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TCS 359
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
TCS 359图片
CAS NO:301305-73-7
包装与价格：
包装价格(元)
10mM (in 1mL DMSO)电议
10mg电议
50mg电议

产品介绍
TCS 359 是一种 2-acylaminothiophene-3-carboxamide，是一种有效的选择性 FLT3 抑制剂，IC50 为 42 nM。 TCS 359 抑制 MV4-11 细胞增殖，IC50 为 340 nM。
Cas No.301305-73-7
化学名2-[(3,4-dimethoxybenzoyl)amino]-4,5,6,7-tetrahydro-1-benzothiophene-3-carboxamide
Canonical SMILESCOC1=C(C=C(C=C1)C(=O)NC2=C(C3=C(S2)CCCC3)C(=O)N)OC
分子式C18H20N2O4S
分子量360.43
溶解度≥ 9mg/mL in DMSO
储存条件4°C, protect from light
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

TCS 359 is a potent inhibitor against the fms-like tyrosine kinase-3 (FLT3) [1] [2] with an IC50 value of 0.042 ±0.03 μM [2].

FLT3 is a receptor tyrosine kinase. Via hematopoietic regulation, it plays its important role in the pathogenesis of acute myeloid leukemia (AML) [3].

To the proliferation of MV4-11 cell line (a human acute myeloid leukemia cell line expressing a constitutively activated mutant FLT3), the IC50 of TCS 359 was 0.34 μM [2].

TCS 359 blocked the ability of FLT3 ligand to promote the development of two-cell-embryos to the hatched blastocyst stage in mice. TCS 359 also decreased the expression of FLT3 ligand in early embryos after the four-cell stage. Without exogenous FLT3 ligand, TCS 359 did not affect embryo development [4]. Treated with another FLT3 inhibitor SU5416, 21 of 22 analyzed patients expressed FLT3 protein, 17 expressed phosphorylated FLT3 at baseline. Among these 17 patients expressed phosphorylated FLT3, inhibition of more than 50% relative to baseline was apparent in seven cases, while inhibition ranged from 20-50% relative to baseline was apparent in an additional three cases. FLT3 phosphorylation was detected in whole blood lysates in the majority of AML patients treated with SU5416. Activated FLT3 was detectable in bone marrow aspirates from approximately 50% AML patients [5].

References:
[1].  Trzci'nska-Daneluti A.M., Nguyen L., Jiang C., et al. Use of Kinase Inhibitors to Correct ΔF508-CFTR Function. Molecular & Cellular Proteomics, 2012, 11(9):745-757.
[2].  Patch R.J., Baumann C.A., Liu J., et al. Identification of 2-acylaminothiophene-3-carboxamides as potent inhibitors of FLT3. Bioorganic & Medicinal Chemistry Letters, 2006, 16: 3282-3286.
[3].  Kar R.K., Suryadevara P., Roushan R., et al. Quantifying the Structural Requirements for Designing Newer FLT3 Inhibitors. Medicinal Chemistry, 2012, 8:913-927.
[4].  Nishijima C., Kawamura K., Okamoto N., et al. Regulation of Preimplantation Embryo Development in Mice by FMS-like Tyrosine Kinase 3 Ligand. Journal of Mammalian Ova Research, 2014, 31(1):45-51.
[5].  O'Farrell A.M., Yuen H.A., Smolich B., et al. Effects of SU5416, a small molecule tyrosine kinase receptor inhibitor, on FLT3 expression and phosphorylation in patients with refractory acute myeloid leukemia. Leuk. Res., 2004, 28(7):679-89.