DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 1EE — 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 1EE 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 1ee 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.
What the evidence adds up to
A 1994 follow-up of 235 patients aged 16–70 enrolled on a register from 1978 to 1992 reported that two-year and four-year survival in dilated cardiomyopathy improved across three consecutive five-year periods. Two-year survival rose from 73.8% in group 1 (1978–1982, 26 patients) to 87.7% in group 2 (1983–1987, 65 patients) and 90.3% in group 3 (1988–1992, 144 patients). Four-year survival rose from 53.8% to 72.3% to 82.9% (P = 0.02). The authors noted that patients in later periods were younger and less severely affected, which partly explained the improvement, but the survival curves diverged progressively and the improvement remained significant after stratification for disease severity, suggesting a sustained treatment effect. A progressively higher proportion of patients received ACE inhibitors and later beta blockers. In group 2, patients treated with ACE inhibitors showed better survival than those not treated, after stratification for heart failure severity. In group 3, beta blockers had a significant additive effect with conventional therapy. Four-year survival in patients with mild heart failure treated with beta blockers, usually with digitalis and ACE inhibitors, was 90%; in those with moderate to severe heart failure it was 87.5%.
A 2014 case report described a previously healthy 45-year-old man with visceral leishmaniasis who developed acute dilated cardiomyopathy during treatment with amphotericin B. Other causes of heart failure and known predisposing factors were ruled out. His cardiac function returned to normal shortly after the drug was stopped. The authors noted that only four previous cases of reversible dilated cardiomyopathy associated with amphotericin B had been reported, all in patients with a predisposing factor for heart failure. This was the first case in a patient without any known predisposing factor. The authors concluded that available evidence suggests amphotericin B may induce cardiotoxicity and that further investigations are needed.
A 2016 review stated that dilated cardiomyopathy is characterised by ventricular dilation and progressive systolic dysfunction and is the most common form of cardiomyopathy. Causative genetic mutations have been identified in more than 40 genes encoding proteins belonging to different cellular structures and pathways. The review described major genes and pathophysiologic mechanisms but provided no new clinical trial data or treatment outcomes.
What is still missing is a prospective trial that tests a specific drug for repurposing in dilated cardiomyopathy, with adequate sample size and stratification by genetic subtype. The 1994 data are now three decades old and reflect an era before modern heart failure pharmacotherapy. The amphotericin B observation is limited to a single case without predisposing factors. No abstract provides randomised evidence for any repurposed agent, and no trial addresses the genetic heterogeneity described in the 2016 review. Money for a properly powered, genetically stratified trial is lacking.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Heart · 1994 · 76 citations · open access
Changing mortality in dilated cardiomyopathy
AbstractOBJECTIVE: To analyse the changes in mortality in dilated cardiomyopathy over the past 15 years and to identify the factors that might have influenced survival. DESIGN: Follow up study of 235 patients (aged 16-70) systematically enrolled on a register from 1 January 1978 to 31 December 1992. SETTING: Hospital department of cardiology. PATIENTS: Three groups corresponding to three periods of 5 years: group 1 (diagnosis between 1 January 1978 and 31 December 1982) 26 patients; group 2 (diagnosis between 1 January 1983 and 31 December 1987) 65 patients; and group 3 (diagnosis between 1 January 1988 and 31 December 1992) 144 patients. MAIN OUTCOME MEASURES: Death or heart transplantation. RESULTS: Two and four year survival was 73.8% and 53.8% in group 1, 87.7% and 72.3% in group 2, and 90.3% and 82.9% in group 3 (P = 0.02). During the 15 years of the study period the number of cases increased progressively and the baseline clinical characteristics changed (that is, patients were younger and less severely affected), partly explaining the improvement in survival. None the less, the three mortality curves tended to diverge progressively and the improvement in survival in the different groups was still significant after stratification for the severity of the disease, suggesting that treatment had a sustained effect. A progressively higher proportion of patients were treated with angiotensin converting enzyme (ACE) inhibitors and more recently with beta blockers. In group 2, after stratification for the severity of heart failure, patients who were treated with ACE inhibitors showed a better survival than patients who were not. Furthermore, analysis of group 3 showed that beta blockers had a significant additive effect with conventional therapy both by intention to treat and actual treatment. Four year survival in patients with mild and moderate to severe heart failure treated with beta blockers, and usually digitalis and ACE inhibitors, was respectively 90% and 87.5%. CONCLUSIONS: The improvement in the survival of patients with dilated cardiomyopathy over the past 15 years may be explained by earlier diagnosis, new treatments, and a change in the clinical characteristics of the patients at enrolment.
Journal of Clinical Pharmacy and Therapeutics · 2014 · 22 citations
Reversible dilated cardiomyopathy associated with amphotericin B therapy
AbstractWHAT IS KNOWN AND OBJECTIVE: Amphotericin B (AmB) is commonly used to treat a broad spectrum of fungal infections and leishmaniasis. Its use is limited by numerous adverse effects. Reversible dilated cardiomyopathy associated with AmB is a rare disorder with only four previously reported cases, and all of them referring to patients who presented with a predisposing factor for heart failure. CASE SUMMARY: A previously healthy 45-year-old man with visceral leishmaniasis treated with AmB developed acute dilated cardiomyopathy. Other causes of heart failure as well-known predisposing factors for this condition were ruled out. As with previously reported cases, the cardiac function of our patient returned to normal shortly after. WHAT IS NEW AND CONCLUSION: We describe the first case of dilated cardiomyopathy associated with the administration of AmB in a patient without any known predisposing factor for developing cardiac dysfunction. Available evidence suggests that AmB may induce cardiotoxicity. Further investigations are needed to clarify this issue.
Journal of Cardiovascular Medicine · 2016 · 15 citations
Genetic bases of dilated cardiomyopathy
AbstractCardiomyopathies represent a wide and heterogeneous group of diseases wherein a genetic cause has been consistently identified.Dilated cardiomyopathy (DCM) is characterized by ventricular dilation and progressive systolic dysfunction, and it is the most common form of cardiomyopathy.Causative genetic mutations have been identified in more than 40 genes encoding proteins belonging to different cellular structures and pathways.A great diversity of pathways has been implied in the pathogenesis of DCM, depending on the affected genes and on the dislodged intracellular structures or mechanisms.This review describes the major genes and focus on the pathophysiologic mechanisms of DCM, with a special consideration of the most recent discoveries in the field.
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.
