies, sorted by most relevant.
Jafarzadeh A, Pour Mohammad A, Khosravi M, et al.
2024
- Hypopigmentation
- Vitiligo
- Sulfonamides
Aims and objectivesThe purpose of this study is to investigate the effectiveness and safety of oral and injectable systemic treatments, such as methotrexate, azathioprine, cyclosporine, tofacitinib, baricitinib, corticosteroids, statins, zinc, apremilast, etc., for treating vitiligo lesions.MethodDatabases including PubMed, Scopus, and Web of Science were meticulously searched for studies spanning from 2010 to August 2023, focusing on systemic oral and injectable therapies for vitiligo, using comprehensive keywords and search syntaxes tailored to each database. Key data extracted included study design, treatment efficacy, patient outcomes, patient satisfaction, and safety profiles.ResultsIn a total of 42 included studies, oral mini-pulse corticosteroid therapy (OMP) was the subject of six studies (14.2%). Minocycline was the focus of five studies (11.9%), while methotrexate, apremilast, and tofacitinib each were examined in four studies (9.5%). Antioxidants and Afamelanotide were the subjects of three studies each (7.1%). Cyclosporine, simvastatin, oral zinc, oral corticosteroids (excluding OMP) and injections, and baricitinib were each explored in two studies (4.8%). Azathioprine, mycophenolate mofetil, and Alefacept were the subjects of one study each (2.4%).ConclusionSystemic treatments for vitiligo have been successful in controlling lesions without notable side effects. OMP, Methotrexate, Azathioprine, Cyclosporine, Mycophenolate mofetil, Simvastatin, Apremilast, Minocycline, Afamelanotide, Tofacitinib, Baricitinib, Antioxidants, and oral/injectable corticosteroids are effective treatment methods. However, oral zinc and alefacept did not show effectiveness.
Abstract licence: CC BY
Heerfordt IM, Lerche CM, Philipsen PA, et al.
2023
- Protoporphyria, Erythropoietic
- Genetic Diseases, X-Linked
- Photosensitivity Disorders
Erythropoietic protoporphyria (EPP) and X-linked protoporphyria (XLP) are characterized by skin photosensitivity caused by accumulation of protoporphyrin IX. We aimed to review the clinical evidence of efficacy and safety of skin photosensitivity treatments in individuals with EPP or XLP. We systematically searched MEDLINE, Embase, the Cochrane Library, and ClinicalTrials.gov. A total of 40 studies with data on 18 treatment modalities were included. Comprehensive treatment safety data were obtained from the European Medicines Agency and the United States Food and Drug Administration. The studies used different outcome measures to evaluate the sensitivity without a generally accepted method to assess treatment effect on skin photosensitivity. Of the included studies, 13 were controlled trials. Gathered, the trials showed moderate positive effect of inorganic sunscreen application and subcutaneous implant of afamelanotide and no effect of organic sunscreen application, or oral treatment with beta-carotene, cysteine, N-acetylcysteine, vitamin C, or warfarin. Studies without control groups suggested treatment effect of foundation cream, dihydroxyacetone/lawsone cream, narrow-band ultraviolet B phototherapy, erythrocyte transfusion, extracorporeal erythrocyte photodynamic therapy, or oral treatment with zinc sulphate, terfenadine, cimetidine, or canthaxanthin, but the real effect is uncertain. Assessment of treatment effect on photosensitivity in patients with EPP or XLP carries a high risk of bias since experienced photosensitivity varies with both weather conditions, exposure pattern, and pigmentation. Controlled trials of promising treatment options are important although challenging in this small patient population.
Abstract licence: CC BY-NC-ND
Maverakis Ramirez N, Jaeger ZJ, Lee DJ
2026
Vitiligo is a depigmentation disorder whose treatment remains a serious challenge. While it is generally accepted that topicals and phototherapy are helpful for generalized symmetric disease, randomized controlled trials (RCTs) provide the best evidence for treatment. Our objective was to identify and summarize RCTs for vitiligo from 2013 to 2023. A systematic review registered with the International Prospective Register of Systematic Reviews (PROSPERO) was performed per PRISMA guidelines. We searched CENTRAL, ClinicalTrials.gov, Embase, PubMed, and Web of Science for RCTs using keywords such as 'vitiligo' and/or 'treatment' or 'intervention.' A total of 652 studies underwent full-text review, and 151 studies met the inclusion criteria. We focused our study on RCTs using the vitiligo area scoring index (VASI) as the primary outcome measure, leading to 36 studies. We further narrowed our focus to studies that could be aggregated into the intervention categories: phototherapy and systemic combination therapy (n=10), topical and topical combination therapy (n=15), and systemic monotherapy (n=5). Treated versus control subjects showed statistically improved VASI after the following interventions were added to phototherapy: oral psoralen, oral minipulsed prednisone, implanted afamelanotide, topical ethyl vanillate, topical bimatoprost, and oral vitamins A and E. Effective topical therapies were ruxolitinib, calcipotriol and betamethasone, tacrolimus and mometasone, and microdermabrasion and tacrolimus. None of the systemic monotherapies was superior to their corresponding comparator.
Abstract licence: CC BY
Janneke G. Langendonk, Manisha Balwani, Karl E. Anderson, et al.
New England Journal of Medicine, 2015
Jessica Wu, Ronald Cotliar
Journal of Drugs in Dermatology, 2021
- Orphan Drug Production
- Skin Diseases
- alpha-MSH
Seth Orlow
Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature, 2016
Henry W. Lim, Pearl E. Grimes, Oma Agbai, et al.
JAMA Dermatology, 2015
Adriana Polańska, Joanna Wegner, Paula Nutbohm, et al.
Advances in Dermatology and Allergology, 2024
Esther S. Kim, Karly P. Garnock-Jones
American Journal of Clinical Dermatology, 2016
Perez-Bootello J, Cova-Martin R, Naharro-Rodriguez J, et al.
2023
- Vitiligo
- Janus Kinase Inhibitors
- Phototherapy
Vitiligo is a complex disease with a multifactorial nature and a high impact on the quality of life of patients. Although there are multiple therapeutic alternatives, there is currently no fully effective treatment for this disease. In the current era, multiple drugs are being developed for the treatment of autoimmune diseases. This review assesses the available evidence on the pathogenesis of vitiligo, and a comprehensive review of treatments available for vitiligo now and in the near future is provided. This qualitative analysis spans 116 articles. We reviewed the mechanism of action, efficacy and safety data of phototherapy, afamelanotide, cyclosporine, phosphodiesterase 4 inhibitors, trichloroacetic acid, basic fibroblast growth factor, tumor necrosis factor (TNF) inhibitors, secukinumab, pseudocatalase and janus kinase (JAK) inhibitors. At the moment, there is no clearly outstanding option or fully satisfactory treatment for vitiligo, so it is necessary to keep up the development of new drugs as well as the publication of long-term effectiveness and safety data for existing treatments.
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
30 minutes
Mechanism
Patients with erythropoietic porphyria (EPP) have a deficiency of ferrochelatase…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
48 hours
Half-life
30 minutes
[L9086]
The apparent half-life following administration of a slow-release subcutaneous implant is 15 hours.
[L9134]
…
Volume of distribution
0.54 L/kg
[A187202]
Metabolism
Elimination
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L9086]
[L9086]
Afamelanotide mimics endogenous alpha melanocyte-stimulating hormone (α-MSH), a hormone typically released in response to UV-induced skin damage. Both afamelanotide and α-MSH bind to the melanocortin-1 receptor (MC1R) on melanocytes which stimulates the synthesis of eumelanin, a photoprotective compound. Eumelanin is incorporated into small vesicles called melanosomes which are then distributed to surrounding keratinocytes. Melanosomes are concentrated above the nucleus of these keratinocytes, thus protecting them from UV-induced damage.[A187202] While endogenous α-MSH requires UV-induced skin damage in order to be produced, afamelanotide increases eumelanin biosynthesis independent of UV exposure.[A187205]
Activation of MC1R signalling by afamelanotide also instigates other protective processes, including an increase in antioxidant activity, DNA repair, and secretion of immunomodulatory proteins such as interleukin-10.[A187202]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L9086]
Following administration of a single subcutaneous implant, the median Tmax was 36 hours, the mean Cmax was 3.7 ± 1.3 ng/mL, and the mean AUC0-∞ was 138.9 ± 42.6 hr.ng/mL.
[L9134]
[L9086]
The apparent half-life following administration of a slow-release subcutaneous implant is 15 hours.
[L9134]
[A187202]
[L9086][L9134]
It has been suggested that afamelanotide may be degraded in the same manner as α-MSH but at a much slower rate, or may instead be degraded intracellularly via endocytosis or non-specific proteases.
[A187202]
[A187202]
[L9086][A187205]
Proteins and enzymes this drug interacts with in the body
PMID:11442765 PMID:11707265 PMID:1325670 PMID:1516719 PMID:8463333
The activity of this receptor is mediated by G proteins which activate adenylate cyclase .
PMID:11707265 PMID:1325670 PMID:16463023 PMID:19737927
Mediates melanogenesis, the production of eumelanin (black/brown) and phaeomelanin (red/yellow), via regulation of cAMP signaling in melanocytes PMID:31097585
PMID:32327598 PMID:33858992
Plays a role in regulating food intake: activation by a stimulating hormone such as anorexigenic alpha-melanocyte stimulating hormone (alpha-MSH) inhibits appetite, whereas binding to a natural antagonist like Agouti-related protein/AGRP promotes appetite. G-protein-coupled receptor that activates conventional Galphas signaling leading to induction of anorexogenic signaling in the hypothalamus to result in negative energy balance .
PMID:33858992
Regulates the firing activity of neurons from the hypothalamus by alpha-MSH and AGRP independently of Galphas signaling by ligand-induced coupling of closure of inwardly rectifying potassium channel KCNJ13 (By similarity). In intestinal epithelial cells, plays a role in the inhibition of hepatic glucose production via nesfatin-1/NUCB2 leading to increased cyclic adenosine monophosphate (cAMP) levels and glucagon-like peptide 1 (GLP-1) secretion in the intestinal epithelium PMID:39562740
ATC D02BB02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Afamelanotide
Additional database identifiers
ChemSpider
17310725
BindingDB
82411
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6929
GenAtlas
MC1R
GeneCards
MC1R
GenBank Gene Database
X65634
Guide to Pharmacology
282
UniProt Accession
MSHR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6932
GeneCards
MC4R
Guide to Pharmacology
285
UniProt Accession
MC4R_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