Ketoprofen

證據等級: L5 預測適應症: 10

目錄

  1. Ketoprofen
  2. Ketoprofen: From Pain and Inflammation 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. Denmark Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## 藥師評估報告

Using the report structure directly (this is a content-generation task per the provided template, not a coding task — no other skill applies).

Ketoprofen: From Pain and Inflammation to Acromesomelic Dysplasia, Hunter-Thompson Type

One-Sentence Summary

Ketoprofen is a non-selective COX-1/COX-2 inhibitor used for pain, inflammation, and fever. The TxGNN model predicts it may be effective for Acromesomelic Dysplasia, Hunter-Thompson Type, a rare skeletal developmental disorder, but this prediction is currently supported by no clinical trials and no published literature, and the model’s own rationale flags the mechanistic link as biologically implausible.


Quick Overview

Item Content
Original Indication Not available — Ketoprofen holds no marketing authorisation in Denmark, so no Danish-approved indication text exists in this Evidence Pack
Predicted New Indication Acromesomelic Dysplasia, Hunter-Thompson Type
TxGNN Prediction Score 99.98%
Evidence Level L5 (model prediction only, no supporting studies)
Denmark Market Status Not marketed
Number of Marketing Authorisations 0
Recommended Decision Hold

Why is This Prediction Reasonable?

Detailed mechanism of action data for this candidate is not available in the Evidence Pack (marked as a Data Gap). Based on the mechanistic notes accompanying the prediction, Ketoprofen is a non-selective COX-1/COX-2 inhibitor with anti-inflammatory, analgesic, and antipyretic activity — a well-established NSAID pharmacology.

However, the predicted indication, Acromesomelic Dysplasia, Hunter-Thompson Type, is a rare genetic skeletal dysplasia caused by GDF5 mutations, with a pathophysiology centered on bone/cartilage developmental signaling rather than inflammation. The Evidence Pack’s own repurposing rationale explicitly states that there is no known pathological link between the COX/prostaglandin pathway and this disorder, and that the high TxGNN score most likely reflects graph-embedding similarity rather than a biologically grounded mechanism.

This pattern repeats across the other top-ranked candidates in this pack (brachyolmia-amelogenesis imperfecta syndrome, myosclerosis, brachyolmia, and colobomatous microphthalmia-rhizomelic dysplasia syndrome) — all are rare congenital/developmental or fibrotic disorders for which the accompanying rationale text states the mechanistic connection to NSAID pharmacology is weak or absent. This is a case where the model score is high but the biological plausibility narrative is explicitly negative; it should not be read as a validated repurposing hypothesis.


Clinical Trial Evidence

Currently no related clinical trials registered.


Literature Evidence

Currently no related literature available.


Denmark Market Information

Ketoprofen currently has no marketing authorisations registered in this Evidence Pack (0 licenses; market status: Not marketed). No product-level dosage form or indication data is available for Denmark.


Safety Considerations

Please refer to the approved Summary of Product Characteristics (SmPC) for safety information. Note: the underlying data pack flags TFDA/regulatory label warnings and contraindications as a Blocking data gap (DG001) — this must be resolved before any safety pre-assessment (S1) can proceed.


Conclusion and Next Steps

Decision: Hold

Rationale: This candidate has no clinical trial or literature evidence (L5, model prediction only), no Danish marketing authorisation to anchor safety/dosing, and the mechanistic rationale supplied with the prediction itself states the biological link to Ketoprofen’s COX-inhibitory pharmacology is weak or absent. There is no basis to advance past the S0 screening stage.

To proceed, the following is needed:

  • TFDA/SmPC-sourced warnings and contraindications (currently a Blocking data gap)
  • Confirmed mechanism of action (MOA) data from DrugBank or equivalent source
  • An independent, disease-specific biological plausibility assessment for Acromesomelic Dysplasia, Hunter-Thompson Type (given the model’s own rationale is skeptical)
  • Any preclinical or case-level evidence connecting NSAID pharmacology to GDF5-related skeletal dysplasias, should such data emerge

    Disclaimer

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



Copyright © 2026 藥提醒科技有限公司 (yao.care). For research purposes only. Not medical advice.

This site uses Just the Docs, a documentation theme for Jekyll.