DeCure for Autosomal dominant nonsyndromic hearing loss 30
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for autosomal dominant nonsyndromic hearing loss 30 — 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.
Disease moduleAutosomal dominant nonsyndromic hearing loss 30 maps to a 1-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 autosomal dominant nonsyndromic hearing loss 30 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
myosin IIIA (MYO3A) — MYO3A 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 6JLE · 1.55 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
No drug treatment is mentioned in any of these abstracts for autosomal dominant nonsyndromic hearing loss 30. The papers are genetic mapping and gene identification studies. By 2003, 80 loci for nonsyndromic hearing loss had been mapped to the human genome and 30 genes identified, including genes for myosins, cytoskeletal proteins, channel and gap junction components, transcription factors, and extracellular matrix proteins. A 2004 clinical genetic study of 144 patients with nonsyndromic hearing loss examined sex distribution, type, degree, symmetry, laterality, progression, and inheritance pattern, but did not test any drug. By 2020, 119 nonsyndromic genes had been associated with hearing loss, and the authors note that gene therapy is emerging but not yet a viable management option.
The 2000 paper states that 11 genes mutated in autosomal dominant inherited hearing loss had been isolated, along with 6 for autosomal recessive forms, but estimates that 50 to 80 hearing loss genes remain to be discovered. No abstract provides any data on survival, response rates, or sample sizes for a drug intervention because no drug was studied. The papers consistently describe the state of knowledge as incomplete: the 2003 review says the identification of genes "holds the promise" of future therapeutic measures, and the 2020 review calls gene therapy a future possibility.
What is still missing is any drug that has been tested in patients with this specific condition, any clinical trial of a repurposed or novel compound for autosomal dominant nonsyndromic hearing loss 30, and any patient stratification or biomarker that would allow a trial to be designed. Money for drug development and for the basic functional studies needed to identify a druggable target in this particular genetic form of hearing loss has not been reported in these abstracts.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Ear and Hearing · 2003 · 66 citations
Nonsyndromic Hearing Loss
AbstractIn Brief The past decade has seen extremely rapid progress in the field of hereditary hearing loss. To date, 80 loci for nonsyndromic hearing loss have been mapped to the human genome. Furthermore, 30 genes have been identified. These genes belong to a wide variety of protein classes: from myosins and other cytoskeletal proteins, over channel and gap junction components, to transcription factors, extracellular matrix proteins and genes with an unknown function. The identification of these genes has enabled geneticists to offer DNA diagnostic tests for some types of nonsyndromic hearing loss. Moreover, it holds the promise to significantly improve the molecular knowledge on the auditory and vestibular organs and on the pathological mechanisms leading to hearing loss. This opens perspectives for future therapeutic and/or preventive measures for hearing loss. This review attempts to give an overview of the current knowledge of the genes responsible for nonsyndromic hearing loss, their expression and functions in the cochlea. A broad review of genes responsible for nonsyndromic hearing loss, their expression and function in the cochlea. Also discusses the genetic tests currently offered for different types of nonsyndromic hearing loss.
Genetics of pediatric hearing loss: A functional perspective
AbstractOBJECTIVES: This article reviews the current role of genetics in pediatric hearing loss (HL). METHODS: A review of the current literature regarding the genetic basis of HL in children was performed. RESULTS: To date, 119 nonsyndromic genes have been associated with HL. There are also hundreds of syndromic causes that have HL as part of the clinical phenotype. CONCLUSIONS: Identifying HL genes coupled with clinical characteristics ("genotype-phenotype") yields a more accurate diagnosis and prognosis. Although the complexity of the auditory apparatus presents challenges, gene therapy is emerging and may be a viable management option in the future.
American Journal of Audiology · 2004 · 1 citations
Clinical Genetic Study of 144 Patients With Nonsyndromic Hearing Loss
AbstractHearing loss constitutes an important category of congenital defects that can be isolated or part of the phenotypic spectrum of several syndromes. A clinical genetic study was performed on a sample of 144 patients with nonsyndromic hearing loss, establishing the sex distribution, type, degree, symmetry, laterality, progression, etiology, and, when possible, inheritance pattern.
Zurich Open Repository and Archive (University of Zurich) · 2000 · 0 citations · open access
Erbliche Schwerhörigkeit: neue Möglichkeiten der Diagnostik
AbstractMutations in many different genes can result in hearing loss. Using different molecular genetic methods, the disease-causing gene mutations can often be identified or at least localised to defined regions of the genome. These new diagnostic possibilities result from the localisation and identification of a number of hearing-loss genes in the last five years. Diagnostic investigations should always be accompanied by a genetic counselling of the family. In addition, the isolation thus far of 11 genes mutated in autosomal dominant inherited hearing loss, as well as of 6 genes mutated in autosomal recessive inherited hearing loss, has contributed to a better understanding of the molecular pathology of hearing loss in general. However, we are only beginning to see the whole picture, as an estimated 50 to 80 hearing loss genes remain to be discovered.
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.
