Maraviroc

Evidence Level: L5 Predicted Indications: 10

Table of Contents

  1. Maraviroc
  2. Maraviroc: From HIV-1 Infection to Multiple Endocrine Neoplasia
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. EU Market Information
    7. Safety Considerations
    8. Conclusion and Next Steps
    9. Disclaimer

## Pharmacist Assessment Report

Maraviroc: From HIV-1 Infection to Multiple Endocrine Neoplasia

One-Sentence Summary

Maraviroc is a CCR5 antagonist originally used to treat HIV-1 infection (CCR5-tropic strains) by blocking viral entry into immune cells. The TxGNN model predicts it may be effective for Multiple Endocrine Neoplasia, with a prediction score of 99.82%, but no clinical trials and no supporting literature currently exist for this indication — the drug’s own repurposing rationale explicitly notes there is no known biological connection.


Quick Overview

Item Content
Original Indication HIV-1 infection (CCR5-tropic strains) — inferred from known drug class; not present in this evidence pack’s license data
Predicted New Indication Multiple Endocrine Neoplasia
TxGNN Prediction Score 99.82%
Evidence Level L5
EU Market Status Not marketed
Number of Authorizations 0
Recommended Decision Hold

Why is This Prediction Reasonable?

Currently, detailed mechanism of action data is not available in this evidence pack (original_moa: [Data Gap]). Based on background information referenced in the repurposing rationale, Maraviroc is a CCR5 antagonist, acting on HIV-1 co-receptor binding to block viral entry and on chemokine-mediated immune cell trafficking. Its efficacy in HIV-1 infection is well established in this drug class.

Multiple endocrine neoplasia (MEN), however, is driven by germline mutations in the RET or MEN1 genes, causing tumor development across endocrine glands. There is no known mechanistic overlap between CCR5 signaling and RET/MEN1-driven tumorigenesis.

The evidence pack’s own rationale is explicit on this point: “與多發性內分泌腫瘤(MEN)之腫瘤發生機轉(RET/MEN1基因突變)無已知生物學連結,純屬TxGNN高分預測,無機轉支持” — i.e., this is a high-scoring statistical prediction from the TxGNN model with no mechanistic or biological support. It should be treated as a research hypothesis at most, not a plausible repurposing candidate at this stage.


Clinical Trial Evidence

Currently no related clinical trials registered.


Literature Evidence

Currently no related literature available.


EU Market Information

No marketing authorizations currently registered — this drug is not marketed in this jurisdiction (market_status: Not marketed, total_licenses: 0).


Safety Considerations

Please refer to the SmPC for safety information.


Conclusion and Next Steps

Decision: Hold

Rationale: This is an L5-level prediction — a TxGNN score with zero supporting clinical trials or literature. The rationale text itself confirms there is no known biological link between Maraviroc’s CCR5-antagonist mechanism and MEN pathogenesis, so there is no basis to advance this candidate.

To proceed, the following is needed:

  • TFDA/regulatory label (warnings, contraindications) — currently a blocking data gap (DG001)
  • Full mechanism of action (MOA) data via DrugBank — currently a high-severity data gap (DG002)
  • Preclinical or mechanistic studies directly linking CCR5 antagonism to RET/MEN1-driven tumorigenesis
  • If no such mechanistic link can be established, this candidate should be deprioritized in favor of other predicted indications in this drug’s portfolio (e.g., HER2-positive breast carcinoma, rank 10, which has direct CCL5/CCR5-ERK pathway evidence and may warrant separate evaluation)

    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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