DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for atrial fibrillation — screening already-approved drugs against its 48-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAtrial fibrillation maps to a 48-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 atrial fibrillation 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
nuclear receptor subfamily 3 group C member 2 (NR3C2) — NR3C2 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 2,2-difluoro-3-hydroxypropyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4PF3 · 1.1 Å · ligand 6-[1-(2,2-difluoro-3-hydroxypropyl)-5-(4-fluorophenyl)-3-methyl-1H-pyrazol-4-yl]-2H-1,4-benzoxazin-3(4H)-one (HFN). Experimental structure, not a prediction.
What the evidence adds up to
Atrial fibrillation is the most commonly diagnosed arrhythmia and a major risk factor for thromboembolic events. A 2020 review states that fibrosis plays an important role in the onset and perpetuation of AF through structural and electrical remodelling processes, and that multiple molecular pathways are involved in atrial substrate modification. The review aims to recapitulate these pathways and indicate existing gaps in the complex interplay of atrial fibrosis and AF, but it does not report any clinical trial results, survival data, or response rates.
A 2017 review on atrial fibrillation genetics notes that diseases such as hypertension, valvular heart disease, and heart failure may induce AF, which increases the risk of stroke and sudden cardiac death. Clinical studies from the last two decades have provided evidence that genetics play a key role: a family history of the disease has been identified in up to 30% of clinically diagnosed patients. In genotyped families, most carry rare genetic variants in genes associated with ionic channels, calcium handling protein, or predisposing to fibrosis, conduction system disease, and inflammatory processes. The review concludes that pathophysiological mechanisms are complex and that better understanding of the molecular basis will help improve risk stratification and clinical management, but no specific drug or intervention is tested.
A 2017 article on gene therapy for atrial fibrillation in heart failure states that current treatments for AF are suboptimal, in large part because the molecular mechanisms underlying AF are not well understood. It describes recent advances leading to preclinical development of gene-based therapies targeted to key molecular mechanisms involved in the genesis and maintenance of AF. No human trial results, efficacy data, or survival numbers are reported.
A 2008 chapter on electrical and structural remodelling in AF focuses on identifying signalling pathways that might be specifically and individually targeted for improved pharmacologic treatment or prevention of AF, perhaps simultaneously lowering stroke risk. It does not present any clinical outcomes, patient numbers, or comparative treatment results. What is still missing are large-scale, randomised clinical trials that test any specific molecular target or gene therapy in patients, adequate funding for such trials, and reliable patient stratification based on genetic or fibrotic markers.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
EP Europace · 2020 · 95 citations
Atrial fibrosis as a dominant factor for the development of atrial fibrillation: facts and gaps
AbstractAtrial fibrillation (AF), the most commonly diagnosed arrhythmia, affects a notable percentage of the population and constitutes a major risk factor for thromboembolic events and other heart-related conditions. Fibrosis plays an important role in the onset and perpetuation of AF through structural and electrical remodelling processes. Multiple molecular pathways are involved in atrial substrate modification and the subsequent maintenance of AF. In this review, we aim to recapitulate underlying molecular pathways leading to atrial fibrosis and to indicate existing gaps in the complex interplay of atrial fibrosis and AF.
Current Opinion in Cardiology · 2017 · 13 citations
Update about atrial fibrillation genetics
AbstractPURPOSE OF REVIEW: Atrial fibrillation is an important cause of morbidity in the aging population. The mechanisms responsible for the triggering and maintenance of the chaotic atrial rhythm are still poorly understood. In this review, we will focus on the genetic aspects of atrial fibrillation, to understand causality, with special emphasis on recent studies published in the field. RECENT FINDINGS: Diseases such as hypertension, valvular heart disease, and heart failure may induce atrial fibrillation, which increases the risk of stroke and sudden cardiac death. Clinical studies published in these last two decades have provided evidence that genetics play a key role in atrial fibrillation. Thus, a family history of the disease has been identified in up to 30% of clinically diagnosed patients. In those genotyped families, most carry rare genetic variants in genes associated with ionic channels, calcium handling protein, or predisposing to fibrosis, conduction system disease, and inflammatory processes. SUMMARY: Currently, atrial fibrillation is the most common sustained arrhythmia in clinical practice. The pathophysiological mechanisms of atrial fibrillation are complex. A better understanding of the molecular basis will help improve both current risk stratification and clinical management.
Gene Therapy for Atrial Fibrillation in Heart Failure
AbstractAtrial fibrillation (AF) is the most common arrhythmia and a major cause of morbidity and mortality in an aging population. Unfortunately, current treatments for AF are suboptimal, in large part because the molecular mechanisms underlying AF are not well understood. Recent advances in our understanding of the AF disease state have led to the preclinical development of gene-based therapies that are targeted to key molecular mechanisms involved in the genesis and maintenance of AF.
Techniques to Improve and Confirm Pulmonary Vein Isolation
AbstractAtrial fibrillation is the most common acquired arrhythmia and is increasing in frequency as the population ages. Treatment for atrial fibrillation ranges from minimal intervention to complex catheter ablations. The strategy used to treat atrial fibrillation largely rests on the extent of symptoms in an individual patient. This review will focus on ablation for atrial fibrillation and efforts to improve the success of the procedure.
AbstractOne of the most clinically important objectives of therapy for atrial fibrillation is the prevention of stroke/thromboembolism. The risk of ischemic stroke in patients with atrial fibrillation may be related to multifactorial pathogenesis. The only therapy for atrial fibrillation with the effect of reducing mortality is anticoagulation with warfarin, not antiarrhythmic therapy. However, the management of atrial fibrillation includes a lot of modulating factors and should be carefully carried out on a case-by-case basis.
Electrical and Structural Remodeling in Atrial Fibrillation
AbstractIntense research efforts since 1995 have sought to characterize the pathways that contribute to the occurrence and persistence of atrial fibrillation (AF). This chapter focuses on recent studies elucidating several of the molecular mechanisms that underlie the electrical and structural remodeling processes that promote persistent AF. Here there is a particular focus on the identification of signaling pathways that might be specifi cally and individually targeted for improved pharmacologic treatment or prevention of AF, perhaps simultaneously lowering the risk of stroke associated with AF.
International Journal of Angiology · 2020 · 0 citations · open access
Contemporary Surgical Management of Atrial Fibrillation
AbstractAtrial fibrillation is a common arrhythmia which may cause symptoms that significantly impact quality of life and is associated with increased risk of stroke, heart failure, and sudden death. Over the past three decades many surgical techniques as well as catheter-bases procedures have been developed to treat atrial fibrillation. In this review we describe the indications, treatments, outcomes, surgical techniques, and technical advances reported in the literature.
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.
