DeCure for Punctate palmoplantar keratoderma type III
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for punctate palmoplantar keratoderma type III — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease modulePunctate palmoplantar keratoderma type III maps to a 2-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 punctate palmoplantar keratoderma type iii 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.
Molecular view
endothelin 3 (EDN3) — EDN3 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 2rdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6IGK · 2.0 Å · ligand (2R)-2,3-dihydroxypropyl (9Z)-octadec-9-enoate (OLC). Experimental structure, not a prediction.
What the evidence adds up to
Punctate palmoplantar keratoderma type III is a hereditary disorder of keratinisation characterised by hyperkeratosis of the palms and soles. The three major clinical patterns of palmoplantar keratoderma are diffuse, focal and punctate. No molecular or genetic data specific to type III punctate PPK are provided in the available abstracts. The 2017 review of two cases of focal acral hyperkeratosis, a subtype of punctate PPK, states that the nosography and classification of punctate PPKs have been confused in published literature, and that the article aims to clarify terminology and classification rather than report treatment outcomes.
The 1998 study of epidermolytic palmoplantar keratoderma found mutations in the keratin 9 gene in two of three Korean families, causing R162Q and R162W substitutions in the 1A rod domain. That study does not address punctate PPK type III. The 2019 review of hereditary palmoplantar keratoderma notes wide genetic and phenotypic heterogeneity and states that molecular studies, despite high cost, are imperative for accurate classification, but provides no specific mutation or treatment data for any subtype. The 2013 eponym review similarly offers no genetic or therapeutic information specific to punctate PPK type III.
No clinical trial, drug repurposing study, or treatment outcome data for punctate palmoplantar keratoderma type III appear in these abstracts. The literature reviewed consists entirely of classification and diagnostic guidance. What is missing is any molecular characterisation of type III punctate PPK, any patient cohort with measured response to any drug, and any trial design that could test a repurposed agent. Without genetic stratification and a defined outcome measure, no drug can be assessed for this condition.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Indian Dermatology Online Journal · 2019 · 42 citations · open access
Hereditary palmoplantar keratoderma: A practical approach to the diagnosis
Abstractor as a feature of several dermatological or systemic diseases. There is a wide genetic and phenotypic heterogeneity in hereditary PPK, due to which reaching an accurate diagnosis only on the basis of clinical features may be sometimes challenging for the clinicians in the absence of molecular studies. Nevertheless, recognizing the clinical patterns of keratoderma, extent of involvement, degree of mutilation, and associated appendageal and systemic involvement may help in delineating different forms. Molecular studies, despite high cost, are imperative for accurate classification, recognizing clinical patterns in resource poor settings is important for appropriate diagnosis, genetic counseling, and management. This review intends to develop a practical approach for clinical diagnosis of different types of hereditary PPK with reasonable accuracy.
Mutations in the 1A Rod Domain Segment of the Keratin 9 Gene in Epidermolytic Palmoplantar Keratoderma
AbstractPalmoplantar keratodermas (PPK) constitute a heterogeneous group of diseases marked by the thickening of palms and soles of affected individuals. They are divided into autosomal dominant and autosomal recessive groups by the mode of transmission. The autosomal dominantly transmitted group is further divided into epidermolytic (EPPK, Voerner) and non-epidermolytic (NEPPK, Unna-Thost) types according to the histopathologic findings. Recent development of molecular approaches has confirmed that EPPK and NEPPK are caused by the mutations in keratin 9 and 1 genes, respectively. We have studied three families of EPPK to find the mutation in the keratin 9 gene. DNA sequence analyses revealed single base changes in sequences encoding the highly conserved 1A rod domain segment of the keratin 9 gene in two of the three families. These mutations caused Arg (CGG) to Glu (CAG; R162Q) and Arg (CGG) to Try (TGG; R162W) substitutions. The same arginine position has been mutated in the keratin 10 gene in epidermolytic hyperkeratosis, the keratin 14 gene in epidermolysis bullosa simplex, and the keratin 9 gene in hereditary EPPK in Western patients. In this study we show that unrelated Korean patients have similar mutations.
Eponyms in the dermatology literature linked to Palmo-Plantar Keratoderma
AbstractPalmoplantar keratodermas (PPKs) represent a diverse group of hereditary and acquired disorders characterized by hyperkeratosis of the skin on the palms and soles The three major patterns of involvement are diffuse, focal and punctate. There are clinical distinguishing features for each disease in this group, for example, transmigration to areas beyond the palmoplantar skin. Also the extent of associated systemic symptoms if present help in characterization of each type.
Dermatology and Dermatitis · 2017 · 0 citations · open access
A Unique Type of Hereditary Punctate Palmoplantar Keratodermas
AbstractKeratodermas encompass a wide spectrum of disorders of keratinization that may be acquired or hereditary. We present two cases of focal acral hyperkeratosis (FAH), a subtype of punctate palmoplantar keratoderma. We review the literature and attempt to clarify the confusing classification of the heritable punctate palmoplantar keratodermas. Capsule Summary 1. (First bullet) what is already known on this topic a. Punctate PPK is an esoteric topic within the field of dermatology that has been discussed both clinically and histologically. 2. (Second bullet) what this article adds to our knowledge a. Despite this, the nosography and classification of punctate PPKs have been confused in published literature. 3. (Third bullet) How this information impacts clinical practice and/or changes patient care a. This article hopes to clarify the terminology and classification of punctate PPKs, thereby increasing awareness of this disease, with the hope of advancing treatment options.
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.
