Targeting the JAK-STAT pathway in lymphoma: a focus on pacritinib

Expert Opin Investig Drugs. 2013 Jun;22(6):775-85. doi: 10.1517/13543784.2013.775244. Epub 2013 Feb 26.

Abstract

Introduction: The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway mediates signaling by cytokine, chemokine and growth factor receptors on cell surface to the nucleus. JAK/STAT pathway is aberrantly activated in a variety of lymphomas, with a dual role of promoting cell survival/proliferation and immune evasion.

Areas covered: This review describes the preclinical rationale behind the development of JAK inhibitors in lymphoma, some of which are being evaluated in Phase I/II studies, and summarizes the characteristics and clinical results of different JAK inhibitors in clinical development. Available preclinical and clinical data about JAK inhibition in lymphoid malignancies were reviewed using a PubMed access. To date, pacritinib (SB1518), a selective JAK2/FLT3 inhibitor is the first and only JAK inhibitor that has been evaluated in patients with relapsed lymphoma.

Expert opinion: The preclinical rationale behind the development of pacritinib in lymphoproliferative neoplasms is strong, as the deregulation of the JAK/STAT pathway is involved in the pathogenesis of multiple lymphoma subtypes, although with different mechanisms. Pacritinib demonstrated safety and early clinical efficacy in a variety of lymphoma histologic types, providing the first proof of principle of the potential clinical value of targeting JAK/STAT pathway in lymphoma.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / pharmacology
  • Bridged-Ring Compounds / adverse effects
  • Bridged-Ring Compounds / pharmacology*
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Drug Design
  • Humans
  • Janus Kinase 2 / antagonists & inhibitors*
  • Lymphoma / drug therapy*
  • Lymphoma / pathology
  • Neoplasm Recurrence, Local
  • Protein Kinase Inhibitors / adverse effects
  • Protein Kinase Inhibitors / pharmacology
  • Pyrimidines / adverse effects
  • Pyrimidines / pharmacology*
  • STAT Transcription Factors / metabolism
  • fms-Like Tyrosine Kinase 3 / antagonists & inhibitors

Substances

  • 11-(2-pyrrolidin-1-ylethoxy)-14,19-dioxa-5,7,26-triazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8,10,12(27),16,21,23-decaene
  • Antineoplastic Agents
  • Bridged-Ring Compounds
  • Protein Kinase Inhibitors
  • Pyrimidines
  • STAT Transcription Factors
  • fms-Like Tyrosine Kinase 3
  • Janus Kinase 2