DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for spermatogenic failure 19 — 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 moduleSpermatogenic failure 19 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 spermatogenic failure 19 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.
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 Application of Clinical Genetics · 2018 · 4 citations · open access
Independent of DAZL-T54A variant and AZF microdeletion in a sample of Egyptian patients with idiopathic non-obstructed azoospermia
AbstractBackground: The microdeletion events that occur in the Y chromosome-azoospermia factor ( AZF ) region may lead to dyszoospermia. Also, the deleted azoospermia ( DAZ ) gene on AZFc and autosomal deleted azoospermia like gene ( DAZL ) are suggested to represent impairment, so it is interesting to determine the independency pattern of the AZF region and DAZL gene in azoospermic patients. Aim: To study the molecular characterization of AZFc and DAZL in 64 idiopathic non-obstructed azoospermia patients and 30 sexually reproductive men. Methods: SYBR Green I (Q-PCR) and AZF -STS analysis was used for DAZ gene, and SNV-PCR and confirmative Sanger sequencing for DAZL gene. Results: The present study observed that 15.6% had AZFc microdeletion, out of which 10% had DAZ1/2 deletion, and no T54A variant in the DAZL gene was found. Conclusion: In the current work, the novelty is that spermatogenic impairment phenotype, present with AZFc microdeletions, is independent of the T54A variant in the DAZL gene, and AZFc microdeletions could be a causative agent in spermatogenic impairment. Keywords: male infertility, azoospermia, AZF, DAZL, deletion
GPR56 gene down-regulation in patients with Klinefelter syndrome: a candidate for infertility?
AbstractBACKGROUND: The etiology of azoospermia in patients with Klinefelter Syndrome (KS) is still unknown. The protein codified by the G protein-couple receptor 56 (GPR56) belongs to the adhesion family of G protein-coupled receptors (GPRs). Its mutations are involved in the pathogenesis of intellectual disability and, according to animal studies, infertility. As the expression of GPR56 in patients with KS has not been investigated so far, this study was undertaken with the purpose of evaluating its expression in peripheral blood mononuclear cells (PBMCs) of patients with KS and normal controls. METHODS: This age-matched case-control study was performed in 10 patients with KS and 10 controls. Patients and controls underwent to blood sampling for next-generation sequencing (NGS) analysis, and differentially expressed mRNAs were identified using DESeq2 v.1.12. QRT-PCR was used to validate the results obtained by NGS analysis. TaqMan Gene Expression Assay primers were used to carry out the real-time PCR analysis for GPR56. RESULTS: GPR56 was down-regulated by -2081-fold (q-value <0.05) in PBMCs of patients with KS compared to controls. NGS data were confirmed by QRT-PCR. CONCLUSIONS: The possible contribution of the GPR56 gene down-regulation in the pathogenesis of spermatogenic failure in patients with KS is worthy to be further explored.
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.
