Regadenoson

證據等級: L5

預測適應症: 4 個

Regadenoson: From Cardiac Stress Test Agent to Anaphylaxis

One-Sentence Summary

Regadenoson is a selective adenosine A2A receptor agonist used clinically as a pharmacologic cardiac stress agent for myocardial perfusion imaging, not as a disease-treating drug. The TxGNN model predicts it may be effective for Anaphylaxis, with a score of 99.85%, but this is supported by only 1 loosely related clinical trial and 0 publications — and the mechanistic evidence points the opposite direction.

Quick Overview

Item	Content
Original Indication	Pharmacologic cardiac stress agent (myocardial perfusion imaging) — not formally structured in source data; no Finland-approved indication text available
Predicted New Indication	Anaphylaxis
TxGNN Prediction Score	99.85%
Evidence Level	L5
Finland Market Status	✗ Not Marketed
Number of Authorizations	0
Recommended Decision	Hold

Why is This Prediction Reasonable?

Detailed mechanism-of-action data is marked as a data gap in the structured record, but the evidence pack's own mechanistic analysis identifies regadenoson as a selective adenosine A2A receptor agonist, used clinically to pharmacologically simulate exercise stress during cardiac perfusion imaging in patients who cannot exercise adequately.

The predicted link to anaphylaxis does not follow a plausible treatment mechanism. Adenosine A2A receptor activation is mechanistically associated with mast cell degranulation and vasodilation — this is precisely why regadenoson's own label already carries a known risk of anaphylactoid/hypersensitivity reactions (flushing, dyspnea, hypotension) as an adverse effect, not a therapeutic one. The single clinical trial retrieved for this indication (NCT06854458) confirms this pattern: it is a cardiac stress-MRI perfusion study where regadenoson is used as the stress-inducing agent, and anaphylaxis appears only as a monitored adverse event, not a treatment endpoint (relevance grade C).

This concern is reinforced by the broader prediction set: of the top 4 TxGNN candidates for this drug, three (anaphylaxis, food-dependent exercise-induced anaphylaxis, pseudoallergy) are all hypersensitivity/mast-cell-mediated conditions. This clustering strongly suggests the knowledge graph has encoded a drug→adverse-event relationship as a drug→indication relationship — i.e., a likely direction-inverted signal rather than a genuine repurposing opportunity.

Clinical Trial Evidence

Trial Number	Phase	Status	Enrollment	Key Findings
NCT06854458	N/A	Recruiting	1000	Multicenter stress cardiac MRI perfusion imaging study; regadenoson used as the pharmacologic stress agent. Anaphylaxis is not a treatment target — at most a monitored adverse event. Relevance graded C (low relevance to the treatment hypothesis).

No clinical trials were found for the other predicted indications (food-dependent exercise-induced anaphylaxis, esotropia, pseudoallergy).

Literature Evidence

Currently no related literature available.

Finland Market Information

Regadenoson is not currently marketed in Finland (0 authorizations on record); no product/license data is available.

Safety Considerations

Structured safety fields (key warnings, contraindications, DDI) are not populated in the source data. However, the evidence pack's mechanistic rationale flags that regadenoson has a known risk of anaphylactoid/hypersensitivity reactions (flushing, dyspnea, hypotension) as part of its established adverse-effect profile — directly relevant given that this is also the predicted "new indication." Full labeling data (TFDA/package insert warnings and contraindications) is currently a blocking data gap and has not yet been retrieved.

Please refer to the package insert for complete safety information once available.

Conclusion and Next Steps

Decision: Hold

Rationale: Evidence level is L5 (model prediction only) — the one retrieved clinical trial does not actually support treating anaphylaxis with regadenoson, and no literature exists. More importantly, the mechanistic pattern (adenosine A2A agonism triggering mast-cell-mediated reactions) and the clustering of hypersensitivity-related predictions across this drug's top candidates both suggest this is a safety signal misclassified as a treatment signal, not a genuine repurposing hypothesis.

To proceed, the following is needed:

Retrieve TFDA/package insert warnings and contraindications (currently a blocking gap for S1 safety evaluation)
Confirm mechanism-of-action data via DrugBank to formally rule in/out the signal-inversion hypothesis
If pursued further, obtain preclinical or mechanistic studies that directly link A2A receptor agonism to an anti-anaphylactic (rather than pro-anaphylactic) effect before advancing past S0
Disclaimer

This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.