DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for spermatogenic failure 86 — 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 86 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 86 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.
Human Reproduction · 1993 · 76 citations
Sperm/egg binding patterns and oocyte cytology in retrospective analysis of fertilization failure in vitro
AbstractFailures of fertilization in in-vitro fertilization have been often linked to visually recognizable defects in spermatozoa, and occasionally to anti-sperm antibodies. However, some total failures and the frequent lack of fertilization in some eggs of normal appearance (partial failure) often remain unexplained. Simple evaluation of the configuration of sperm binding to the zona pellucida and of the oocyte features revealed by acetic alcohol fixation and lacmoid staining, may provide diagnostic clues in this respect. Among 25 cases of unanticipated total failure, this approach identified some men with normal semen analyses whose spermatozoa displayed either a total inability to bind to the zona or, after binding, an inability to intrude into the zona matrix. However, in 10 of these cases significant numbers of spermatozoa were bound to and intruded deep into the zona, a pattern consistent with the possibility of an egg defect, specifically a resistance to the passage of spermatozoa past the inner portion of the zona pellucida. Such a block also appeared to be the main cause of fertilization failure among 442 unfertilized eggs from 154 partial failure patients. As in the total failures, the inability of apparently competent spermatozoa to penetrate the zona was often associated with ooplasmic anomalies (refractile bodies, extra groups of chromosomes, chromatin rings or masses, one or more pronuclei with one or no polar bodies, and other occasional anomalies). These anomalies occurred in 79.4% of this unfertilized oocyte subset, in contrast to a 27.4% incidence in 238 oocytes not fertilized because of sperm defects. Simple retrospective assessment of sperm binding patterns and oocyte cytology can be a valuable complement to semen analysis in diagnosis of fertilization failure in vitro.
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.
