Rare & Orphan Lab · DeCure for X

DeCure for Dentinogenesis imperfecta

DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for dentinogenesis imperfecta — 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 module2 genesLead labRare & Orphan
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Rare & OrphanDOID:4154$DeCureRare

The disease map

Disease moduleDentinogenesis imperfecta 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 dentinogenesis imperfecta 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

collagen type I alpha 2 chain (COL1A2)COL1A2 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 apo structuredrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 8YV3 · 1.68 Å · ligand none (apo structure). Experimental structure, not a prediction.

What the evidence adds up to

Dentinogenesis imperfecta is a hereditary condition that affects dentine development in both primary and permanent teeth, occurring at a rate of about 1 in 8000 births. It is an autosomal dominant disorder with high penetrance and a low mutation rate. Two main types are described: type I associated with osteogenesis imperfecta, and type II, the classical hereditary opalescent dentin. The formerly proposed type III appears to be only a modified expression of the same gene as type II. The presentation varies depending on type and severity, leading to tooth discolouration and attrition.

Diagnosis is based on family history, clinical examination, and pedigree construction. Treatment principles focus on preservation of teeth, removal of infection, and restoration of function and aesthetics. Early intervention is considered important for both psychosocial and functional reasons. No drug therapy is mentioned in any of the abstracts.

What is still missing is any molecular target for pharmacological intervention, any clinical trial testing a drug, and any evidence that a drug can alter dentine structure or tooth integrity in this condition. The abstracts provide no data on survival, response rates, or sample sizes because no treatment was tested. Without a candidate drug, a trial design, or patient stratification by genetic subtype, there is no basis for repurposing any existing medicine.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Dental Update · 2010 · 11 citations

Dentinogenesis Imperfecta - Clinical Presentation and Management

AbstractUNLABELLED: Dentinogenesis imperfecta (DI) is a hereditary condition which affects the development of dentine in both the primary and permanent dentitions. Three types of DI have been described in the literature. The presentation of DI is variable, depending on the type and severity of the disease. Early intervention in the treatment of a patient with DI is extremely important both for psycho-social and for functional reasons. This paper attempts to describe the clinical presentation and management of DI, and explores its association with certain medical conditions. CLINICAL RELEVANCE: Recognition of DI is important, so that correct treatment principles may be instituted.

https://doi.org/10.12968/denu.2010.37.6.364
International journal of odontostomatology · 2012 · 1 citations · open access

Capdepont's Teeth - a Hereditary Dentin Defect: Case Report & Review

AbstractDentinogenesis imperfecta is an autosomal dominant genetic disorder with abnormal dentin structure affecting both primary and permanent dentitions leading to discolouration and attrition of teeth. Diagnosis is usually based on family history, a detailed clinical examination and pedigree construction. Treatment involves preservation of teeth, removal of infection, restoration of function and esthetics.

https://doi.org/10.4067/s0718-381x2012000200018
DOAJ (DOAJ: Directory of Open Access Journals) · 2015 · 0 citations · open access

Dentinogenesis Imperfekta : Aspek Genetika Molekular, Klasifikasi dan Upaya Penanggulangannya

AbstractDentinogenesis Imperfecta (DI) is a hereditary simple autosomal dominant disorder showing abnormalities in the dentin of developing teeth and occuring at a rate of about 1 in 8000 births affecting both primary and secondary dentitions. The expression of DI shows a high penetrance and a low mutation rate. Two main types of DI appear to exist: type 1 which is the defect associate with osteogenesis imperfecta, and type II which is the classical hereditary opalescent dentin. The formerly proposed DI type III appears to be only a modified expression of the same gene as in the classical DI type II. This paper reviews molecular genetic aspects of DI.

https://doi.org/10.14693/jdi.v6i2.814

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.