Cardio Lab · DeCure for X

DeCure for Catecholaminergic polymorphic ventricular tachycardia 4

DeCure's autonomous Cardio AI scientist is researching a drug-repurposing hypothesis for catecholaminergic polymorphic ventricular tachycardia 4 — 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 module1 genesLead labCardio
All cures
CardioDOID:0060678$DeCureCardio

The disease map

Disease moduleCatecholaminergic polymorphic ventricular tachycardia 4 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 catecholaminergic polymorphic ventricular tachycardia 4 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 2010 case report describes a patient with catecholaminergic polymorphic ventricular tachycardia (CPVT) whose arrhythmia was refractory to beta-blockade and an implanted cardioverter defibrillator. After a selective serotonin re-uptake inhibitor (SSRI) was added to the regimen, no further episodes of ventricular tachycardia occurred during the following two years. This is a single patient observation, not a controlled trial.

A 2007 review discusses the molecular pathophysiology of CPVT, linking mutations in the cardiac ryanodine receptor and calsequestrin to disrupted calcium homeostasis and arrhythmogenesis. It mentions potentially innovative strategies for controlling calcium-handling abnormalities but provides no clinical data on any specific drug. A 2020 review describes the mechanistic progression from beta-adrenergic stimulation to ventricular tachycardia in CPVT and discusses hypotheses about cellular and tissue origins of the arrhythmias, but again offers no treatment results.

No controlled studies have tested SSRIs in CPVT. The only clinical evidence is a single case report from 2010. No data exist on response rates, survival, or sample sizes beyond that one patient. What is missing is any prospective trial, any replication of the SSRI finding, and any patient stratification to identify who might benefit.

Evidence

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

Cardiovascular Research · 2007 · 59 citations

Disruption of calcium homeostasis and arrhythmogenesis induced by mutations in the cardiac ryanodine receptor and calsequestrin

AbstractDevelopment of cardiac arrhythmias in several degenerative cardiac disorders such as heart failure is precipitated by abnormalities in intracellular calcium regulation. Recently, the identification of mutations in proteins responsible for the control of intracellular calcium has been associated with an inherited arrhythmogenic syndrome called catecholaminergic polymorphic ventricular tachycardia (CPVT). Here, we review the current knowledge about the molecular pathophysiology of CPVT and we discuss some potentially innovative strategies for controlling calcium-handling abnormalities in CPVT that may provide novel therapeutic options for affected patients.

https://doi.org/10.1093/cvr/cvm004
Cardiovascular journal of South Africa/Cardiovascular journal of Southern Africa · 2010 · 9 citations · open access

Serotonin and catecholaminergic polymorphic ventricular tachycardia : a possible therapeutic role for SSRIs?

AbstractCatecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare malignant arrhythmia, usually diagnosed in the adolescent years. The diagnosis can typically be made by one or more of the following: a positive family history, exercise electrocardiography, ambulatory ECG monitoring and/or an intra-cardiac, electrophysiological examination. This is a case report of a patient with CPVT that was refractory to treatment with beta-blockade and an implanted automatic cardioverter defibrillator. However, after a selective serotonin re-uptake inhibitor (SSRI) was added to the therapeutic regimen, no further episodes of ventricular tachycardia occurred during the following two years.

https://doi.org/10.5830/cvja-2010-023
The Journal of Physiology · 2020 · 0 citations

AbstractCatecholaminergic polymorphic ventricular tachycardia (CPVT) is a cardiac arrhythmia characterized by the presence of ventricular tachycardia in response to β-adrenergic receptor stimulation. Here, we describe the mechanistic progression from β-adrenergic stimulation to the formation of mono/polymorphic ventricular tachycardia. The goal of this review is to highlight the current molecular mechanisms that lead to CPVT followed by a discussion of the current hypotheses and research around the cellular/tissue origin of the arrhythmias.

https://doi.org/10.1113/tjp.v598.14

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.