DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for dilated cardiomyopathy 1A — screening already-approved drugs against its 26-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 1A maps to a 26-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 1a 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
LIM domain binding 3 (LDB3) — LDB3 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 gludrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4YDP · 1.4 Å · ligand GLUTAMIC ACID (GLU). Experimental structure, not a prediction.
What the evidence adds up to
A 1994 follow-up of 235 patients aged 16–70 with dilated cardiomyopathy, enrolled from 1978 to 1992, reported improving survival across three five-year periods. Two-year survival rose from 73.8% in group 1 (1978–1982, n=26) to 87.7% in group 2 (1983–1987, n=65) and 90.3% in group 3 (1988–1992, n=144). Four-year survival increased 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, and that a progressively higher proportion 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 was 90% for mild heart failure and 87.5% for moderate to severe heart failure in patients treated with beta blockers, usually alongside digitalis and ACE inhibitors.
A 2016 review stated that dilated cardiomyopathy is characterised by ventricular dilation and progressive systolic dysfunction, and that causative genetic mutations have been identified in more than 40 genes encoding proteins from different cellular structures and pathways. A 2024 review gave an annual incidence of 5–8 cases per 100,000 for European and North American populations, and listed non-genetic causes including viruses, cardiotoxicity, recreational drugs, and chemotherapeutic medications. That review focused on cytoskeletal and sarcomeric protein genes and described mouse models incorporating human mutations, stating that knowledge from these models might lead to new therapeutic approaches.
No drug is mentioned in the 2016 or 2024 reviews beyond the general categories of chemotherapeutic medications as a cause. The 1994 study does not test a single drug in a randomised trial; it is an observational comparison across time periods with changing patient characteristics. What is still missing is a randomised controlled trial of any specific repurposed drug for dilated cardiomyopathy 1A, a defined genetic subtype, and patient stratification by genotype rather than by heart failure severity alone. Funding for such a trial and for the necessary genetic screening has not been reported in these abstracts.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Circulation · 1981 · 273 citations · open access
Verapamil: its potential for causing serious complications in patients with hypertrophic cardiomyopathy.
AbstractVerapamil is extremely effective in the treatment of patients with hypertrophic cardiomyopathy. However, the basic physiologic actions of the drug may lead to serious adverse effects. An appreciation of this and an understanding of when these adverse effects are most likely to occur will minimize the potential of verapamil to cause serious complications in patients with hypertrophic 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.
Cleveland Clinic Journal of Medicine · 2002 · 44 citations
Idiopathic dilated cardiomyopathy: a common but mystifying cause of heart failure.
AbstractWhile researchers try to elucidate the origins of idiopathic dilated cardiomyopathy, clinicians continue to face the challenges of identifying and treating the causes of this condition to improve symptoms and survival. We review classification schemes for dilated cardiomyopathy and the current range of diagnostic and therapeutic options and treatment goals.
Journal of the American Heart Association · 2025 · 17 citations · open access
Disopyramide Revisited for Treatment of Symptomatic Obstructive Hypertrophic Cardiomyopathy: Efficacy and Safety in Patients Treated for at Least 5 Years
AbstractBackground Disopyramide is used to treat heart failure symptoms in patients with obstructive hypertrophic cardiomyopathy (HCM) with known medium‐term efficacy and safety, while long‐term outcomes are unknown. Methods and Results A total of 92 consecutive patients with symptomatic obstructive HCM with peak left ventricular outflow tract gradients of ≥30 mm Hg at rest or with provocation who were maintained on disopyramide for ≥5 years at 2 dedicated HCM centers were included: 92 patients; mean age, 62.5 years; 54% women; treated with disopyramide for median 7.2 years (left ventricular wall thickness 18±4 mm; median peak outflow gradient 95 mm Hg). At last follow‐up, 62 (67%) patients continued disopyramide, including 57 with symptom improvement ≥1 New York Heart Association class. The other 30 (33%) patients discontinued disopyramide due primarily to incomplete symptom resolution and required surgical myectomy or alcohol septal ablation (n=23) at 7.4 years from initiation. With disopyramide, resting left ventricular outflow gradients were reduced by 37% (to median 19 mm Hg), and provoked gradients decreased by 57% (to median 41 mm Hg), with no residual outflow obstruction (<30 mm Hg at rest or with provocation) in 42 (46%) patients and no change in ejection fraction (69%±6% versus 69%±9%, P =0.51). Ventricular tachyarrhythmias and left ventricular systolic dysfunction were uncommon (n=3 and n=1) and were not attributed to disopyramide. Death on disopyramide was exceedingly rare (n=3 [5%]) and non–HCM‐related occurring at age ≥90 years. Conclusions In patients with obstructive HCM, disopyramide is safe and effective at relieving heart failure symptoms from outflow obstruction in a subgroup of patients who were maintained on disopyramide for >5 years.
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.
Does Disopyramide Still Have a Place in the Management of Obstructive Hypertrophic Cardiomyopathy?
AbstractHypertrophic cardiomyopathy (HCM) is a relatively common inherited cardiac disorder associated with a left ventricular hypertrophy that cannot be explained by another cardiac or systemic disorder. One of the core pathophysiology features is left ventricular outflow tract obstruction (obstructive HCM [oHCM]), and this pathology could lead to complications, including sudden cardiac death and heart failure. Current treatment strategies for symptomatic oHCM consist of historical pharmacologic agents that are often based on nonrandomized, limited data or expert opinion. This article presents a critical appraisal of disopyramide, one of the pharmacologic options available in Canada for managing oHCM. The author concludes that robust clinical evidence supporting the use of disopyramide in treating oHCM is lacking, and that disopyramide should be reserved as a last resort for nonresponders to pharmacologic treatment and for those in whom invasive therapies are not indicated.
Medical Research Archives · 2024 · 7 citations · open access
Dilated Cardiomyopathy – Exploring the Underlying Causes
AbstractCardiovascular disease is one of the world's leading causes of natural mortality, taking approximately 18 million lives each year. Dilated cardiomyopathy, a subgroup of cardiac diseases, has an annual incidence of 5 - 8 cases per 100,000 for European and North American populations. Common features of dilated cardiomyopathy include cardiac chamber enlargement, impaired systolic function, reduced ejection fraction, and arrhythmias, with an endpoint of ventricular dilation and heart failure. The focus of this paper is to review the non-genetic and genetic etiologies that lead to dilated cardiomyopathy. The non-genetic causes of dilated cardiomyopathy that are discussed include viruses, cardiotoxicity, recreational drugs, and chemotherapeutic medications. For the genes that lead to dilated cardiomyopathy, the focus of this paper is on cytoskeletal and sarcomeric protein genes. Our scope in defining this area will be to explore numerous mouse models that incorporate mutations found in humans that lead to dilated cardiomyopathy. The purpose of the paper is to define the morphological and physiological consequences of these mutations and how this information has furthered our understanding of the disease. Having gained invaluable knowledge from these animal models, it is hoped that new and improved therapeutic approaches can be developed for the treatment and prevention of dilated cardiomyopathy.
Journal of clinical practice · 2014 · 2 citations · open access
MODERN APPROACH TO MANAGEMENT OF DILATED CARDIOMYOPATHY: CASE REPORT
AbstractDescription of case reports of a patient with diagnosis of dilated cardiomyopathy granting of a historical reference and modern ideas about the etiology, pathogenesis, course, and management of the disease. Performed surgical treatment (orthotopic transplantation of putrid heart), along with medication, allowed to improve the quality of life and prognosis of the disease.
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.
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