figshare
Browse
ieid_a_1312338_sm4903.docx (20.25 kB)

Duvelisib: a phosphoinositide-3 kinase δ/γ inhibitor for chronic lymphocytic leukemia

Download (20.25 kB)
Version 2 2020-08-24, 13:02
Version 1 2017-04-24, 07:28
journal contribution
posted on 2017-04-24, 07:28 authored by Hima V. Vangapandu, Nitin Jain, Varsha Gandhi

Introduction: Frontline chemotherapy is successful against chronic lymphocytic leukemia (CLL), but results in untoward toxicity. Further, prognostic factors, cytogenetic anomalies, and compensatory cellular signaling lead to therapy resistance or disease relapse. Therefore, for the past few years, development of targeted therapies is on the rise. PI3K is a major player in the B-cell receptor (BCR) signaling axis, which is critical for the survival and maintenance of B cells. Duvelisib, a PI3K δ/γ dual isoform specific inhibitor that induces apoptosis and reduces cytokine and chemokine levels in vitro, holds promise for CLL.

Areas covered: Herein, we review PI3K isoforms and their inhibitors in general, and duvelisib in particular; examine literature on preclinical investigations, pharmacokinetics and clinical studies of duvelisib either as single agent or in combination, for patients with CLL and other lymphoid malignancies.

Expert opinion: Duvelisib targets the PI3K δ isoform, which is necessary for cell proliferation and survival, and γ isoform, which is critical for cytokine signaling and pro-inflammatory responses from the microenvironment. In phase I clinical trials, duvelisib as a single agent showed promise for CLL and other lymphoid malignancies. Phase II and III trials of duvelisib alone or in combination with other agents are ongoing.

Funding

This work was supported in part by grant CLL PO1 CA81534 from the National Cancer Institute, Department of Health and Human Services; Alliance grant from the CLL Global Research Foundation; and Sponsored Research Agreement from Infinity Pharmaceuticals.

History

Usage metrics

    Expert Opinion on Investigational Drugs

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC