DeCure for Dilated cardiomyopathy-hypergonadotropic hypogonadism syndrome
DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy-hypergonadotropic hypogonadism syndrome — 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 moduleDilated cardiomyopathy-hypergonadotropic hypogonadism syndrome 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 dilated cardiomyopathy-hypergonadotropic hypogonadism syndrome 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
lamin A/C (LMNA) — LMNA 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 6JLB · 3.205 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
The 1997 review on dilated cardiomyopathy describes it as a syndrome of ventricular enlargement, abnormal systolic and diastolic function, congestive heart failure, and premature death from heart failure or arrhythmias. It lists causes including coronary artery disease, valvular disease, viral infection, toxins, autoimmunity, and primary genetic abnormalities, but notes that in many patients the cause remains idiopathic. The review states that advanced dilated cardiomyopathy from any cause shows remarkable similarities in clinical course, histopathology, and haemodynamics.
A 2017 study on infertility in men with hypogonadotropic hypogonadism calls for a unified clinical algorithm and for research into effective and safe treatment for patients with hypergonadotropic hypogonadism. It does not provide any patient numbers, response rates, or survival data.
A 2025 retrospective cohort study of 14 patients with hypertrophic cardiomyopathy who required heart transplantation found that 10 developed a dilated/hypokinetic phenotype and 4 a restrictive phenotype. At least one pathogenic or likely pathogenic genetic variant was identified in 13 patients (93%). Dilated remodelling was associated with loss-of-function variants in LAMP2 (3 cases, all female), ALPK3 homozygous (1), MYH7 (1), MYBPC3 (1), a heterozygous missense variant in TRIM63 (1), FLNC truncating variant (1), and TTN truncating variant (2). For the TTN and FLNC variants, electrophoretic analysis of titin isoform composition and protein content in explanted heart fragments confirmed functional significance. The restrictive phenotype in adults was associated with multiple pathogenic sarcomere gene variants: MYL3 homozygous (1), MYBPC3 plus TPM1 (1), an MYH7 converter domain variant (1), and in one child a TNNT2 variant. The authors conclude that hypertrophic cardiomyopathy progressing to transplantation has a higher frequency of variants in non-sarcomeric genes and Danon disease compared to the general HCM cohort.
No abstract in this set directly studies dilated cardiomyopathy-hypergonadotropic hypogonadism syndrome. No abstract reports any drug treatment, any survival benefit, or any response rate for this specific combined condition. What is missing is any dedicated clinical trial, any prospective cohort, any validated animal model, and any funding for a disease-specific study that would stratify patients by both cardiac and gonadal phenotypes.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
New England Journal of Medicine · 1997 · 64 citations
The Genetics of Dilated Cardiomyopathy — Emerging Clues to the Puzzle
AbstractDespite recent advances in both medical and surgical therapies, dilated cardiomyopathy remains a leading cause of cardiovascular morbidity and mortality. This syndrome consists of ventricular enlargement, abnormal systolic and diastolic left ventricular function, symptoms of congestive heart failure, and premature death due predominantly to heart failure and cardiac arrhythmias. Coronary artery disease, valvular heart disease, viral infection, toxins, autoimmunity, and primary genetic abnormalities can all cause dilated cardiomyopathy, but in many patients it is idiopathic. The remarkable similarities in the clinical course, histopathological findings, and hemodynamic abnormalities in patients with advanced dilated cardiomyopathy, whatever the cause, suggest that a common . . .
Andrology and Genital Surgery · 2017 · 1 citations · open access
INFERTILITY IN MEN WITH PRIMARY HYPOGONADOTROPIC HYPOGONADISM
AbstractIn this study, an analysis data on the etiology, pathogenesis, diagnosis and treatment of male sterility with hypogonadotropic hypogonadism. Examination of the patients requires attention of urologist, andrologist, endocrinologist, neurosurgeon, medical geneticist. Clinical case, described by us, shows the necessity of development of a unified algorithm for working with these patients and search for effective and safe treatment of patients with hypergonadotropic hypogonadism.
Journal of Cardiovascular Development and Disease · 2025 · 1 citations · open access
Genetic Spectrum, Clinical Characteristics, and Molecular Pathogenesis of Hypertrophic Cardiomyopathy Requiring Heart Transplantation
AbstractHypertrophic cardiomyopathy (HCM) progressing to end-stage heart failure and heart transplantation (HT) is a rare clinical scenario with an insufficiently explored genetic background. In this single-center retrospective cohort study, we aimed to characterize the genetic spectrum, variants of HCM adverse remodeling, and aspects of molecular pathogenesis of this subgroup. The study included 14 patients (9 females), among whom 10 developed a dilated/hypokinetic phenotype and 4 a restrictive phenotype. In 13 patients (93%), at least one pathogenic or likely pathogenic genetic variant was identified. Dilated remodeling/hypokinesis was associated with loss-of-function variants in LAMP2 (3) in females, ALPK3homo (1), MYH7 (1), MYBPC3 (1), a heterozygous missense variant in TRIM63 (1), FLNCtv (1), TTNtv (2). For the latter two, electrophoretic analysis of titin isoform composition and protein content in myocardial fragments from explanted hearts confirmed the functional significance of TTN gene variants. The restrictive phenotype in the adult group was associated with carriage of multiple pathogenic sarcomere gene variants: MYL3homo (1), MYBPC3+TPM1 (1), an MYH7 converter domain variant (1), and, in one child, with a TNNT2 variant. This findings support HCM progressing to HT is characterized by a higher frequency of variants in non-sarcomeric genes and Danon disease compared to the general HCM cohort.
Dialnet (Universidad de la Rioja) · 1997 · 0 citations
Mil muertos de un trago: el caso de las bebidas envenenadas con alcohol metílico
AbstractCardiomyopathies are a major cause of mortality and morbidity and this spectrum of disorders tops the list of diseases leading to cardiac transplantation. While significant gains have been made during the past decade clinically, knowledge of the molecular aspects of these disorders has taken longer to advance. During the past 5 years, however, molecular genetic information on a variety of primary cardiomyopathies, such as familial hypertrophic cardiomyopathy and X-linked dilated cardiomyopathy, has been obtained. Other primary and secondary myocardial diseases are now under study with advances occurring more regularly. The purpose of this review is to outline the major advances thus far described for some primary and secondary cardiomyopathies, as well as detailing the slower progress seen for others.
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.
