产品说明书

TMP269

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Chemical Structure| 1314890-29-3 同义名 : -
CAS号 : 1314890-29-3
货号 : A259571
分子式 : C25H21F3N4O3S
纯度 : 99%+
分子量 : 514.519
MDL号 : MFCD26522023
存储条件：

粉末 Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(204.07 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
靶点

  • HDAC4

    HDAC4, IC50:157 nM

  • HDAC9

    HDAC9, IC50:23 nM

  • HDAC7

    HDAC7, IC50:43 nM

  • HDAC5

    HDAC5, IC50:97 nM
描述 TMP269, at a concentration of 10 μM, does not affect mitochondrial activity or the viability of human CD4+ T cells, indicating its safety profile at this dosage for such cells and suggesting its utility in identifying the natural targets of class IIa HDAC enzymes[1]. In IEC-18 intestinal epithelial cells, TMP269 halts cell cycle progression, DNA synthesis, and proliferation that is typically initiated following activation of G protein-coupled receptors/PKD1[2]. Similarly, TMP269 amplifies the cytotoxicity brought on by CFZ in multiple myeloma (MM) cell lines through the upregulation of ATF4 and CHOP, driving apoptosis. This effect is achieved without causing hyperacetylation of histone H3K9 or α-tubulin, confirming its specificity for not inhibiting class I or IIb HDACs. TMP269-induced cytotoxicity correlates with the activation of apoptosis, as evidenced by the cleavage of caspase-8, -9, -3, and PARP[3].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

1.94mL

0.39mL

0.19mL

9.72mL

1.94mL

0.97mL

19.44mL

3.89mL

1.94mL
参考文献

[1]Lobera M, et al. Selective class IIa histone deacetylase inhibition via a nonchelating zinc-binding group. Nat Chem Biol. 2013 May;9(5):319-25.

[2]Sinnett-Smith J, et al. Protein kinase D1 mediates class IIa histone deacetylase phosphorylation and nuclear extrusion in intestinal epithelial cells: role in mitogenic signaling. Am J Physiol Cell Physiol. 2014 May 15;306(10):C961-71.

[3]Kikuchi S, et al. Class IIa HDAC inhibition enhances ER stress-mediated cell death in multiple myeloma. Leukemia. 2015 Sep;29(9):1918-1927.

[4]EricSalgado, et al. Volume 503 HDAC9 overexpression confers invasive and angiogenic potential to triple negative breast cancer cells via modulating microRNA-206. Biochemical and Biophysical Research Communications.