Rare & Orphan Lab · DeCure for X
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for mal de Meleda — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
No approved-drug candidate for mal de meleda 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.
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
AbstractLuca Stulli of Dubrovnik (Ragusa), 1772-1828, was one of the first to make epidemiologic studies of heritable skin disorders. His treatise of what became the 'mal de Meleda' on the Adriatic island of Mljet (Meleda) is a classic in the dermatologic literature. The present study documents his life, his birth record, his portrait and recalls his original publication (in Italian).
https://doi.org/10.1159/000051695AbstractPresent address: R.G.L. Nellen, Department of Dermatology, IJsselland Ziekenhuis, Capelle aan den IJssel, The Netherlands. Funding sources: none. Conflicts of interests: none declared. Madam, Mal de Meleda (MDM; OMIM 248300) is an autosomal recessive monogenic disorder defined by progressive transgredient hyperkeratosis of the palms and soles, hyperhidrosis, malodourous scent due to bacterial superinfection, and minor symptoms such as perioral erythema, mild ichthyosis, pseudoainhum and nail abnormalities. Mutations in the SLURP1 gene, encoding the secreted Ly‐6/uPar related protein‐1, cause mal de Meleda.1 SLURP1 enhances the function of the nicotinic acetylcholine receptor α7 in epidermal keratinocytes, thereby promoting differentiation of keratinocytes in the stratum granulosum to the cells forming the stratum corneum.2, 3 The prevalence of the three most common mutations, c.82delT, p.R96X and p.W15R, has a sharp geographical demarcation (Fig. 1a). The c.82delT mutation was reported in Tunisian, Algerian and Croatian families, and a Scottish patient,1, 4, 5 and cosegregates with a shared haplotype, suggesting a founder effect for this mutation.5 Shared haplotypes were also found in Turkish6, 7 and Croatian1 families homozygous for the p.R96X mutation and in a German family and a Scottish patient harbouring the p.W15R mutation.5
https://doi.org/10.1111/bjd.12203Disease 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.
