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WP1066,一种新型的JAK2抑制剂,可抑制携带JAK2 V617F突变的人类红细胞系细胞的增殖并诱导其凋亡。

WP1066, a novel JAK2 inhibitor, suppresses proliferation and induces apoptosis in erythroid human cells carrying the JAK2 V617F mutation.

作者信息

Verstovsek Srdan, Manshouri Taghi, Quintás-Cardama Alfonso, Harris David, Cortes Jorge, Giles Francis J, Kantarjian Hagop, Priebe Waldemar, Estrov Zeev

机构信息

Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.

出版信息

Clin Cancer Res. 2008 Feb 1;14(3):788-96. doi: 10.1158/1078-0432.CCR-07-0524.

Abstract

PURPOSE

The discovery of an activating somatic mutation in codon 617 of the gene encoding the Janus kinase (JAK)-2 (JAK2 V617F) in patients with myeloproliferative disorders has opened new avenues for the development of targeted therapies for these malignancies. However, no effective JAK2 inhibitors are currently available for clinical use.

EXPERIMENTAL DESIGN

We investigated the activity of (E)-3(6-bromopyridin-2-yl)-2-cyano-N-(S0-1phenylethyl)acrylamide (WP1066), a novel analogue of the JAK2 inhibitor AG490, in JAK2 V617F-positive erythroleukemia HEL cells and in blood cells from patients with polycythemia vera.

RESULTS

We found that WP1066 significantly inhibited JAK2 and its downstream signal transducer and activator of transcription-3, signal transducer and activator of transcription-5, and extracellular signal-regulated kinase-1/2 pathways in a dose- and time-dependent manner. As a result, WP1066 concentrations in the low micromolar range induced time- and dose-dependent antiproliferative and proapoptotic effects in HEL cells. As expected, WP1066 inhibited the proliferation of peripheral blood hematopoietic progenitors of patients with polycythemia vera carrying the JAK2 V617F mutation in a dose-dependent manner.

CONCLUSIONS

Our data suggest that WP1066 is active both in vitro and ex vivo and should be further developed for the treatment of neoplasms expressing the JAK2 V617F mutation.

摘要

目的

在骨髓增殖性疾病患者中发现编码Janus激酶(JAK)-2的基因第617密码子的激活体细胞突变(JAK2 V617F),为这些恶性肿瘤的靶向治疗开辟了新途径。然而,目前尚无有效的JAK2抑制剂可用于临床。

实验设计

我们研究了JAK2抑制剂AG490的新型类似物(E)-3(6-溴吡啶-2-基)-2-氰基-N-(S0-1-苯乙基)丙烯酰胺(WP1066)在JAK2 V617F阳性红白血病HEL细胞和真性红细胞增多症患者血细胞中的活性。

结果

我们发现WP1066以剂量和时间依赖性方式显著抑制JAK2及其下游信号转导和转录激活因子-3、信号转导和转录激活因子-5以及细胞外信号调节激酶-1/2途径。结果,低微摩尔范围内的WP1066浓度在HEL细胞中诱导了时间和剂量依赖性的抗增殖和促凋亡作用。正如预期的那样,WP1066以剂量依赖性方式抑制携带JAK2 V617F突变的真性红细胞增多症患者外周血造血祖细胞的增殖。

结论

我们的数据表明WP1066在体外和体内均具有活性,应进一步开发用于治疗表达JAK2 V617F突变的肿瘤。

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