DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hearing loss, autosomal dominant 80 — 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 moduleHearing loss, autosomal dominant 80 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 hearing loss, autosomal dominant 80 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 VIIA (MYO7A) — MYO7A 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 5MV9 · 2.6 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
A 1993 prospective phase-II study treated 37 patients with sudden sensorineural hearing loss using intravenous flunarizine followed by oral flunarizine. Mean absolute hearing gains were 17 dB after one week and 21 dB after four weeks. A placebo group of 67 patients from an earlier double-blind study at the same institutions had gains of 16 dB and 24 dB. Relative gains were 35% and 43% for flunarizine versus 33% and 42% for placebo. The authors concluded that flunarizine does not improve recovery of sudden hearing loss.
No abstract in this set reports a clinical trial of any drug for autosomal dominant hearing loss (DFNA). The 1999 review describes phenotyping of DFNA1, DFNA2, DFNA5, DFNA6/14, DFNA8/12, DFNA9, DFNA13, DFNA17, and DFNA21, but gives no treatment data. A 2025 review on gene therapy for hereditary hearing loss mentions three strategies—gene replacement, gene suppression, and gene editing—and refers to successful preclinical trials and approved clinical trial results, but does not name any specific drug or compound. A 2004 study of 144 patients with nonsyndromic hearing loss describes inheritance patterns and audiometric features without testing any intervention.
A 2023 study of subclinical hearing loss in aging found that normal-hearing adults had worse high-frequency thresholds and poorer speech-in-noise performance than younger subjects, with no significant association between age and auditory brainstem response after controlling for hearing level. This is not a treatment study. A 1995 review presents a pipeline from family identification to gene-based therapy but states that each mutation is at a different stage of investigation. A 2025 collection of 31 papers on hearing loss includes basic mechanisms, protection methods, and gene therapy, but no abstract provides a positive drug result for DFNA80 or any autosomal dominant hearing loss.
What is missing: a clinical trial of any drug or gene therapy specifically for DFNA80; any evidence that flunarizine or any other compound alters the course of autosomal dominant hearing loss; patient stratification by genotype; and funding for a trial that tests a mechanism-based intervention in a defined DFNA cohort.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
British Journal of Audiology · 1999 · 23 citations
Non-Syndromal Autosomal Dominant Hearing Impairment: Ongoing Phenotypical Characterization of Genotypes
AbstractThis review is concerned with the present state of phenotypical characterization of known genotypes of non-syndromal autosomal dominant hearing impairment. A brief outline of history and context of phenotyping and genotyping of hearing impairment is given with particular reference to the most recent developments in this field, followed by descriptions of DFNA1, DFNA2, DFNA5, DFNA6/14, DFNA8/12, DFNA9, DFNA 13, DFNA17 and DFNA21. Phenotyping those known genotypes may support the ongoing search for mutations in the corresponding gene and enhance genetic counselling. It is recommended that sufficient attention is given to a detailed description of the phenotype in each (newly) described hereditary hearing impairment disorder.
Ergebnisse einer prospektiven offenen Studie zur Therapie des Hörsturzes mit Flunarizine
AbstractThe treatment effect of the lipophilic calcium antagonist flunarizine on the recovery of sudden hearing loss was evaluated in a prospective phase-II study. Thirty-seven patients presenting with recent and sudden onset of unilateral sensorineural hearing loss were treated with 50 mg flunarizine intravenously for the first two days followed by 10 mg flunarizine orally for four weeks. Pure-tone audiometry was done before the beginning of the treatment and after one and four weeks. The absolute and relative hearing gains after one and four weeks were compared to those of 67 similar patients previously treated with saline infusions and placebo tablets in the same institutions during a double blind study (Probst et al. Acta Otolaryngol. 112 (1992) 435-443). The mean absolute hearing gains of the flunarizine group was 17 dB and 21 dB, after one and four weeks respectively (placebo group: 16 dB and 24 dB). The corresponding relative hearing gains (defined as absolute gain divided by initial hearing loss) were 35% and 43% for the flunarizine group and 33% and 42% for the placebo group. We conclude that flunarizine treatment does not improve the recovery of sudden hearing loss.
Sensory Neuroscience · 2025 · 7 citations · open access
Update on Gene Therapy in the Treatment of Hereditary Hearing Loss
AbstractABSTRACT Gene therapy is a promising therapeutic approach for genetic disorders, involving genetic modification to repair or reconstruct faulty genetic material. It is particularly relevant to hereditary hearing loss (HHL), a common monogenic condition that can lead to congenital deafness. The recent approval of clinical trial results using gene therapy for HHL underscores the growing interest in this field. To further advance inner ear gene therapy and its application in genetic diseases, it is crucial to review the progress of gene therapy for HHL. This review focuses on the three major gene therapy strategies—gene replacement, gene suppression, and gene editing—highlighting their application across different monogenic disorders and successful preclinical trials in HHL. We summarize the primary gene therapy strategies used in recent years, discuss recent achievements in preclinical studies, and explore potential advancements in this field.
Journal of Otology · 2023 · 5 citations · open access
Subclinical hearing loss associated with aging
AbstractObjective: Contribute to clarifying the existence of subclinical hearing deficits associated with aging. Design: In this work, we study and compare the auditory perceptual and electrophysiological performance of normal-hearing young and adult subjects (tonal audiometry, high-frequency tone threshold, a triplet of digits in noise, and click-evoked auditory brainstem response). Study sample: ." Results: presented significantly worse tonal thresholds in the high frequencies (12 and 16 kHz) and worse performance in the digit triplet tests in noise. In the electrophysiological test using the auditory brainstem response technique, the adult group presented significantly lower I and V wave amplitudes and higher V wave latencies at the supra-threshold level. At the threshold level, we observed a significantly higher latency in wave V in the adult group. In addition, in the partial correlation analysis, controlling for the hearing level, we observed a relationship (negative) between age and speech in noise performance and high-frequency thresholds. No significant association was observed between age and the auditory brainstem response. Conclusion: The results are compatible with subclinical hearing loss associated with aging.
Current Opinion in Otolaryngology & Head & Neck Surgery · 1995 · 2 citations
Modern clinical methods in genetic hearing loss
AbstractClinical methods in cases of genetic hearing loss have been influenced recently by both methodologic advances and specific findings made in the many research laboratories devoted to human genetic investigation. For the clinician, reports from these laboratories seem to suggest significant breakthroughs accompanied by allusions to clinical applicability. This review presents a rationale for the analysis of the many reports related to genetic hearing loss and their attending clinical impact. This rationale is based on a simplified view of the laboratory effort as a pipeline. A disease (mutation) passes through this pipeline on its way from family identification, through linkage analysis (chromosome localization), to gene sequencing and disease mechanism identification, and finally to gene-based therapy. Each stage of the investigation process has its own impact on clinical methods, and each mutation is in a particular spot in the pipeline at present. The pipeline itself is presented in this paper, along with the nature of the clinical impact of each level of laboratory findings.
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.
Advanced Science · 2025 · 1 citations · open access
Hearing Loss: From Basic to Clinical Science
AbstractHearing loss (HL) affects over 1.5 billion people globally, with genetic factors accounting for ≈50% of congenital cases. Therefore, HL has become a global health issue, driving extensive research from basic science to clinical applications. This Special Collection includes a total of 31 papers, among which 9 are review papers, 21 are research article papers, 1 is a perspective paper, that highlight the basic mechanisms and possible protection methods of HL, the application of gene therapy for treating HL, and the clinical study and application in HL.
AbstractOur findings confirm the complex genetic landscape of hearing loss and the limitations of WES in achieving a 100% diagnostic rate, especially in conditions characterized by genetic heterogeneity. These results contribute to our understanding of the genetic basis of hearing loss and emphasize the need for further research and comprehensive genetic analyses to elucidate the underlying causes of this condition.
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.
