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Related Experiment Video

Updated: Jun 24, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Bortezomib and Waldenstrom's macroglobulinemia.

Laurent Pascal1, Julie Gay, Christophe Willekens

  • 1Service des Maladies du Sang, Hopital Huriez, CHRU Lille, Rue Michel Polonovski, Lille, France.

Expert Opinion on Pharmacotherapy
|April 9, 2009
PubMed
Summary

Waldenstrom's macroglobulinemia (WM) is incurable, necessitating new treatments. Bortezomib, a proteasome inhibitor targeting the NFkB pathway, shows promise for Waldenstrom's macroglobulinemia therapy.

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Area of Science:

  • Hematology
  • Oncology
  • Pharmacology

Background:

  • Waldenstrom's macroglobulinemia (WM) remains an incurable hematologic malignancy.
  • Current therapies offer limited complete response rates and median survival.
  • Novel therapeutic strategies are essential for improving patient outcomes in WM.

Purpose of the Study:

  • To review biological studies and clinical efforts investigating bortezomib for Waldenstrom's macroglobulinemia.
  • To evaluate the potential of targeting the NFkB pathway in WM treatment.
  • To update on the development of bortezomib as a therapeutic agent for WM.

Main Methods:

  • Review of preclinical studies on NFkB pathway inhibition in WM.
  • Analysis of clinical trial data for bortezomib in WM.

Related Experiment Videos

Last Updated: Jun 24, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

  • Examination of bortezomib's mechanism of action, including NFkB pathway inhibition.

    • Main Results:

    • The NFkB pathway is a validated therapeutic target in WM.
    • Bortezomib, a proteasome inhibitor, effectively inhibits the NFkB pathway.
    • Clinical efforts are underway to establish bortezomib as a treatment for WM.

    Conclusions:

    • Bortezomib demonstrates potential as a novel therapeutic agent for Waldenstrom's macroglobulinemia.
    • Targeting the NFkB pathway represents a promising strategy for WM treatment.
    • Further clinical development of bortezomib is warranted for WM.