Melanotan I (Afamelanotide)

Median EPP QoL score rose from 11.11 (IQR 3.03-19.44) before treatment to 79.17 (IQR 75.00-97.22) on therapy.; Median phototoxic burn tolerance time increased from 15 minutes (IQR 10-25) to 250 minutes (IQR 120-300).; Phototoxic reactions occurred in 88% of patients before therapy versus 33% on therapy.; Treatment side effects were only mild and transient.

29 trials including patients with EPP were retrieved; 16 evaluated afamelanotide and three new pharmacotherapies: dersimelagon, bitopertin, and cimetidine.; Safety and efficacy of all new pharmacotherapies are currently being investigated against placebo-control groups or against baseline.; Results of the trials cannot be directly compared because of differences in outcome measures and included patient populations.; Methodologically challenging aspects and ethical issues were identified in some trial protocols.

Non-swelling silica-based resin enabled peptide synthesis with a 50% reduction in solvent consumption.; 2-hour coupling was favored over standard 1-hour coupling.; Peptides including linear oxytocin, angiotensin II, and afamelanotide were synthesized with more than acceptable purity.; Overall yields were reduced despite acceptable purity.

Vitiligo is caused by progressive melanocyte destruction involving oxidative stress, inflammation, genetics, and autoimmunity.; Recent advances in understanding etiopathogenesis have led to more effective treatments.; Janus kinase inhibitors, prostaglandin analogues, and antioxidants are among the promising new therapies.; Targeted phototherapy and excimer lasers offer additional therapeutic possibilities.

EPP1, XLEPP, and EPP2 are ultra-rare disorders leading to protoporphyrin IX accumulation in erythrocytes and severe phototoxic skin pain from early childhood.; Diagnosis is confirmed by metal-free PPIX levels 3 times the upper limit of normal; complications include liver failure, gallstones, mild anemia, and vitamin D deficiency.; Iron supplementation is contraindicated in EPP1 but can reduce PPIX levels and phototoxicity in XLEPP.; Afamelanotide is the only approved specific treatment, increasing pain-free sunlight exposure and quality of life.

Median time to phototoxic symptom onset rose from 12.5 min (IQR 5-20) pre-treatment to 120 min (IQR 60-240) after two implants (p < 0.001); Quality of life improved during treatment as measured by two tools that correlated well with each other; No improvement in median metal-free erythrocyte protoporphyrin, plasma protoporphyrin, or liver biochemistries; 26 of 29 patients (72.2%) received two afamelanotide implants

Afamelanotide is a synthetic alpha melanocyte stimulating hormone with higher activity than natural hormones.; It enhances eumelanin production by agonistically binding to the melanocortin-1 receptor.; Since 2016, it has been applied to treat erythropoietic protoporphyria (EPP), reducing painful photosensitivity.; Subcutaneous administration improved tolerance to artificial white light and increased pain-free time in direct sunlight.

What is Melanotan I (Afamelanotide)?

**Mechanism of Action** Melanotan I (Afamelanotide) is a synthetic tridecapeptide analog of α-melanocyte-stimulating hormone (α-MSH) that acts as a selective agonist at the melanocortin-1 receptor (MC1R). Activation of MC1R on melanocytes stimulates the cAMP-dependent signaling pathway, leading to increased transcripti

How does Melanotan I (Afamelanotide) work?

Selective MC1R agonist approved (Scenesse) to prevent phototoxicity in erythropoietic protoporphyria by stimulating eumelanin.

What is the research status of Melanotan I (Afamelanotide)?

Melanotan I (Afamelanotide) is currently classified as approved, with 106 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Melanotan I (Afamelanotide)?

Melanotan I (Afamelanotide) has a molecular weight of approximately 1646.8 g/mol (formula C78H111N21O19).