DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for frontometaphyseal dysplasia — 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 moduleFrontometaphyseal dysplasia 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 frontometaphyseal dysplasia 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
mitogen-activated protein kinase kinase kinase 7 (MAP3K7) — MAP3K7 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 adndrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 2EVA · 2.0 Å · ligand ADENOSINE (ADN). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
American Journal of Medical Genetics · 1995 · 193 citations
AbstractFrontometaphyseal dysplasia (FMD) is an uncommon genetic syndrome affecting bone and connective tissue. This condition is characterized by hyperostosis of the skull and prominence of the supraorbital ridges; long bones have flared metaphyses. Frontometaphyseal dysplasia is an X-linked dominant trait with more severe manifestations in males and with extreme variability in females. Diagnosis in the neonatal period is difficult. We present 2 newborn boys with the radiographic findings of FMD.
Human Genome Variation · 2021 · 5 citations · open access
A novel TAB2 mutation detected in a putative case of frontometaphyseal dysplasia
AbstractFrontometaphyseal dysplasia (FMD) type 2 is an autosomal dominant disorder characterized by skeletal abnormalities and caused by MAP3K7 mutation. We identified a novel missense mutation in TAB2 associated with FMD in a child with multiple congenital malformations. This case was diagnosed as FMD due to joint contractures and bone deformities. This is the third report of FMD caused by a TAB2 mutation located in the TAK1-binding region.
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.
