2. Academic Validation
  3. NS-018, a selective JAK2 inhibitor, preferentially inhibits CFU-GM colony formation by bone marrow mononuclear cells from high-risk myelodysplastic syndrome patients

NS-018, a selective JAK2 inhibitor, preferentially inhibits CFU-GM colony formation by bone marrow mononuclear cells from high-risk myelodysplastic syndrome patients

  • Leuk Res. 2014 May;38(5):619-24. doi: 10.1016/j.leukres.2014.03.001.
Junya Kuroda 1,  Ayumi Kodama 2,  Yoshiaki Chinen 3,  Yuji Shimura 3,  Shinsuke Mizutani 3,  Hisao Nagoshi 3,  Tsutomu Kobayashi 3,  Yosuke Matsumoto 3,  Yohei Nakaya 2,  Ayako Tamura 2,  Yutaka Kobayashi 4,  Haruna Naito 2,  Masafumi Taniwaki 3
Affiliations

Affiliations

  • 1 Division of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan. Electronic address: [email protected].
  • 2 Discovery Research Laboratories, Nippon Shinyaku Co., Ltd, Kyoto, Japan.
  • 3 Division of Hematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
  • 4 Department of Hematology, Kyoto Second Red Cross Hospital, Kyoto, Japan.
PMID: 24679585 DOI: 10.1016/j.leukres.2014.03.001
Abstract

JAK2/STAT signaling promotes survival and expansion of myelodysplastic syndrome (MDS) clones, but little is known about the potential of JAK2/STAT as a therapeutic target in MDS. We investigated the effect of NS-018, a novel antagonist for JAK2, on the colony-forming ability of bone marrow mononuclear cells (BMMNCs) from high-risk MDS patients. NS-018 decreased colony-forming unit-granulocyte/macrophage (CFU-GM) colony numbers from MDS-derived BMMNCs in a dose-dependent manner, and this effect was significantly more potent than against normal BMMNCs. In addition, NS-018 suppressed the phosphorylation of STAT3 in colony-forming cells from MDS patients. Collectively, NS-018 could be a new therapeutic option for high-risk MDS.

Keywords

CFU-GM; JAK2; Myelodysplastic syndrome; NS-018; STAT.

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