DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for dyschromatosis symmetrica hereditaria — screening already-approved drugs against its 4-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDyschromatosis symmetrica hereditaria maps to a 4-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 dyschromatosis symmetrica hereditaria 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
adenosine deaminase RNA specific (ADAR) — ADAR 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 ihpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9B83 · 3.01 Å · ligand INOSITOL HEXAKISPHOSPHATE (IHP). Experimental structure, not a prediction.
What the evidence adds up to
In 1952 two familial cases of dyschromatosis universalis hereditaria were reported, with the same dermatosis appearing across five generations. Unexposed skin was as strongly affected as exposed areas, including palms and soles. The authors concluded the pigmentary disturbance was caused by genotype with epistasis of factors other than photosensitivity, and rejected a relationship with dyschromatosis symmetrica hereditaria despite clinical resemblance. By 2009, dyschromatosis universalis hereditaria was described as a rare autosomal dominant disease with generalised hyper- and hypo-pigmentation, mostly reported from east Asia. Early studies had suggested dyschromatosis symmetrica hereditaria might be a subtype, but later work on pathogenic genes established them as distinct entities.
Dyschromatosis symmetrica hereditaria is a highly penetrant autosomal-dominant skin disease characterised by a mixture of hyper- and hypo-pigmented macules on the dorsal aspects of the hands and feet. Onset is typically in infancy or early childhood, stops spreading before adolescence, and lasts for life. In 2003 it was clarified that a heterozygous mutation in the adenosine deaminase acting on RNA1 gene (ADAR1) causes the disorder. A 2011 case report described dyschromatosis symmetrica hereditaria with acral hypertrophy, but no numbers or sample sizes are given in that abstract.
No drug treatment is mentioned in any of these abstracts. No clinical trial data, no response rates, no survival figures are reported. What is still missing is any therapeutic intervention tested in patients, any trial design, any patient stratification, and any funding directed toward treatment development for either 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.
The Tohoku Journal of Experimental Medicine · 1952 · 32 citations · open access
Genetical Studies on Skin Diseases
Abstract1. Two familial cases of dyschromatosis universalis hereditaria are reported. 2. In the same family the occurrence of similar dermatoses is noted in five generations. 3. Unexposed parts of the body is as strongly affected as the exposed area. And even the palm and sole are involved. 4. The pigmentary disturbance is caused by genotype with epistases of some other factors than photosensitivity. 5. Thus the relationship with dyschromatosis symmetrica hereditaria is rejected in spite of clinical resemblance.
European Journal of Dermatology · 2011 · 3 citations
Dyschromatosis symmetrica hereditaria with acral hypertrophy
Abstractejd.2011.1486 Auteur(s) : Teruasa Murata1, Yosuke Yagi2, Miki Tanioka3, Tamio Suzuki4, Yoshiki Miyachi3, Kazumasa Morita1, Atsushi Utani2 [email protected] 1 Tenri Hospital, Nara, Japan 2 Department of Dermatology, Nagasaki University 1-7-1 Sakamoto, Nagasaki. 852-8501, Japan 3 Department of Dermatology, Kyoto University, Kyoto, 606-8507, Japan 4 Department of Dermatology, Yamagata University, Yamagata, Japan Dyschromatosis symmetrica hereditaria (DSH) is a hereditary disorder caused by a mutation [...]
European Journal of Dermatology · 2014 · 3 citations
A frameshift mutation in the ADAR gene in a Korean family with dyschromatosis symmetrica hereditaria
AbstractDyschromatosis symmetrica hereditaria (DSH; MIM 127400) is a rare autosomal dominant skin disorder characterized by a mixture of hyper- and hypopigmented macules on the dorsal surface of the extremities and face. Onset of the disease is usually during infancy or early childhood. Dyschromatosis stops spreading before adolescence and lasts for life. The skin lesions are otherwise asymptomatic and do not affect the general health of the patient. The prevalence of DSH was estimated to be ∼1.5 per 100,000 [...]
Dyschromatosis Symmetrica Hereditaria and RNA Editing Enzyme
AbstractDyschromatosis symmetrica hereditaria (DSH) is a highly penetrant autosomal-dominant skin disease. It is characterized by a mixture of hyperand hypo-pigmented macules on the dorsal aspects of the hands and feet (Figure 1). The disorder typically has its onset during infancy or early childhood, stops spreading before adolescence and lasts for life. It was clarified in 2003 that a heterozygous mutation in the adenosine deaminase acting on RNA1 gene (ADAR1) causes DSH [1).
International Journal of Dermatology and Venereology · 2009 · 0 citations
Dyschromatosis universalis hereditaria
AbstractDyschromatosis universalis hcreditaria is a rare autosomal dominant inherited disease characterized by generalized hyper-and hypo-pigmentation of the skin. Most of the reported cases of this disease are from east Asian. Early studies suggested that dyschromatosis symmetrica hereditaria might be a subtype of this disease. However, recent studies on pathogenic genes have revealed that dyschromatosis symmetrica hereditaria and dyschromatosis univcrsalis hereditaria belong to two distinct disease entities.
Key words:
Heredity ; Pigmentation disorders ;
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.
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