A Phase Ib/II Study of the JAK1 Inhibitor, Itacitinib, plus

Publication/Presentation Date

1-1-2019

Abstract

LESSONS LEARNED: Itacitinib in combination with

BACKGROUND: Cytokine-mediated signaling via JAK/STAT is central to tumor growth, survival, and systemic inflammation, which is associated with cancer cachexia, particularly in pancreatic cancer. Because of their centrality in the pathogenesis of cancer cachexia and progression, JAK isozymes have emerged as promising therapeutic targets. Preclinical studies have demonstrated antiproliferative effects of JAK/STAT pathway inhibition in both in vitro and in vivo models of cancer, including pancreatic cancer.

METHODS: This phase Ib/II dose-optimization study assessed itacitinib, a selective JAK1 inhibitor, combined with

RESULTS: Among 55 patients in Part 1, 6 developed seven hematologic dose-limiting toxicities (Cycle 1). Itacitinib 300 mg plus

CONCLUSION: Itacitinib plus chemotherapy demonstrated acceptable safety and clinical activity in patients with advanced solid tumors including pancreatic cancers. This study was terminated early (sponsor's decision) based on negative phase III results for a JAK1/2 inhibitor in previously treated advanced pancreatic cancer.

Volume

24

Issue

1

First Page

14

Last Page

14

ISSN

1549-490X

Disciplines

Medicine and Health Sciences

PubMedID

30115734

Department(s)

Hematology-Medical Oncology Division

Document Type

Article

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