GSK1838705A
- 型號： HY-13020
- 更新時間： 2024-06-03
- 上一個：HY-13011CH5424802
- 下一個：13274555mm配重透析袋夾子
訂貨咨詢：；；；
： 865512910 1656711470
備注：本公司銷售的所有產(chǎn)品僅用于生化科研試驗
HY-13020 GSK1838705A的機制（別名GSK1838705A）：ALK
技術參數(shù)：價格和可用性
M.Wt：532.57
分子式：C27H29FN8O3
純度：> 98％
貯存：貯存在-20℃2年
CAS號：1116235-97-2
溶解性：DMSO≥107mg/mL;水濃度為1mg/mL;乙醇濃度為1mg/mL
生物活性的：
是一種有效的小分子IGF-IR，胰島素受體和間變性淋巴瘤激酶（ALK）抑制劑的IC50分別為2.0，1.6和0.5海里。 防止來自固體和惡性血液病，包括多發(fā)性骨髓瘤，尤因氏肉瘤，并阻礙在體內(nèi)生長的人類腫瘤異種移植的細胞系在體外增殖。盡管胰島素受體的抑制作用，對葡萄糖穩(wěn)態(tài)的影響zui小，得到在有效劑量。在0.1和0.3毫克/公斤口服單劑量的導致到35％和65％的預防，IGF-IR的磷酸化，分別，而劑量≥1毫克/公斤，導致完成的配體誘導的IGF-IR的磷酸化的抑制。同時，在30毫克/公斤的劑量，預防持續(xù)？化合物注射后的24小時。 也抑制了間變性淋巴瘤激酶（ALK），介導的異常??增長的間變性大細胞淋巴瘤，神經(jīng)母細胞瘤，非小細胞肺癌的一個子集。由于其抑制ALK中，提供了良好的耐受劑量在體內(nèi)引起的ALK-依賴性腫瘤*消退。
HY-13020 (Synonyms GSK 1838705A) Mechanisms:ALK
Technical Data: Price and Availability of
M.Wt: 532.57
Formula: C27H29FN8O3
Purity: >98%
Storage: at -20℃ 2 years
CAS No.: 1116235-97-2
Solubility: DMSO ≥107mg/mL; Water <1mg/mL; Ethanol <1mg/mL
5mg
10mg
50mg
200mg
Biological Activity of :
is a potent small-molecule IGF-IR, the insulin receptor and anaplastic lymphoma kinase (ALK) inhibitor with IC50 of 2.0, 1.6 and 0.5 nM, respectively. prevents the in vitro proliferation of cell lines derived from solid and hematologic malignancies, including multiple myeloma and Ewing’s sarcoma, and retards the growth of human tumor xenografts in vivo. Despite the inhibitory effect of on insulin receptor, minimal effects on glucose homeostasis were obtained at efficacious doses. A single oral dose of at 0.1 and 0.3 mg/kg led to 35% and 65% prevention of IGF-IR phosphorylation, respectively, whereas doses ≥1 mg/kg led to complete inhibition of ligand-induced IGF-IR phosphorylation. Meanwhile, at a dose of 30 mg/kg, prevention was lasted for ?24 hours after compound injection. also suppresses the anaplastic lymphoma kinase (ALK), which mediates the aberrant growth of anaplastic large-cell lymphomas, some neuroblastomas, and a subset of non–small cell lung cancers. Due to its inhibition of ALK, gives rise to complete regression of ALK-dependent tumors in vivo at well-tolerated doses