Neuro Lab · DeCure for X

DeCure for Wolff-Parkinson-White Syndrome

DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for Wolff-Parkinson-White Syndrome — screening already-approved drugs against its 45-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.

Disease module45 genesLead labNeuro
All cures
NeuroDOID:384$DeCureNeuro

The disease map

Disease moduleWolff-Parkinson-White Syndrome maps to a 45-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 wolff-parkinson-white 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

T-box transcription factor 5 (TBX5)TBX5 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-[2-(2-ethoxy-ethoxydrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 2X6U · 1.9 Å · ligand 2-{2-[2-(2-{2-[2-(2-ETHOXY-ETHOXY)-ETHOXY]-ETHOXY}-ETHOXY)-ETHOXY]-ETHOXY}-ETHANOL (PE4). Experimental structure, not a prediction.

What the evidence adds up to

Family studies and molecular genetic investigations indicate that Wolff-Parkinson-White syndrome can have a substantial genetic component, sometimes inherited as a single gene disorder, though the abstract from 2005 offers no concrete numbers on prevalence or specific genes. A retrospective study from 2009 followed 124 asymptomatic children with ventricular pre-excitation, average age 7 years, for a mean of 4.2 years. During follow-up, all patients remained in good health. An intermittent pathway was detected in 18 patients (15%), and four of them (3.4%) showed a supraventricular tachycardia despite being asymptomatic. An ergometric test in 76 asymptomatic patients showed total abrupt vanishing of the delta wave in 16 children (21%). The authors concluded that asymptomatic Wolff-Parkinson-White syndrome in children has a good outcome over a short-term follow-up, and that the predictive value of electrophysiological evaluation is uncertain.

A 2018 case report describes one infant with asymptomatic Wolff-Parkinson-White syndrome and severe left ventricular dyssynchrony and dysfunction who was given flecainide and had a complete response. The authors suggest flecainide is a suitable resynchronisation therapy for such infants, but this is a single patient, not a trial. No other drugs are mentioned in any of the abstracts.

No randomised controlled trials, no survival data, and no large-scale comparisons of treatments for asymptomatic Wolff-Parkinson-White syndrome are reported in these abstracts. What is missing is prospective trial data with sufficient follow-up to establish whether pharmacologic intervention alters long-term outcomes, and any evidence that would justify treating asymptomatic patients beyond the rare infant with documented dyssynchrony.

Evidence

Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.

Journal of Cardiovascular Electrophysiology · 2005 · 39 citations

Is Wolff‐Parkinson‐White Syndrome a Genetic Disease?

AbstractFamily studies, and more recent molecular genetic investigations, indicate that the Wolff-Parkinson-White (WPW) syndrome and associated preexcitation disorders can have a substantial genetic component. Because preexcitation disorders are sometimes inherited as single gene disorders, key mechanistic insights can be gained that are expected to be relevant also to the more common multifactorial forms of these traits. Potentially, such insights will inform the future management of these conditions. Where WPW is inherited as a familial trait, with or without associated cardiac defects or a systemic syndrome, there are clinical genetic ramifications that are already of practical importance.

https://doi.org/10.1111/j.1540-8167.2005.50139.x
Journal of Cardiovascular Medicine · 2009 · 17 citations

Asymptomatic ventricular pre-excitation in children

AbstractOBJECTIVE: This retrospective study was planned for a good risk assessment of asymptomatic patients affected by ventricular pre-excitation. METHODS: From 1985 to 2007, 124 patients with an atrioventricular pathway (electrocardiographic signs of ventricular pre-excitation) were admitted to our cardiology division. The average age was 7 years (range 1 month to 18 years). The mean follow-up period in the whole population of patients was 4.2 years (range 1-13 years). Four patients were lost during the follow-up. During this period, all patients remained in good health. In all of them, we performed a Holter evaluation every year. An intermittent pathway was detected in 18 patients (15%), and four of them (3.4%) showed a supraventricular tachycardia even though they were asymptomatic patients. An ergometric test was performed in 76 asymptomatic patients; 16 children (21%) showed a total abrupt vanishing of delta wave. A transoesophageal electrophysiological evaluation was performed in 14 patients. CONCLUSION: According to our data, asymptomatic Wolff-Parkinson-White syndrome in children has a good outcome during a short-term (4 years) follow-up. The usefulness of electrophysiological evaluation (in particular its predictive value) is uncertain.

https://doi.org/10.2459/jcm.0b013e32831a98c2
Cardiology in the Young · 2018 · 7 citations

Pharmacologic therapy with flecainide for asymptomatic Wolff–Parkinson–White syndrome in an infant with severe left ventricular dyssynchrony

AbstractSome asymptomatic patients with Wolff-Parkinson-White syndrome have severe left ventricular dyssynchrony and dysfunction. We describe a patient who was given a diagnosis of Wolff-Parkinson-White syndrome in infancy and had a complete response to pharmacologic therapy with flecainide. Our findings suggest that flecainide is a suitable resynchronisation therapy for such infants.

https://doi.org/10.1017/s1047951118000252

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.