Ketoprofen

證據等級: L5 預測適應症: 10

目錄

  1. Ketoprofen
  2. Ketoprofen: From NSAID Therapy to Acromesomelic Dysplasia, Hunter-Thompson Type
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. Taiwan Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## 藥師評估報告

Ketoprofen: From NSAID Therapy to Acromesomelic Dysplasia, Hunter-Thompson Type

One-Sentence Summary

Ketoprofen is a non-selective NSAID (propionic acid class, COX-1/COX-2 inhibitor) generally used for inflammatory pain conditions, though its specific original indication record is not available for this evidence pack. The TxGNN model’s top-ranked prediction is Acromesomelic Dysplasia, Hunter-Thompson Type, but this candidate is supported by 0 clinical trials and 0 publications, and the evidence pack itself flags the prediction as likely graph noise with no known mechanistic basis.


Quick Overview

Item Content
Original Indication Not available (no TFDA license record; drug is pharmacologically classified as a propionic acid NSAID / COX-1,2 inhibitor used for inflammatory pain)
Predicted New Indication Acromesomelic Dysplasia, Hunter-Thompson Type
TxGNN Prediction Score 99.98%
Evidence Level L5
Taiwan Market Status 未上市 (Not Marketed)
Number of Licenses 0
Recommended Decision Hold

Why is This Prediction Reasonable?

Detailed mechanism of action data for ketoprofen is not directly available in this evidence pack ([Data Gap], DG002). What is known from the accompanying rationale text is that ketoprofen is a non-selective COX-1/COX-2 inhibitor of the propionic acid NSAID class, working through suppression of prostaglandin synthesis to achieve anti-inflammatory and analgesic effects.

Acromesomelic Dysplasia, Hunter-Thompson Type is a rare congenital skeletal dysplasia driven by disruption of BMP signaling (GDF5/CDMP1), not by an inflammatory or prostaglandin-mediated process. The evidence pack’s own repurposing rationale explicitly states there is no known mechanistic relationship between NSAID/COX inhibition and this disorder, and characterizes the prediction as a “graph-noise-type” output — i.e., the TxGNN score is very high, but no pharmacological, clinical, or literature signal supports it.

Consequently, this specific prediction should not be interpreted as a validated repurposing hypothesis. It is worth noting that other candidates lower in this same prediction set carry more biological plausibility — for example, spondyloarthropathy susceptibility (rank 8, L3, supported literature) and LACC1-defect juvenile arthritis (rank 10, L4, inflammatory mechanism overlap) — both of which align with ketoprofen’s known anti-inflammatory pharmacology and may be more productive directions for further evaluation.


Clinical Trial Evidence

Currently no related clinical trials registered.


Literature Evidence

Currently no related literature available.


Taiwan Market Information

Ketoprofen currently has no approved license record in Taiwan (0 licenses; market status: 未上市/Not Marketed).


Safety Considerations

Please refer to the package insert for safety information.


Conclusion and Next Steps

Decision: Hold

Rationale: The top-ranked prediction carries a very high TxGNN score but zero supporting clinical trials, zero literature, and no plausible mechanistic link — the evidence pack’s own rationale identifies it as likely model noise (Evidence Level L5). Combined with the drug’s absence from the Taiwan market (0 licenses) and a Blocking data gap on TFDA labeling/contraindication data (DG001), there is no basis to advance this specific candidate.

To proceed, the following is needed:

  • TFDA package insert (warnings/contraindications) — currently a Blocking data gap (DG001), required before any safety-stage (S1) review
  • Mechanism of action (MOA) data via DrugBank — currently a High-severity data gap (DG002)
  • If pursuing ketoprofen repurposing further, prioritize the higher-evidence candidates in this prediction set instead — spondyloarthropathy susceptibility (rank 8, L3, literature-supported) and LACC1-defect juvenile arthritis (rank 10, L4, mechanistically plausible) — rather than the rank-1 candidate evaluated here
  • Taiwan market/licensing status confirmation, given the drug is not currently marketed domestically

    Disclaimer

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



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