Idelalisib

證據等級: L5 預測適應症: 10

目錄

  1. Idelalisib
  2. IDELALISIB: From B-cell Hematologic Malignancies to Mantle Cell Lymphoma
    1. One-Sentence Summary
    2. Quick Overview
    3. Why is This Prediction Reasonable?
    4. Clinical Trial Evidence
    5. Literature Evidence
    6. US Market Information
    7. Cytotoxicity
    8. Safety Considerations
    9. Conclusion and Next Steps
    10. Disclaimer

## 藥師評估報告

IDELALISIB: From B-cell Hematologic Malignancies to Mantle Cell Lymphoma

One-Sentence Summary

Idelalisib is a selective PI3Kδ inhibitor originally developed for B-cell hematologic malignancies such as chronic lymphocytic leukemia (CLL), follicular lymphoma, and small lymphocytic lymphoma (SLL), based on literature evidence in this dataset (structured license/indication fields are not populated for this jurisdiction). The TxGNN model predicts it may also be effective for Mantle Cell Lymphoma (MCL), with 9 clinical trials and 19 publications currently supporting this direction, though the strongest single trial in this set (NCT01796470) was terminated.


Quick Overview

Item Content
Original Indication Not available in structured license data (0 licenses on file); literature evidence in this pack consistently describes idelalisib (Zydelig®) as approved for relapsed CLL, follicular lymphoma, and SLL
Predicted New Indication Mantle Cell Lymphoma
TxGNN Prediction Score 99.84%
Evidence Level L2
US Market Status Not Marketed
Number of NDAs 0
Recommended Decision Research Question

Why is This Prediction Reasonable?

Currently, a structured mechanism-of-action record is not available for this drug (data gap DG002). Based on evidence within the literature corpus, idelalisib is a first-in-class, orally administered, selective inhibitor of the delta isoform of phosphatidylinositol 3-kinase (PI3Kδ). PI3Kδ is expressed predominantly in hematopoietic cells and sits downstream of the B-cell receptor (BCR), where it drives proliferation and survival signaling in B-cell malignancies.

Idelalisib’s established efficacy in CLL, follicular lymphoma, and SLL stems from blocking this BCR/PI3Kδ survival pathway, which is broadly active across B-cell derived neoplasms — including MCL. This provides a plausible mechanistic bridge to MCL, since MCL is also a B-cell lymphoproliferative disorder in which PI3K pathway activation contributes to pathogenesis (as reflected in several of the MCL-specific publications below).

However, the mechanistic case for MCL specifically is weaker than for CLL/iNHL: MCL’s clinical response has historically been driven more strongly by BTK inhibition (e.g., ibrutinib) than by PI3Kδ inhibition, and idelalisib has shown intrinsic resistance in MCL in some preclinical models. The most directly relevant combination trial in this indication (NCT01796470, entospletinib + idelalisib) was terminated, while the strongest positive signal comes from a smaller Phase 1/randomized Phase 2 study of idelalisib + lenalidomide (NCT01838434) specifically in relapsed/refractory MCL.


Clinical Trial Evidence

Trial Number Phase Status Enrollment Key Findings
NCT01838434 Phase 1 / Randomized Phase 2 Completed 106 Idelalisib + lenalidomide in relapsed/refractory MCL — direct, most relevant trial for this population
NCT01088048 Phase 1 Completed 241 Safety of idelalisib combined with anti-CD20 mAb, chemotherapy, or other agents in relapsed indolent NHL, MCL, or CLL
NCT01796470 Phase 2 Terminated 66 Entospletinib + idelalisib in relapsed/refractory hematologic malignancies incl. MCL; terminated
NCT02603445 Phase 1b Completed 20 BCL201 + idelalisib safety/tolerability in follicular lymphoma and MCL
NCT03151057 Phase 1 Terminated 16 Idelalisib as post-allogeneic HSCT maintenance in B-cell derived malignancies
NCT02824159 N/A Completed 121 Real-world association of idelalisib/ibrutinib plasma concentration with side effects in hematologic malignancies including MCL
NCT02457598 Phase 1 Terminated 203 Tirabrutinib combined with targeted anti-cancer therapies in relapsed/refractory B-cell lymphoproliferative malignancies
NCT03740529 Phase 1/2 Completed 803 Oral pirtobrutinib in CLL/SLL/NHL; idelalisib not the study drug, indirect relevance
NCT04985214 N/A Unknown 464 Quality-of-life assessment of lymphoma patients treated with oral therapies including idelalisib

Literature Evidence

PMID Year Type Journal Key Findings
24795031 2014 Review (Tier 1) Cancer Discovery The PI3Kδ inhibitor idelalisib was effective in heavily pretreated patients with MCL
24615778 2014 Phase 1 clinical study Blood Phase 1 study of idelalisib (50–350 mg) in 40 patients with relapsed/refractory MCL; evaluated safety, DLT, ORR, PFS
27342398 2017 Cohort (Tier 2) Clin Cancer Res Idelalisib impacts MCL cell growth by disrupting translation-regulatory mechanisms
33850273 2022 Review (Tier 2) Acta Pharmacol Sin P300/CBP inhibition sensitizes MCL to idelalisib, overcoming intrinsic resistance
40466505 2025 Review (Tier 2) Phytomedicine CBX5 loss drives PI3Kδ inhibitor resistance in MCL; propolis restores sensitivity
38815797 2024 Cancer Letters Idelalisib enhances anti-tumor effects of CDK4/6 inhibitor palbociclib via PLK1 in B-cell lymphoma incl. MCL
22361516 2012 Oncotarget Novel targeted therapies for MCL, including PI3K/Akt pathway inhibition
24974852 2014 Br J Haematol Current regimens and novel agents for MCL
23512567 2013 Curr Treat Options Oncol Current and emerging therapies in MCL
26360791 2015 Expert Opin Pharmacother Overview of standard and novel treatment options for MCL

US Market Information

Idelalisib currently holds no active marketing authorization on file in this dataset — 0 licenses recorded and market status “Not Marketed.” No product/dosage-form/indication records are available to tabulate.


Cytotoxicity

Idelalisib is an antineoplastic agent (oncology indication class evident throughout the literature evidence — CLL, SLL, follicular lymphoma, MCL), so this section applies.

Item Content
Cytotoxicity Classification Targeted therapy — selective PI3Kδ (phosphatidylinositol 3-kinase delta) inhibitor, not a conventional cytotoxic agent
Myelosuppression Risk Please refer to the package insert warnings and precautions
Emetogenicity Classification Please refer to the package insert warnings and precautions
Monitoring Items Standard monitoring for this drug class as referenced in the literature includes CBC with differential, liver function tests, and infection surveillance; specific institutional protocols should follow the package insert
Handling Protection Please refer to the package insert warnings and precautions

Safety Considerations

Please refer to the package insert for safety information.


Conclusion and Next Steps

Decision: Research Question

Rationale: The mechanistic rationale (PI3Kδ/BCR pathway relevance to B-cell malignancies) is plausible for MCL, and one directly relevant Phase 1/randomized Phase 2 trial (NCT01838434) was completed, supporting an L2 evidence level. However, the most disease-specific combination trial (NCT01796470) was terminated, and MCL’s clinical dependency is more strongly tied to BTK than PI3Kδ inhibition, so the signal is not yet strong enough for a Go or Guardrails decision.

To proceed, the following is needed:

  • TFDA/FDA label data (warnings, contraindications) to close data gap DG001 before any safety evaluation
  • DrugBank-confirmed mechanism of action to close data gap DG002
  • Detailed efficacy outcomes (ORR, PFS) from NCT01838434 and the completed Phase 1 study (PMID 24615778)
  • Clarification on why NCT01796470 was terminated (efficacy vs. safety vs. business reasons) before weighting it further

    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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