RARE DISEASE
Solar urticaria
Solar urticaria
Solar urticaria
Drug discovery
2
drugs
With orphan designations
Overview
Solar urticaria is a rare IgE-mediated photodermatosis characterized by urticarial lesions within minutes of UV/visible light exposure, with potential systemic symptoms (e.g., anaphylaxis). It involves mast cell degranulation triggered by photoallergens, though the exact antigen remains unidentified. Chronic and often refractory to treatment, it requires phototesting for diagnosis and management [1][4][16].
Population
Therapies
1st-line: High-dose 2nd-gen H1 antihistamines (75.8% efficacy) ± H2 blockers (42.9% efficacy) [5][16].
2nd-line: UVA hardening therapy (88.9% efficacy for UVA-triggered cases) or omalizumab (80% response rate) [3][5][8][16].
Refractory cases: Immunosuppressants (cyclosporine), IVIG, plasmapheresis, or combination therapies [4][12][16].
Categories: rare skin diseases
Research Papers
234 drug discovery papers about Solar urticaria, with 1 first-in-class and 4 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
234 drug discovery papers about Solar urticaria, with 1 first-in-class and 4 next-in-class emerging drug candidates forecasted to outperform the average preclinical success rate. Recent publications:
categories:
Small molecules
small molecules
2026-04-22 | Refractory chronic spontaneous urticaria management in resource-poor settings: A critical appraisal
Urticaria is characterized by the occurrence of wheals, angioedema, or both. When urticaria duration is >6 weeks, it is known as chronic urticaria (CU). CU is classified as spontaneous (CSU) and inducible (CIndU). When the clinical course has no definite physical eliciting factor involved and shows a spontaneous course, it is described as CSU, and when a physical eliciting factor is present, it is called CIndU. CIndU is further subclassified as symptomatic dermographism, cold urticaria, delayed pressure urticaria, solar urticaria, heat urticaria, and vibratory angioedema, as well as cholinergic urticaria, contact urticaria, and aquagenic urticaria. CU patients can simultaneously present with more than one form of CU, especially CIndU. The management of CSU commences with the second-generation H1 anti-histamine. A few CSU patients do not respond to a single dose of 2 nd- generation anti-histamine; then, the dose is escalated to 4 fold the usual dose. About 10–50% patients do not respond to even 4-fold increased doses of which end up necessitating the repeated use of oral corticosteroids to control disease exacerbations is classified to have refractory CSU. Various drugs and biologics are in the armamentarium of dermatologists and allergologists; however, there are financial constraints in the developing world in resource-poor settings. Omalizumab, dupilumab, remibrutinib, and cyclosporine are the agents that are used in refractory urticaria. The financial burden of these agents restricts patients in poor settings to use for long-term therapy. The agents such as methotrexate, tofacitinib, and mycophenolate mofetil have been used with success anecdotally. However, azathioprine has shown a ray of hope in refractory urticaria patients, which may be an alternative in difficult-to-treat cases of CSU.
2026-01-06 | O07 Solar urticaria is associated with novel rare missense variants in ACACA
Abstract Introduction and aims Solar urticaria (SU) is a rare, poorly understood photodermatosis characterized by inappropriate mast cell degranulation following cutaneous exposure to sunlight. Based on a lack of Mendelian inheritance in families and its onset in adulthood with limited impact on reproductive fitness, SU is likely a complex trait whose development is determined by genetic and environmental factors. Its rarity and unusual phenotype, which constitutes an extreme aberration of physiological responses to sunlight, imply that its genetic architecture may be underpinned by rare, highly penetrant and deleterious variants. To investigate this, we performed a case–control whole-exome sequencing gene association study in SU. Methods Forty-six patients of European ancestry with phototest-confirmed SU underwent whole-exome sequencing. Healthy control whole exomes (n = 971) were derived from the 1958 British Birth Cohort. Following quality control, joint variant calling and variant filtering to retain rare, high-impact variants, burden testing was performed. Sanger sequencing and bioinformatic resources were used to validate and explore identified genes/variants. Results Burden testing revealed exome-wide significant enrichment of rare, high-impact variants in ACACA among SU cases (P = 4.7 × 10−7). This gene encodes acetyl-coenzyme A carboxylase alpha, an enzyme that catalyses the rate-limiting step in de novo lipogenesis. Six of 46 SU cases carried rare, heterozygous missense variants in ACACA compared with 3 of 971 controls. Sanger sequencing validated the presence of these variants in ACACA. Structural analyses demonstrated that ACACA variants were predicted to decrease protein stability. Reanalysis of single-cell RNA sequencing data from skin confirmed ACACA expression in all cell types, including mast cells. Conclusions Enrichment of rare, deleterious ACACA variants among patients with SU suggests a role for altered lipid metabolism, potentially affecting mast cell function, in SU pathogenesis. Characterization of lipid-mediated disease mechanisms in SU should form the basis of future investigations.
2026-01-05 | Visible Light Protection Strategies for Diverse Populations.
Visible light (VL; 400-700 nm) constitutes nearly half of solar radiation and has distinct biological effects on human skin. High-energy visible light (HEVL), particularly blue light (400-490 nm), contributes to erythema, persistent pigmentation, and photoaging. Emerging data also demonstrate synergistic pigmentary interactions between VL and long-wavelength ultraviolet A1 (UVA1). Individuals with skin of colour (SOC) and patients with visible-light-sensitive dermatoses are particularly susceptible to the cutaneous effects of visible light. This review aims to provide an evidence-based overview of VL interactions with skin, the mechanisms driving VL-induced cutaneous changes, and current VL-directed photoprotection strategies, with emphasis on their relevance for SOC populations and visible-light-sensitive dermatoses. PubMed and Google Scholar were searched to identify studies addressing VL properties, cutaneous biological effects, and VL-specific photoprotection, including sunscreens, pigments, novel organic filters, antioxidants, and behavioural approaches. VL, especially blue light, induces oxidative stress, melanogenesis via opsin 3-mediated pathways, and degradation of dermal extracellular matrix. Tinted sunscreens containing iron oxides and pigmentary titanium dioxide provide the most effective and cosmetically acceptable VL protection, reducing HEVL transmission by up to 80-97% and improving clinical outcomes in melasma and other hyperpigmentation disorders. Novel organic UV filters such as TriAsorB™ expand absorbance into the VL spectrum, while adjunctive topical and oral antioxidants may attenuate VL-induced oxidative stress. VL may exacerbate photodermatoses, including autoimmune connective tissue diseases, porphyria, and solar urticaria. VL is a biologically active and clinically relevant component of sunlight with disproportionate effects in SOC and certain photosensitive dermatoses. Optimal photoprotection requires a multimodal approach integrating UV and VL protection through physical measures, tinted formulations, emerging broad-spectrum filters, antioxidants, and patient-centred photoeducation. Standardised VL-protection labelling and further clinical research are needed to guide future practice.
2025-12-07 | Solar urticaria in an infant: a case report
BACKGROUND: Urticaria remains a relevant issue in modern medicine, including pediatric practice. The prevalence of chronic urticaria among children under 15 years of age is approximately 1.1%. A rare form of chronic inducible urticaria is solar urticaria, which accounts for about 0.5% of chronic urticaria cases. Solar urticaria most often manifests with typical symptoms such as erythema and wheals. However, severe cases have been described, accompanied by headache, dizziness, nausea, bronchospasm, hypertension, tachycardia, and pronounced allergic reactions up to anaphylactic shock—particularly when large areas of the skin are exposed to the provoking light spectrum. Despite the distinctive clinical manifestations, diagnosing solar urticaria poses a challenge, especially in infants and young children. An additional difficulty in pediatric patients is the lack of standardized provocation diagnostic tests, which use is limited by ethical and legal considerations. This clinical case of solar urticaria in an infant underscores the importance of early diagnosis for timely management of this rare form of chronic urticaria. CASE DESCRIPTION: This article presents a clinical case of solar urticaria in an infant. From the first weeks of life, the mother noted facial redness after walks in sunny weather. At the age of 1.5–2 months, erythema was accompanied by wheals and itching on the face, prompting consultation with a pediatrician and subsequently an allergist-immunologist. The therapeutic approach included laboratory testing, differential diagnosis, and treatment measures. After diagnosing solar urticaria, implementing appropriate elimination measures, and providing adequate symptomatic therapy, a stable remission was achieved. CONCLUSION: This rare clinical case of solar urticaria in a 2-month-old infant confirms the need for timely differential diagnosis and referral to a specialist for verification of the diagnosis and initiation of appropriate treatment measures. Adherence to therapy by the child’s parents plays a crucial role in disease management.
2025-12-01 | Solar Urticaria‐Like Symptoms Induced by Conjugated Estrogen
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
antibodies
2026-07-24 | Differential Effects of Dupilumab in a Patient With Localized Heat Urticaria, Delayed Solar Urticaria, and Symptomatic Dermographism.
Physical urticaria is a subtype of chronic inducible urticaria characterized by wheals and/or angioedema triggered by physical stimuli. We report a refractory case of combined localized heat urticaria, delayed solar urticaria, and symptomatic dermographism in a 16-year-old girl. Provocation testing showed erythematous and edematous lesions after thermal stimulation at 42°C and after the application of warm water at 40°C and 42°C. An intradermal test using the patient's serum heated to 42°C for 5 min yielded a positive result, leading to the diagnosis of localized heat urticaria. Visible light irradiation induced no immediate wheals; however, wheals developed at all irradiated sites 4.5 h later, accompanied by intense pruritus without burning sensation or pain, consistent with delayed solar urticaria. A FricTest provoked wheals, confirming symptomatic dermographism. Antihistamines were ineffective, and omalizumab, administered as a second-line treatment, improved only the symptomatic dermographism, with no effect on the heat or solar urticaria. Dupilumab was subsequently administered 12 times. Repeated provocation testing during treatment showed resolution of symptomatic dermographism, whereas localized heat urticaria persisted and delayed solar urticaria showed no meaningful improvement. The Urticaria Control Test score also did not improve. These findings suggest that the pathogenesis of symptomatic dermographism in this case may involve IgE- and IL-4/IL-13-mediated pathways, whereas localized heat urticaria and delayed solar urticaria may be driven by distinct mechanisms.
2026-04-10 | Omalizumab Therapy Results in Defined Behavioural Changes and Improvements in Quality of Life in Solar Urticaria.
Solar urticaria is a rare photodermatosis in which exquisite photosensitivity can require extreme behavioural adaptations, resulting in a substantial impact on quality of life (QoL). Omalizumab therapy has been demonstrated to improve several clinical outcome measures, but the impact on behavioural measures is poorly understood. Our objectives were to examine daylight exposure behaviours and QoL measures pre- and post-omalizumab therapy. Daylight exposure diaries were completed by n = 5 patients with solar urticaria and n = 7 healthy participants during different seasons in England, UK (51.1-53.5oN). These incorporated a range of measures, including time spent outdoors and clothing worn, and Dermatology Life Quality Index (DLQI) data were also collected. Prior to omalizumab, patients spent less time outdoors in sunny vs. non-sunny conditions in spring (mean 10 vs. 29 min/day, p < 0.05) and less than healthy volunteers (44 min in sunny conditions/day). On omalizumab, patients increased their time outdoors in sunny conditions, reaching similar levels to healthy volunteers in spring (45 min/day) and further increasing to 85 min/day in summer. This was accompanied by fewer days with symptoms (symptoms on 75% days in spring pre-omalizumab vs. 26% days in summer on omalizumab), an apparent doubling of skin surface area exposure and substantial improvement in patients' QoL (mean past-year DLQI pre-omalizumab vs. past-week summer on omalizumab 22 vs. 5, p < 0.001). Omalizumab therapy was associated with behavioural changes that increase daylight exposure, accompanied by improved QoL. This study highlights the importance of considering a range of outcome measures in assessing response to therapy.
2025-12-20 | [Omalizumab for the treatment of severe solar urticaria].
Solar urticaria is a rare condition induced by exposure to ultraviolet radiation. Although it typically resolves spontaneously, like other dermatoses, it often affects patients' quality of life. We report the case of a patient with solar urticaria successfully treated with omalizumab. A 36-year-old female patient with a history of allergies presented with pruritic wheals in sun-exposed areas for four years. Despite unremarkable physical findings, erythematous-edematous plaques were observed. Serum IgE levels were elevated (507 IU/ml), and antinuclear antibodies and rheumatoid factor were negative. Initial treatment with levocetirizine (up to 20 mg/day) and photoprotection failed, with a UCT score of 10. Omalizumab (300 mg/4 weeks) was added, achieving complete control of the condition (UCT score 16) after five months, allowing for a reduction in the dose and dosing interval. However, episodes during the spring season (UCT score 6) necessitated reintroducing the initial dose to regain full disease control. Omalizumab is a second-line anti-IgE monoclonal antibody for the off-label treatment of patients who do not respond to systemic antihistamines.
2025-11-06 | Efficacy of monoclonal antibodies and Janus kinase inhibitors in the treatment of idiopathic photosensitive skin disorders: a systematic review.
Idiopathic photosensitive skin disorders, or idiopathic photodermatoses, are characterized by abnormal reactions to sunlight and ultraviolet (UV) radiation. They encompass conditions such as actinic prurigo, chronic actinic dermatitis, solar urticaria, photoaggravated psoriasis, polymorphic light eruption and photoaggravated eczema. Treatment options remain limited, but monoclonal antibodies (such as dupilumab, omalizumab, adalimumab, ustekinumab) and Janus kinase (JAK) inhibitors (such as tofacitinib, baricitinib, upadacitinib) have emerged as promising potential therapies. To evaluate the short- and long-term efficacy of these biologics and JAK inhibitors in managing these conditions, despite their lack of formal approval. A literature search was conducted using PubMed, Google Scholar and the Wiley Online Library. Inclusion criteria focused on studies published between 1960 and 2025 investigating monoclonal antibodies and JAK inhibitors for idiopathic photodermatoses, excluding other treatment modalities. Thirty-two studies involving 96 patients met the inclusion criteria. Most studies were case series or reports. Findings indicated significant reductions in disease activity and improvement in quality-of-life metrics (such as the Dermatology Life Quality Index) across various conditions. The lack of high-quality studies and the reliance on case reports limit generalizability. Variations in treatment regimens and outcome measures pose additional challenges. Monoclonal antibodies and JAK inhibitors demonstrate promise in reducing symptoms and improving quality of life in idiopathic photosensitive skin disorders. As these treatments are not formally indicated for these conditions, further research is warranted to confirm their efficacy and safety. This review highlights the need for clinical trials to enhance understanding and management of these challenging dermatological conditions.
2025-08-30 | Efficacy of Therapies for Solar Urticaria: A Systematic Review and Meta-Analysis.
Background: Solar urticaria is a rare and disabling photodermatosis. Due to its low prevalence, most available data regarding treatment are derived from observational studies and case series, and a systematic evaluation of treatment efficacy is lacking. This systematic review and meta-analysis aims to assess therapeutic outcomes across treatment modalities in order to guide clinical care. Methods: We conducted a systematic literature search across PubMed, ScienceDirect, the Cochrane Library, and ClinicalTrials.gov. Studies reporting treatment outcomes in patients with solar urticaria were included. Pooled response rates were calculated for each treatment modality. Results: Out of 508 studies initially identified, 38 met the inclusion criteria. Antihistamines were evaluated in 21 studies (376 patients), with a pooled response rate (partial or complete) of 83.0% (95% CI, 70.4-91.1%) and a complete response rate of 7.7% (95% CI, 1.7-28.3%). Phototherapy was assessed in 11 studies (145 patients), showing a similar overall response (89.8%; 95% CI, 77.9-95.3%) but a higher complete response rate (39.8%; 95% CI, 18.3-66.1%). Omalizumab, evaluated in nine studies (76 patients), demonstrated the highest efficacy, with 93.2% (95% CI, 73.8-98.5%) achieving response and 68.4% (95% CI, 48.5-83.2%) complete remission. Limited data on IVIG, cyclosporine, and plasmapheresis suggested partial efficacy in selected refractory cases. Conclusions: This meta-analysis may support clinical decision-making by clinicians. A stepwise approach is suggested: high-dose H1 antihistamines as first-line therapy, phototherapy as an alternative option in patients with access to treatment centers, and omalizumab for those with insufficient response. In refractory cases, additional options might be considered.
proteins
2023-06-01 | PD03 Afamelanotide reduces the ultraviolet radiation erythemal response soon after application in healthy volunteers with skin phototypes II–III
Abstract Afamelanotide is a potent α-melanocyte stimulating hormone analogue that binds to the melanocortin 1 receptor and, over time, promotes tanning, conferring systemic photoprotection. Afamelanotide also has antioxidant properties and may promote repair of ultraviolet (UV) radiation (UVR)-induced DNA damage. The objectives of this study were to examine the short-term impact of afamelanotide on DNA damage repair mechanisms, UVR erythema and melanogenic responses in healthy human skin following exposure to UVR. Healthy men and women (n = 10) volunteers aged 27–43 years (median 34) of skin phototypes II–III were recruited. Reflectance spectrophotometry was performed on six body sites (photoexposed and photoprotected) to assess skin pigmentation, and then a geometric series of erythemally weighted doses (7–80 mJ cm−2) of broadband UVB (∼60% UVB, 40% UVA; Philips TL12) was applied to unexposed upper buttock skin. After 24 h, the minimal erythema dose (MED) was assessed and erythema intensity (CIE a*) was measured at each dose site. A subcutaneous implant of afamelanotide 16 mg was administered; 5 days later, the same UVR dose series was applied to unexposed contralateral upper buttock skin. After 24 h, the MED was assessed and repeat skin reflectance measurements were performed. The overall UVR–erythema dose response (area under curve) showed a significant decrease post-afamelanotide (mean 3.5 vs. 2.7; P = 0.018). There was an apparent increase in the median MED post-afamelanotide (24.5 vs. 29.9 mJ cm−2; not statistically significant). Reflectance measurements showed skin lightness (CIE L*) significantly decreased at only one site (central forehead, from 63.0 to 61.0; P = 0.015), while determination of melanin density by reflectance at 420 and 400 nm showed a statistically significant increase in density at all sites except the right abdomen, with a mean overall increase from 2.5% to 2.9% (P = 0.001). Our results indicate that afamelanotide reduces the overall UVR–erythema dose response in healthy human skin shortly after administration, with a small increase in melanogenesis, suggesting other nonmelanogenic properties of this agent contribute to the erythema protection. Further investigation will examine whether enhanced repair of UVR-induced DNA damage plays a role. Funding sources: research sponsored by CLINUVEL (UK) Ltd.
2021-07-08 | Afamelanotide: An Orphan Drug with Potential for Broad Dermatologic Applications.
Afamelanotide (SCENESSE®) is a synthetic analogue of α-melanocyte-stimulating hormone that is FDA-approved to increase pain-free sunlight exposure in adult patients with erythropoietic protoporphyria. Its dual photoprotective and anti-inflammatory effects also make it a promising therapy for other photosensitive dermatologic diseases that are resistant to treatment. The PubMed/MEDLINE and ClinicalTrials.gov databases were searched for literature and ongoing trials describing the use of afamelanotide in treating cutaneous diseases. There is randomized controlled trial (RCT) evidence for the successful use of afamelanotide in several conditions beyond erythropoietic protoporphyria, including polymorphic light eruption and vitiligo. Smaller studies have also demonstrated its efficacy in treating acne vulgaris, Hailey-Hailey disease, and solar urticaria. No serious adverse effects with afamelanotide use have been reported, though diffuse hyperpigmentation is experienced by almost all patients. Larger scale studies are needed to confirm the efficacy of afamelanotide in treating dermatologic conditions beyond erythropoietic protoporphyria, and further research should focus on determining the safety, efficacy, and optimal dosing of afamelanotide for pediatric patients.J Drugs Dermatol. 2021;20(3):290-294. doi:10.36849/JDD.5526.
2020-05-29 | [Medicaments and oral healthcare. Hyperpigmentation of oral soft tissues due to afamelanotide].
The medicament afamelanotide is an analogue of endogenous ?-melanocyte-stimulating hormone. It promotes cutaneous pigmentation, providing protection from sunlight. In dermatology, afamelanotide seems to establish therapeutic results for polymorphic light eruption, solar urticaria, erythropoietic protoporphyria, Hailey-Hailey disease, vitiligo and acne vulgaris. Afamelanotide is available for non-medical use to realise quick and easy skin tanning. Adverse effects of afamelanotide mentioned in the scientific literature are development and aggravation of melanocytic naevi, degeneration of melanocytic naevi to melanomas, melanonychia, systemic toxicity, rhabdomyolysis, posterior reversible encephalopathy syndrome, priapism and hyperpigmentation of oral soft tissues. Furthermore, numerous adverse effects of afamelanotide have been reported to the Netherlands pharmacovigilance centre LAREB as well as numerous adverse effects due to overdosage of afamelanotide to the National Poisons Information Centre. Dentists should be alert to hyperpigmentation of oral soft tissues due to afamelanotide. Het medicament afamelanotide is een analoog van ?-melanocytstimulerend hormoon. Het bevordert de pigmentatie van de huid en biedt daardoor bescherming tegen zonlicht. In de dermatologie lijkt afamelanotide heilzaam bij polymorfe lichteruptie, zonne-urticaria, erytropoëtische protoporfyrie, de ziekte van Hailey-Hailey, vitiligo en acne vulgaris. Voor niet-medicinale toepassing is afamelanotide verkrijgbaar voor het snel en eenvoudig bruinen van de huid. In de wetenschappelijke literatuur is als bijwerking van afamelanotide melding gemaakt van ontwikkeling en verergering van melanocytaire naevi, ontaarding van melanocytaire naevi in melanomen, melanonychia, systemische intoxicatie, rabdomyolyse, posterieur reversibel encefalopathiesyndroom, priapisme en hyperpigmentatie van orale slijmvliezen. Daarnaast zijn tal van bijwerkingen gemeld bij het Bijwerkingencentrum LAREB en tal van bijwerkingen bij overdosering van afamelanotide bij het Nationaal Vergiftigingen Informatie Centrum. Tandartsen moeten attent zijn op hyperpigmentatie van de orale slijmvliezen door afamelanotide.
2018-11-08 | Mechanisms and Therapeutic Prospects of Peptides in Skin Pigmentation
Clinically modifying skin pigmentation is a valuable approach that can treat pigmentation and photosensitivity disorders and provide a degree of protection from skin cancers.Skin pigmentation is due to the presence of eumelanin, a biological pigment that is generated by the highly regulated melanogenesis pathway.Proteins within this pathway, including the melanocortin 1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), and tyrosinase, can be activated or deactivated in order to bring about the desired change in eumelanin content, and thus pigmentation.A novel platform to modulate skin pigmentation is the use of oligopeptides designed with affinity towards the active sites in molecules of the melanogenesis pathway.A useful approach developing such peptides is to imitate active sites of existing hormones and signaling molecules with melanogenesis modulating properties.This platform is especially useful since oligopeptides can be designed to increase activity, prolong in vivo stability, promote penetration into cells and minimize side effects when compared to the molecules they mimic, or other drugs.Abbreviations α-MSH = α-Melanocyte Stimulating Hormone; ASIP = agouti signaling protein; cAMP = cyclic adenosine monophosphate; DCT = dopachrome tautomerase; EPP = erythropoietic protoporphyria; HQ = hydroquinone; IL= interleukin; MC1R = melanocortin 1 receptor; MITF = microphthalmia-associated transcription factor; PLE = polymorphic light eruption; SU = solar urticaria; TGF-β1 = transforming growth factor β; TRP = tyrosinase related protein
2018-04-02 | Pharmacokinetics and Pharmacodynamics of Afamelanotide and its Clinical Use in Treating Dermatologic Disorders.
Afamelanotide, the first α-melanocyte-stimulating hormone (MSH) analogue, synthesized in 1980, was broadly investigated in all aspects of pigmentation because its activity and stability were higher than the natural hormone. Afamelanotide binds to the melanocortin-1 receptor (MC1R), and MC1R signaling increases melanin synthesis, induces antioxidant activities, enhances DNA repair processes and modulates inflammation. The loss-of-function variants of the MC1R present in fair-skinned Caucasians are less effectively activated by the natural hormone. Afamelanotide was the first α-MSH analogue to be applied to human volunteers. Ten daily doses of between 0.08 and 0.21 mg/kg in saline injected subcutaneously resulted in long-lasting skin pigmentation and enabled basic pharmacokinetics. Subcutaneous application had full bioavailability, but neither oral nor transdermal application resulted in measurable plasma concentrations or pigmentation response. Two trials in human volunteers showed that neither MC1R variants nor fair skin reduced the afamelanotide-induced increase in skin pigmentation. A controlled-release formulation optimizes administration in man and is effective at a lower dose than the daily saline injections. Promising therapeutic results were published in polymorphic light eruption, erythropoietic protoporphyria (EPP), solar urticaria, Hailey-Hailey disease and vitiligo. In 2014, afamelanotide was approved by the European Medicines Agency for the prevention of phototoxicity in adult patients with EPP. No late effects were reported in volunteers 25 years after the first exposure or after continuous long-term application of up to 8 years in EPP patients, and an immunogenic potential has been excluded. Generally, adverse effects were benign in all trials.
small molecules
2026-04-22 | Refractory chronic spontaneous urticaria management in resource-poor settings: A critical appraisal
Urticaria is characterized by the occurrence of wheals, angioedema, or both. When urticaria duration is >6 weeks, it is known as chronic urticaria (CU). CU is classified as spontaneous (CSU) and inducible (CIndU). When the clinical course has no definite physical eliciting factor involved and shows a spontaneous course, it is described as CSU, and when a physical eliciting factor is present, it is called CIndU. CIndU is further subclassified as symptomatic dermographism, cold urticaria, delayed pressure urticaria, solar urticaria, heat urticaria, and vibratory angioedema, as well as cholinergic urticaria, contact urticaria, and aquagenic urticaria. CU patients can simultaneously present with more than one form of CU, especially CIndU. The management of CSU commences with the second-generation H1 anti-histamine. A few CSU patients do not respond to a single dose of 2 nd- generation anti-histamine; then, the dose is escalated to 4 fold the usual dose. About 10–50% patients do not respond to even 4-fold increased doses of which end up necessitating the repeated use of oral corticosteroids to control disease exacerbations is classified to have refractory CSU. Various drugs and biologics are in the armamentarium of dermatologists and allergologists; however, there are financial constraints in the developing world in resource-poor settings. Omalizumab, dupilumab, remibrutinib, and cyclosporine are the agents that are used in refractory urticaria. The financial burden of these agents restricts patients in poor settings to use for long-term therapy. The agents such as methotrexate, tofacitinib, and mycophenolate mofetil have been used with success anecdotally. However, azathioprine has shown a ray of hope in refractory urticaria patients, which may be an alternative in difficult-to-treat cases of CSU.
2026-01-06 | O07 Solar urticaria is associated with novel rare missense variants in ACACA
Abstract Introduction and aims Solar urticaria (SU) is a rare, poorly understood photodermatosis characterized by inappropriate mast cell degranulation following cutaneous exposure to sunlight. Based on a lack of Mendelian inheritance in families and its onset in adulthood with limited impact on reproductive fitness, SU is likely a complex trait whose development is determined by genetic and environmental factors. Its rarity and unusual phenotype, which constitutes an extreme aberration of physiological responses to sunlight, imply that its genetic architecture may be underpinned by rare, highly penetrant and deleterious variants. To investigate this, we performed a case–control whole-exome sequencing gene association study in SU. Methods Forty-six patients of European ancestry with phototest-confirmed SU underwent whole-exome sequencing. Healthy control whole exomes (n = 971) were derived from the 1958 British Birth Cohort. Following quality control, joint variant calling and variant filtering to retain rare, high-impact variants, burden testing was performed. Sanger sequencing and bioinformatic resources were used to validate and explore identified genes/variants. Results Burden testing revealed exome-wide significant enrichment of rare, high-impact variants in ACACA among SU cases (P = 4.7 × 10−7). This gene encodes acetyl-coenzyme A carboxylase alpha, an enzyme that catalyses the rate-limiting step in de novo lipogenesis. Six of 46 SU cases carried rare, heterozygous missense variants in ACACA compared with 3 of 971 controls. Sanger sequencing validated the presence of these variants in ACACA. Structural analyses demonstrated that ACACA variants were predicted to decrease protein stability. Reanalysis of single-cell RNA sequencing data from skin confirmed ACACA expression in all cell types, including mast cells. Conclusions Enrichment of rare, deleterious ACACA variants among patients with SU suggests a role for altered lipid metabolism, potentially affecting mast cell function, in SU pathogenesis. Characterization of lipid-mediated disease mechanisms in SU should form the basis of future investigations.
2026-01-05 | Visible Light Protection Strategies for Diverse Populations.
Visible light (VL; 400-700 nm) constitutes nearly half of solar radiation and has distinct biological effects on human skin. High-energy visible light (HEVL), particularly blue light (400-490 nm), contributes to erythema, persistent pigmentation, and photoaging. Emerging data also demonstrate synergistic pigmentary interactions between VL and long-wavelength ultraviolet A1 (UVA1). Individuals with skin of colour (SOC) and patients with visible-light-sensitive dermatoses are particularly susceptible to the cutaneous effects of visible light. This review aims to provide an evidence-based overview of VL interactions with skin, the mechanisms driving VL-induced cutaneous changes, and current VL-directed photoprotection strategies, with emphasis on their relevance for SOC populations and visible-light-sensitive dermatoses. PubMed and Google Scholar were searched to identify studies addressing VL properties, cutaneous biological effects, and VL-specific photoprotection, including sunscreens, pigments, novel organic filters, antioxidants, and behavioural approaches. VL, especially blue light, induces oxidative stress, melanogenesis via opsin 3-mediated pathways, and degradation of dermal extracellular matrix. Tinted sunscreens containing iron oxides and pigmentary titanium dioxide provide the most effective and cosmetically acceptable VL protection, reducing HEVL transmission by up to 80-97% and improving clinical outcomes in melasma and other hyperpigmentation disorders. Novel organic UV filters such as TriAsorB™ expand absorbance into the VL spectrum, while adjunctive topical and oral antioxidants may attenuate VL-induced oxidative stress. VL may exacerbate photodermatoses, including autoimmune connective tissue diseases, porphyria, and solar urticaria. VL is a biologically active and clinically relevant component of sunlight with disproportionate effects in SOC and certain photosensitive dermatoses. Optimal photoprotection requires a multimodal approach integrating UV and VL protection through physical measures, tinted formulations, emerging broad-spectrum filters, antioxidants, and patient-centred photoeducation. Standardised VL-protection labelling and further clinical research are needed to guide future practice.
2025-12-07 | Solar urticaria in an infant: a case report
BACKGROUND: Urticaria remains a relevant issue in modern medicine, including pediatric practice. The prevalence of chronic urticaria among children under 15 years of age is approximately 1.1%. A rare form of chronic inducible urticaria is solar urticaria, which accounts for about 0.5% of chronic urticaria cases. Solar urticaria most often manifests with typical symptoms such as erythema and wheals. However, severe cases have been described, accompanied by headache, dizziness, nausea, bronchospasm, hypertension, tachycardia, and pronounced allergic reactions up to anaphylactic shock—particularly when large areas of the skin are exposed to the provoking light spectrum. Despite the distinctive clinical manifestations, diagnosing solar urticaria poses a challenge, especially in infants and young children. An additional difficulty in pediatric patients is the lack of standardized provocation diagnostic tests, which use is limited by ethical and legal considerations. This clinical case of solar urticaria in an infant underscores the importance of early diagnosis for timely management of this rare form of chronic urticaria. CASE DESCRIPTION: This article presents a clinical case of solar urticaria in an infant. From the first weeks of life, the mother noted facial redness after walks in sunny weather. At the age of 1.5–2 months, erythema was accompanied by wheals and itching on the face, prompting consultation with a pediatrician and subsequently an allergist-immunologist. The therapeutic approach included laboratory testing, differential diagnosis, and treatment measures. After diagnosing solar urticaria, implementing appropriate elimination measures, and providing adequate symptomatic therapy, a stable remission was achieved. CONCLUSION: This rare clinical case of solar urticaria in a 2-month-old infant confirms the need for timely differential diagnosis and referral to a specialist for verification of the diagnosis and initiation of appropriate treatment measures. Adherence to therapy by the child’s parents plays a crucial role in disease management.
2025-12-01 | Solar Urticaria‐Like Symptoms Induced by Conjugated Estrogen
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
antibodies
2026-07-24 | Differential Effects of Dupilumab in a Patient With Localized Heat Urticaria, Delayed Solar Urticaria, and Symptomatic Dermographism.
Physical urticaria is a subtype of chronic inducible urticaria characterized by wheals and/or angioedema triggered by physical stimuli. We report a refractory case of combined localized heat urticaria, delayed solar urticaria, and symptomatic dermographism in a 16-year-old girl. Provocation testing showed erythematous and edematous lesions after thermal stimulation at 42°C and after the application of warm water at 40°C and 42°C. An intradermal test using the patient's serum heated to 42°C for 5 min yielded a positive result, leading to the diagnosis of localized heat urticaria. Visible light irradiation induced no immediate wheals; however, wheals developed at all irradiated sites 4.5 h later, accompanied by intense pruritus without burning sensation or pain, consistent with delayed solar urticaria. A FricTest provoked wheals, confirming symptomatic dermographism. Antihistamines were ineffective, and omalizumab, administered as a second-line treatment, improved only the symptomatic dermographism, with no effect on the heat or solar urticaria. Dupilumab was subsequently administered 12 times. Repeated provocation testing during treatment showed resolution of symptomatic dermographism, whereas localized heat urticaria persisted and delayed solar urticaria showed no meaningful improvement. The Urticaria Control Test score also did not improve. These findings suggest that the pathogenesis of symptomatic dermographism in this case may involve IgE- and IL-4/IL-13-mediated pathways, whereas localized heat urticaria and delayed solar urticaria may be driven by distinct mechanisms.
2026-04-10 | Omalizumab Therapy Results in Defined Behavioural Changes and Improvements in Quality of Life in Solar Urticaria.
Solar urticaria is a rare photodermatosis in which exquisite photosensitivity can require extreme behavioural adaptations, resulting in a substantial impact on quality of life (QoL). Omalizumab therapy has been demonstrated to improve several clinical outcome measures, but the impact on behavioural measures is poorly understood. Our objectives were to examine daylight exposure behaviours and QoL measures pre- and post-omalizumab therapy. Daylight exposure diaries were completed by n = 5 patients with solar urticaria and n = 7 healthy participants during different seasons in England, UK (51.1-53.5oN). These incorporated a range of measures, including time spent outdoors and clothing worn, and Dermatology Life Quality Index (DLQI) data were also collected. Prior to omalizumab, patients spent less time outdoors in sunny vs. non-sunny conditions in spring (mean 10 vs. 29 min/day, p < 0.05) and less than healthy volunteers (44 min in sunny conditions/day). On omalizumab, patients increased their time outdoors in sunny conditions, reaching similar levels to healthy volunteers in spring (45 min/day) and further increasing to 85 min/day in summer. This was accompanied by fewer days with symptoms (symptoms on 75% days in spring pre-omalizumab vs. 26% days in summer on omalizumab), an apparent doubling of skin surface area exposure and substantial improvement in patients' QoL (mean past-year DLQI pre-omalizumab vs. past-week summer on omalizumab 22 vs. 5, p < 0.001). Omalizumab therapy was associated with behavioural changes that increase daylight exposure, accompanied by improved QoL. This study highlights the importance of considering a range of outcome measures in assessing response to therapy.
2025-12-20 | [Omalizumab for the treatment of severe solar urticaria].
Solar urticaria is a rare condition induced by exposure to ultraviolet radiation. Although it typically resolves spontaneously, like other dermatoses, it often affects patients' quality of life. We report the case of a patient with solar urticaria successfully treated with omalizumab. A 36-year-old female patient with a history of allergies presented with pruritic wheals in sun-exposed areas for four years. Despite unremarkable physical findings, erythematous-edematous plaques were observed. Serum IgE levels were elevated (507 IU/ml), and antinuclear antibodies and rheumatoid factor were negative. Initial treatment with levocetirizine (up to 20 mg/day) and photoprotection failed, with a UCT score of 10. Omalizumab (300 mg/4 weeks) was added, achieving complete control of the condition (UCT score 16) after five months, allowing for a reduction in the dose and dosing interval. However, episodes during the spring season (UCT score 6) necessitated reintroducing the initial dose to regain full disease control. Omalizumab is a second-line anti-IgE monoclonal antibody for the off-label treatment of patients who do not respond to systemic antihistamines.
2025-11-06 | Efficacy of monoclonal antibodies and Janus kinase inhibitors in the treatment of idiopathic photosensitive skin disorders: a systematic review.
Idiopathic photosensitive skin disorders, or idiopathic photodermatoses, are characterized by abnormal reactions to sunlight and ultraviolet (UV) radiation. They encompass conditions such as actinic prurigo, chronic actinic dermatitis, solar urticaria, photoaggravated psoriasis, polymorphic light eruption and photoaggravated eczema. Treatment options remain limited, but monoclonal antibodies (such as dupilumab, omalizumab, adalimumab, ustekinumab) and Janus kinase (JAK) inhibitors (such as tofacitinib, baricitinib, upadacitinib) have emerged as promising potential therapies. To evaluate the short- and long-term efficacy of these biologics and JAK inhibitors in managing these conditions, despite their lack of formal approval. A literature search was conducted using PubMed, Google Scholar and the Wiley Online Library. Inclusion criteria focused on studies published between 1960 and 2025 investigating monoclonal antibodies and JAK inhibitors for idiopathic photodermatoses, excluding other treatment modalities. Thirty-two studies involving 96 patients met the inclusion criteria. Most studies were case series or reports. Findings indicated significant reductions in disease activity and improvement in quality-of-life metrics (such as the Dermatology Life Quality Index) across various conditions. The lack of high-quality studies and the reliance on case reports limit generalizability. Variations in treatment regimens and outcome measures pose additional challenges. Monoclonal antibodies and JAK inhibitors demonstrate promise in reducing symptoms and improving quality of life in idiopathic photosensitive skin disorders. As these treatments are not formally indicated for these conditions, further research is warranted to confirm their efficacy and safety. This review highlights the need for clinical trials to enhance understanding and management of these challenging dermatological conditions.
2025-08-30 | Efficacy of Therapies for Solar Urticaria: A Systematic Review and Meta-Analysis.
Background: Solar urticaria is a rare and disabling photodermatosis. Due to its low prevalence, most available data regarding treatment are derived from observational studies and case series, and a systematic evaluation of treatment efficacy is lacking. This systematic review and meta-analysis aims to assess therapeutic outcomes across treatment modalities in order to guide clinical care. Methods: We conducted a systematic literature search across PubMed, ScienceDirect, the Cochrane Library, and ClinicalTrials.gov. Studies reporting treatment outcomes in patients with solar urticaria were included. Pooled response rates were calculated for each treatment modality. Results: Out of 508 studies initially identified, 38 met the inclusion criteria. Antihistamines were evaluated in 21 studies (376 patients), with a pooled response rate (partial or complete) of 83.0% (95% CI, 70.4-91.1%) and a complete response rate of 7.7% (95% CI, 1.7-28.3%). Phototherapy was assessed in 11 studies (145 patients), showing a similar overall response (89.8%; 95% CI, 77.9-95.3%) but a higher complete response rate (39.8%; 95% CI, 18.3-66.1%). Omalizumab, evaluated in nine studies (76 patients), demonstrated the highest efficacy, with 93.2% (95% CI, 73.8-98.5%) achieving response and 68.4% (95% CI, 48.5-83.2%) complete remission. Limited data on IVIG, cyclosporine, and plasmapheresis suggested partial efficacy in selected refractory cases. Conclusions: This meta-analysis may support clinical decision-making by clinicians. A stepwise approach is suggested: high-dose H1 antihistamines as first-line therapy, phototherapy as an alternative option in patients with access to treatment centers, and omalizumab for those with insufficient response. In refractory cases, additional options might be considered.
proteins
2023-06-01 | PD03 Afamelanotide reduces the ultraviolet radiation erythemal response soon after application in healthy volunteers with skin phototypes II–III
Abstract Afamelanotide is a potent α-melanocyte stimulating hormone analogue that binds to the melanocortin 1 receptor and, over time, promotes tanning, conferring systemic photoprotection. Afamelanotide also has antioxidant properties and may promote repair of ultraviolet (UV) radiation (UVR)-induced DNA damage. The objectives of this study were to examine the short-term impact of afamelanotide on DNA damage repair mechanisms, UVR erythema and melanogenic responses in healthy human skin following exposure to UVR. Healthy men and women (n = 10) volunteers aged 27–43 years (median 34) of skin phototypes II–III were recruited. Reflectance spectrophotometry was performed on six body sites (photoexposed and photoprotected) to assess skin pigmentation, and then a geometric series of erythemally weighted doses (7–80 mJ cm−2) of broadband UVB (∼60% UVB, 40% UVA; Philips TL12) was applied to unexposed upper buttock skin. After 24 h, the minimal erythema dose (MED) was assessed and erythema intensity (CIE a*) was measured at each dose site. A subcutaneous implant of afamelanotide 16 mg was administered; 5 days later, the same UVR dose series was applied to unexposed contralateral upper buttock skin. After 24 h, the MED was assessed and repeat skin reflectance measurements were performed. The overall UVR–erythema dose response (area under curve) showed a significant decrease post-afamelanotide (mean 3.5 vs. 2.7; P = 0.018). There was an apparent increase in the median MED post-afamelanotide (24.5 vs. 29.9 mJ cm−2; not statistically significant). Reflectance measurements showed skin lightness (CIE L*) significantly decreased at only one site (central forehead, from 63.0 to 61.0; P = 0.015), while determination of melanin density by reflectance at 420 and 400 nm showed a statistically significant increase in density at all sites except the right abdomen, with a mean overall increase from 2.5% to 2.9% (P = 0.001). Our results indicate that afamelanotide reduces the overall UVR–erythema dose response in healthy human skin shortly after administration, with a small increase in melanogenesis, suggesting other nonmelanogenic properties of this agent contribute to the erythema protection. Further investigation will examine whether enhanced repair of UVR-induced DNA damage plays a role. Funding sources: research sponsored by CLINUVEL (UK) Ltd.
2021-07-08 | Afamelanotide: An Orphan Drug with Potential for Broad Dermatologic Applications.
Afamelanotide (SCENESSE®) is a synthetic analogue of α-melanocyte-stimulating hormone that is FDA-approved to increase pain-free sunlight exposure in adult patients with erythropoietic protoporphyria. Its dual photoprotective and anti-inflammatory effects also make it a promising therapy for other photosensitive dermatologic diseases that are resistant to treatment. The PubMed/MEDLINE and ClinicalTrials.gov databases were searched for literature and ongoing trials describing the use of afamelanotide in treating cutaneous diseases. There is randomized controlled trial (RCT) evidence for the successful use of afamelanotide in several conditions beyond erythropoietic protoporphyria, including polymorphic light eruption and vitiligo. Smaller studies have also demonstrated its efficacy in treating acne vulgaris, Hailey-Hailey disease, and solar urticaria. No serious adverse effects with afamelanotide use have been reported, though diffuse hyperpigmentation is experienced by almost all patients. Larger scale studies are needed to confirm the efficacy of afamelanotide in treating dermatologic conditions beyond erythropoietic protoporphyria, and further research should focus on determining the safety, efficacy, and optimal dosing of afamelanotide for pediatric patients.J Drugs Dermatol. 2021;20(3):290-294. doi:10.36849/JDD.5526.
2020-05-29 | [Medicaments and oral healthcare. Hyperpigmentation of oral soft tissues due to afamelanotide].
The medicament afamelanotide is an analogue of endogenous ?-melanocyte-stimulating hormone. It promotes cutaneous pigmentation, providing protection from sunlight. In dermatology, afamelanotide seems to establish therapeutic results for polymorphic light eruption, solar urticaria, erythropoietic protoporphyria, Hailey-Hailey disease, vitiligo and acne vulgaris. Afamelanotide is available for non-medical use to realise quick and easy skin tanning. Adverse effects of afamelanotide mentioned in the scientific literature are development and aggravation of melanocytic naevi, degeneration of melanocytic naevi to melanomas, melanonychia, systemic toxicity, rhabdomyolysis, posterior reversible encephalopathy syndrome, priapism and hyperpigmentation of oral soft tissues. Furthermore, numerous adverse effects of afamelanotide have been reported to the Netherlands pharmacovigilance centre LAREB as well as numerous adverse effects due to overdosage of afamelanotide to the National Poisons Information Centre. Dentists should be alert to hyperpigmentation of oral soft tissues due to afamelanotide. Het medicament afamelanotide is een analoog van ?-melanocytstimulerend hormoon. Het bevordert de pigmentatie van de huid en biedt daardoor bescherming tegen zonlicht. In de dermatologie lijkt afamelanotide heilzaam bij polymorfe lichteruptie, zonne-urticaria, erytropoëtische protoporfyrie, de ziekte van Hailey-Hailey, vitiligo en acne vulgaris. Voor niet-medicinale toepassing is afamelanotide verkrijgbaar voor het snel en eenvoudig bruinen van de huid. In de wetenschappelijke literatuur is als bijwerking van afamelanotide melding gemaakt van ontwikkeling en verergering van melanocytaire naevi, ontaarding van melanocytaire naevi in melanomen, melanonychia, systemische intoxicatie, rabdomyolyse, posterieur reversibel encefalopathiesyndroom, priapisme en hyperpigmentatie van orale slijmvliezen. Daarnaast zijn tal van bijwerkingen gemeld bij het Bijwerkingencentrum LAREB en tal van bijwerkingen bij overdosering van afamelanotide bij het Nationaal Vergiftigingen Informatie Centrum. Tandartsen moeten attent zijn op hyperpigmentatie van de orale slijmvliezen door afamelanotide.
2018-11-08 | Mechanisms and Therapeutic Prospects of Peptides in Skin Pigmentation
Clinically modifying skin pigmentation is a valuable approach that can treat pigmentation and photosensitivity disorders and provide a degree of protection from skin cancers.Skin pigmentation is due to the presence of eumelanin, a biological pigment that is generated by the highly regulated melanogenesis pathway.Proteins within this pathway, including the melanocortin 1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), and tyrosinase, can be activated or deactivated in order to bring about the desired change in eumelanin content, and thus pigmentation.A novel platform to modulate skin pigmentation is the use of oligopeptides designed with affinity towards the active sites in molecules of the melanogenesis pathway.A useful approach developing such peptides is to imitate active sites of existing hormones and signaling molecules with melanogenesis modulating properties.This platform is especially useful since oligopeptides can be designed to increase activity, prolong in vivo stability, promote penetration into cells and minimize side effects when compared to the molecules they mimic, or other drugs.Abbreviations α-MSH = α-Melanocyte Stimulating Hormone; ASIP = agouti signaling protein; cAMP = cyclic adenosine monophosphate; DCT = dopachrome tautomerase; EPP = erythropoietic protoporphyria; HQ = hydroquinone; IL= interleukin; MC1R = melanocortin 1 receptor; MITF = microphthalmia-associated transcription factor; PLE = polymorphic light eruption; SU = solar urticaria; TGF-β1 = transforming growth factor β; TRP = tyrosinase related protein
2018-04-02 | Pharmacokinetics and Pharmacodynamics of Afamelanotide and its Clinical Use in Treating Dermatologic Disorders.
Afamelanotide, the first α-melanocyte-stimulating hormone (MSH) analogue, synthesized in 1980, was broadly investigated in all aspects of pigmentation because its activity and stability were higher than the natural hormone. Afamelanotide binds to the melanocortin-1 receptor (MC1R), and MC1R signaling increases melanin synthesis, induces antioxidant activities, enhances DNA repair processes and modulates inflammation. The loss-of-function variants of the MC1R present in fair-skinned Caucasians are less effectively activated by the natural hormone. Afamelanotide was the first α-MSH analogue to be applied to human volunteers. Ten daily doses of between 0.08 and 0.21 mg/kg in saline injected subcutaneously resulted in long-lasting skin pigmentation and enabled basic pharmacokinetics. Subcutaneous application had full bioavailability, but neither oral nor transdermal application resulted in measurable plasma concentrations or pigmentation response. Two trials in human volunteers showed that neither MC1R variants nor fair skin reduced the afamelanotide-induced increase in skin pigmentation. A controlled-release formulation optimizes administration in man and is effective at a lower dose than the daily saline injections. Promising therapeutic results were published in polymorphic light eruption, erythropoietic protoporphyria (EPP), solar urticaria, Hailey-Hailey disease and vitiligo. In 2014, afamelanotide was approved by the European Medicines Agency for the prevention of phototoxicity in adult patients with EPP. No late effects were reported in volunteers 25 years after the first exposure or after continuous long-term application of up to 8 years in EPP patients, and an immunogenic potential has been excluded. Generally, adverse effects were benign in all trials.
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Drug Discovery Landscape
2 orphan drug designations for Solar urticaria.
2 orphan drug designations for Solar urticaria.
Drug | Therapy type | Regulator | Orphan designation | Approval | Sponsor |
|---|---|---|---|---|---|
afamelanotide | peptides | FDA | 2009-12-11 | — | Clinuvel, Inc. |
Afamelanotide | small molecules | EMA | 2009-07-24 | — | Clinuvel Europe Limited |
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