EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72532_C
酪氨酸激酶抑制剂；抑制ABL、PDGFR和KIT
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总览
甲磺酸伊马替尼是第一代酪氨酸激酶抑制剂，可选择性靶向某些酪氨酸激酶，包括ABL、血小板衍生生长因子受体 (PDGFR) 和KIT (Druker, 2008; Müller)。
分化
·抑制原代培养的人间充质干细胞的增殖，促进成脂性分化而非成骨性分化（Fierro et al.）。
·在培养的成骨细胞中诱导成骨细胞分化，并减少小鼠骨髓培养中的破骨细胞生成（O’Sullivan et al.）。
癌症研究
·在慢性粒细胞白血病 (CML) 中，伊马替尼抑制致癌蛋白BCR-ABL，该蛋白是费城染色体基因融合的产物 (Carroll et al.; Druker et al., 1996)。
·抑制真性红细胞增多症患者外周血单个核细胞的自主红细胞生成（Oehler et al.）。
细胞类型
脂肪细胞，癌细胞及细胞系，白血病/淋巴瘤细胞，间充质干/祖细胞，成骨细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
分化
研究领域
癌症，干细胞生物学
CAS 编号
220127-57-1
化学式
C₂₉H₃₁N₇O · CH₄SO₃
纯度
≥98%
通路
酪氨酸激酶
靶点
ABL，KIT，PDGFR
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (2)
文献 (7)
Imatinib and its successors--how modern chemistry has changed drug development. Current pharmaceutical design 2009 JAN
Abstract
Since protein kinases are frequently mutated or otherwise deregulated in human malignancies, they serve as a target for differentiating between tumor cells and normal tissues. Imatinib mesylat (IM), an inhibitor of the BCR-ABL tyrosine kinase was introduced in 2001 and has revolutionized the treatment of patients with chronic myeloid leukemia (CML). Since 2005 a second generation of tyrosine kinase inhibitors is to follow in Imatinib's footsteps: The development of these new small molecules was promoted by the identification of potential target kinases within the cellular signaling apparatus. Modern biochemical tools provide relevant amounts of these target kinases necessary for high throughput screening (HTS) campaigns and for elucidation of their 3-D structure by crystallography. Supported by computational chemistry the resulting data have enabled rational drug design. In this review low molecular weight inhibitors used for the CML treatment are summarized, pointing out their chemical similarities and differences.
Translation of the Philadelphia chromosome into therapy for CML. Blood 2008 DEC
Abstract
Throughout its history, chronic myeloid leukemia (CML) has set precedents for cancer research and therapy. These range from the identification of the first specific chromosomal abnormality associated with cancer to the development of imatinib as a specific, targeted therapy for the disease. The successful development of imatinib as a therapeutic agent for CML can be attributed directly to decades of scientific discoveries. These discoveries determined that the BCR-ABL tyrosine kinase is the critical pathogenetic event in CML and an ideal target for therapy. This was confirmed in clinical trials of imatinib, with imatinib significantly improving the long-term survival of patients with CML. Continuing in this tradition of scientific discoveries leading to improved therapies, the understanding of resistance to imatinib has rapidly led to strategies to circumvent resistance. Continued studies of hematologic malignancies will allow this paradigm of targeting molecular pathogenetic events to be applied to many additional hematologic cancers.
Imatinib promotes osteoblast differentiation by inhibiting PDGFR signaling and inhibits osteoclastogenesis by both direct and stromal cell-dependent mechanisms. Journal of bone and mineral research 2007 NOV
Abstract
UNLABELLED: Several lines of evidence suggest that imatinib may affect skeletal tissue. We show that inhibition by imatinib of PDGFR signaling in osteoblasts activates osteoblast differentiation and inhibits osteoblast proliferation and that imatinib inhibits osteoclastogenesis by both stromal cell-dependent and direct effects on osteoclast precursors. INTRODUCTION: Imatinib mesylate, an orally active inhibitor of the c-abl, c-kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is in clinical use for the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal cell tumors. Interruption of both c-kit and c-abl signaling in mice induces osteopenia, suggesting that imatinib might have adverse effects on the skeleton. However, biochemical markers of bone formation increase in patients with CML starting imatinib therapy, whereas bone resorption is unchanged, despite secondary hyperparathyroidism. We assessed the actions of imatinib on bone cells in vitro to study the cellular and molecular mechanism(s) underlying the skeletal effects we observed in imatinib-treated patients. MATERIALS AND METHODS: Osteoblast differentiation was assessed using a mineralization assay, proliferation by [(3)H]thymidine incorporation, and apoptosis by a TUNEL assay. Osteoclastogenesis was assessed using murine bone marrow cultures and RAW 264.7 cells. RT and multiplex PCR were performed on RNA prepared from human bone marrow samples, osteoblastic cells, and murine bone marrow cultures. Osteoprotegerin was measured by ELISA. RESULTS: The molecular targets of imatinib are expressed in bone cells. In vitro, imatinib increases osteoblast differentiation and prevents PDGF-induced inhibition of this process. Imatinib inhibits proliferation of osteoblast-like cells induced by serum and PDGF. In murine bone marrow cultures, imatinib inhibits osteoclastogenesis stimulated by 1,25-dihydroxyvitamin D(3) and partially inhibits osteoclastogenesis induced by RANKL and macrophage-colony stimulating factor. Imatinib partially inhibited osteoclastogenesis in RANKL-stimulated RAW-264.7 cells. Treatment with imatinib increases the expression of osteoprotegerin in bone marrow from patients with CML and osteoblastic cells. CONCLUSIONS: Taken together with recent in vivo data, these results suggest a role for the molecular targets of imatinib in bone cell function, that inhibition by imatinib of PDGFR signaling in osteoblasts activates bone formation, and that the antiresorptive actions of imatinib are mediated by both stromal cell-dependent and direct effects on osteoclast precursors.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 220127-57-1 |
| Chemical Formula | C₂₉H₃₁N₇O · CH₄SO₃ |
| 纯度 | ≥ 98% |
| Target | ABL, KIT, PDGFR |
| Pathway | Tyrosine Kinase |
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