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Merck
CN

R0158

Sigma-Aldrich

RepSox

≥98% (HPLC), solid, TGF-β RI kinase inhibitor

别名:

E-616452; 2-[3-(6-甲基-2-吡啶基)-1H-吡唑-4-基]-1,5-萘啶

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About This Item

经验公式(希尔记法):
C17H13N5
分子量:
287.32
MDL编号:
UNSPSC代码:
51111800
PubChem化学物质编号:
NACRES:
NA.77

产品名称

RepSox, ≥98% (HPLC)

质量水平

方案

≥98% (HPLC)

表单

solid

溶解性

DMSO: >20 mg/mL

储存温度

2-8°C

SMILES字符串

Cc1cccc(n1)-c2n[nH]cc2-c3ccc4ncccc4n3

InChI

1S/C17H13N5/c1-11-4-2-5-16(20-11)17-12(10-19-22-17)13-7-8-14-15(21-13)6-3-9-18-14/h2-10H,1H3,(H,19,22)

InChI key

LBPKYPYHDKKRFS-UHFFFAOYSA-N

应用

RepSox已被用于转化生长因子β激酶1型受体(ALK5)的抑制剂。此外,还可用于基本培养基成分,以培养人类多能干细胞。

生化/生理作用

RepSox 抑制 TGF-β 受体信号。
RepSox 抑制 TGF-β 受体信号。逆转录病毒转导 Sox2、Oct4 和 Klf4 基因导致体细胞直接重编程为诱导多能干细胞 (iPSC)。
RepSox通过抑制SMAD族成员3 (Smad3)和c-Jun n -端激酶(JNK)途径/激活蛋白质1 (AP-1)途径,抑制破骨细胞分化、骨组织吸收和卵巢切除术(OVX)诱导的骨质疏松症(OP)。

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Yumiko Mihara et al.
The Journal of clinical endocrinology and metabolism, 105(12) (2020-09-03)
To identify the upstream regulators (URs) involved in the onset and pathogenesis of ovarian endometrioma. Recently, a method called Significance-based Modules Integrating the Transcriptome and Epigenome (SMITE) that uses transcriptome data in combination with publicly available data for identifying URs
Phosphorylation of NEUROG3 links endocrine differentiation to the cell cycle in pancreatic progenitors
Krentz N, et al.
Developmental Cell, 41(2), 129-142 (2017)
Small molecule inhibitor RepSox prevented ovariectomy-induced osteoporosis by suppressing osteoclast differentiation and bone resorption
Mei L, et al.
Journal of Cellular Physiology, 233(12) (2018)
Establishment of a normal-derived estrogen receptor-positive cell line comparable to the prevailing human breast cancer subtype
Hopkinson B, et al.
Testing, 8(6), 10580-10580 (2017)
Alice C Newman et al.
Nature communications, 8(1), 1537-1537 (2017-11-18)
Macroautophagy can regulate cell signalling and tumorigenesis via elusive molecular mechanisms. We establish a RAS mutant cancer cell model where the autophagy gene ATG5 is dispensable in A549 cells in vitro, yet promotes tumorigenesis in mice. ATG5 represses transcriptional activation

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