DeCure's autonomous Dermatology AI scientist is researching a drug-repurposing hypothesis for peeling skin syndrome 1 — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePeeling skin syndrome 1 maps to a 3-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for peeling skin syndrome 1 is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
What the evidence adds up to
Peeling skin syndrome type 1 (PSS1) is an autosomal recessive genodermatosis caused by loss-of-function mutations in the CDSN gene. A 2024 case report describes a Chinese woman with congenital generalised pruritic erythroderma and exfoliation, markedly elevated IgE, and a novel homozygous CDSN variant (c.295C>T, p.Gln99*). Immunohistochemistry confirmed absent corneodesmosin expression and showed overexpression of Th2-related cytokines IL-4 and IL-13. After treatment with the JAK1 inhibitor upadacitinib, both skin rashes and itching were significantly alleviated. This single case suggests JAK1 signalling may be a potential therapeutic target, but no controlled data exist.
Other abstracts in the set do not address PSS1. A 2000 paper describes a chemical peel technique using 70% glycolic acid gel augmented with 40% trichloroacetic acid on more than 3100 patients for cosmetic improvement of nonfacial skin, with reported excellent results for texture, wrinkling, and pigmentation. A 2022 Chinese expert consensus provides guidance on chemical peels for various skin conditions. A 2013 report identifies a novel KRT1 missense mutation in a family with autosomal dominant generalised skin peeling initially mistaken for epidermolysis bullosa simplex superficialis, but this is a distinct disorder from PSS1.
No randomised trial, no larger case series, and no comparative data exist for any treatment in PSS1. The upadacitinib report is a single patient with no long-term follow-up. What is missing is any systematic clinical trial, any funding for such a trial, and any understanding of which patients might respond to JAK inhibition versus other pathways. Patient stratification by CDSN mutation type or cytokine profile has not been attempted.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
PubMed · 1986 · 103 citations
Medium-depth chemical peeling of the skin: a variation of superficial chemosurgery.
AbstractMedium-depth chemical peeling of the skin is an intermediate procedure between superficial trichloroacetic acid application and deep phenolic cauterant application. Combining solid carbon dioxide with trichloroacetic acid promotes both epidermal and dermal regeneration. The technique for treatment of actinic degeneration, acne scarring, rhytids, and pigmentary aberrations is presented.
Chemical Peel of Nonfacial Skin Using Glycolic Acid Gel Augmented with TCA and Neutralized Based on Visual Staging
AbstractBACKGROUND: Until recently, standard techniques for laser or chemical peeling have not always provided consistent results when applied to the nonfacial skin. OBJECTIVE: The author describes a more controlled chemical peel technique for nonfacial skin using 70% glycolic acid gel combined with 40% trichloroacetic acid (TCA). The method has given consistently good results on the skin of the neck, chest, arms, hands, back, and other nonfacial skin. METHODS: More than 3100 patients were given skin peels of the neck, chest, and other areas of the body as indicated. Seventy percent glycolic acid gel was applied to the areas to be peeled, then immediately augmented with 40% TCA. Each area was carefully monitored for the end point and then neutralized with copious amounts of 10% sodium bicarbonate solution. The end point was determined by visual observation using a six-stage classification to determine the degree of peeling. RESULTS: Clinical results were excellent, with smoother skin texture, decreased wrinkling and striae, and fading of lentigines and other pigmentary abnormalities. There was excellent blending into peeled facial skin and into adjacent areas of nonpeeled skin. Complications were minimal. CONCLUSION: This technique can provide the benefits of skin peeling to nonfacial skin with excellent cosmetic results and minimal complications.
BMC Dermatology · 2012 · 19 citations · open access
Acral peeling skin syndrome in two East-African siblings: case report
AbstractBACKGROUND: Acral peeling skin syndrome is a rare autosomal recessive genodermatosis due to a missense mutation in transglutaminase 5. The skin peeling occurs at the separation of the stratum corneum from the stratum granulosum. CASE PRESENTATION: We present a case of two siblings who developed continuous peeling of the palms and soles from the first year of life. This peeling was more severe on the soles than palms and on younger sibling than elder sibling. Peeling is worsened by occlusion and sweating. CONCLUSIONS: Sporadic cases of Acral Peeling Skin Syndrome occur in African population. There is variability in time of presentation and clinical severity even within families.
A case of peeling skin syndrome type 1 with novel <i>CDSN</i> gene variation successfully treated with upadacitinib
AbstractPeeling skin syndrome type 1 (PSS1) is an autosomal recessive genodermatosis caused by the CDSN gene loss-of-function mutation and characterized by widespread superficial skin peeling and erythroderma with unbearable pruritus. Because of its ultra-rarity and unclear mechanism, this rare disease has no established treatment regimen. Herein, we reported a Chinese woman who presented with congenital generalized pruritic erythroderma and exfoliation, notable for significantly elevated IgE levels. The whole exome sequencing identified an unpublished homozygous variant (c.295C>T, p.Gln99*) in the CDSN gene, confirming the diagnosis of PSS1. Immunohistochemistry analysis of the affected skin confirmed the lack of corneodesmosin expression, revealed the overexpression of T helper 2 (Th2)-related cytokines harboring interleukin (IL) 4 and IL-13. After Janus kinase 1 (JAK1) inhibitor upadacitinib administration, both the patient's skin rashes and itching symptoms were significantly alleviated. Our work expanded the PSS1-related CDSN gene mutation spectrums, substantiated the hypothesis regarding the overexpression of Th2-related cytokines, and uncovered the important role of JAK1 underlying PSS1. JAK1 signaling may dominate the pathogenesis in PSS1 and represent a potential therapeutic target.
Archives of Disease in Childhood · 2013 · 1 citations · open access
G28 A Novel Missense Mutation in Keratin 1 Underlying Clinically Mild Epidermolytic Ichthyosis Mimicking Epidermolysis Bullosa Simplex Superficialis
AbstractInherited skin peeling may be autosomal recessive (AR) or autosomal dominant (AD). When AR, this can be localised, as in acral peeling skin syndrome (APSS); or generalised, as in peeling skin syndrome (PSS) types A (non-inflammatory) and B (inflammatory). When AD, this can present in association with ichthyosis as either epidermolytic ichthyosis (EI) or superficial epidermolytic ichthyosis (SIE); or as a further, poorly characterised form of AD skin peeling, termed epidermolysis bullosa simplex superficialis (EBSS), previously described in two families. We report 6 affected individuals from 2 generations with generalised AD skin peeling. All presented neonatally with erosions at trauma-prone sites including the axillae, back and thighs, with ongoing skin fragility caused by friction. All 4 affected children reported slightly dry skin in the first decade of life with very mild hyperkeratosis of the axillae and neck. Some individuals had peeling of fingertips and soles, and one adult had mild diffuse plantar hyperkeratosis. There was no erythema, mucosal, nail or hair involvement. Initially, EBSS was considered based on AD inheritance, the generalised distribution, and lack of inflammation and ichthyosis at presentation. A biopsy of rubbed, uninvolved skin from one affected individual showed a thickened stratum corneum but no signs of blistering or ultrastructural abnormalities at the dermal-epidermal junction or within the epidermis. Sequencing of <i>KRT5</i> and <i>KRT14</i> (keratins 5 and 14) showed no mutations, but whole exome sequencing demonstrated a heterozygous missense mutation in <i>KRT1</i> encoding keratin 1, p.Ser338Pro, in the 4 probands tested. This amino acid substitution is located within the L12 linker region, close to where other pathogenic mutations in keratin 1 have been reported in unrelated individuals with EI. Therefore, the most likely diagnosis in this family is EI due to a novel mutation in <i>KRT1</i>. This clinically mild disorder and new <i>KRT1</i> gene pathology extends genotype-phenotype correlation in EI and underscores the value of next generation sequencing in diagnosing clinically atypical genodermatoses.
International Journal of Dermatology and Venereology · 2023 · 0 citations · open access
Expert Consensus on the Clinical Application of Chemical Peels in China (2022) #
AbstractChemical peels are widely used to treat various skin diseases and photoaging. Their rational, effective, and safe use has become an important issue in clinical practice. To standardize the clinical use of chemical peels, a group of experts developed this consensus based on the latest research and discussions. This consensus provides specific guidance to clinicians on chemical peels with respect to their classification, peeling agents, mechanisms, indications, contraindications, peeling techniques, and complications.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
