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Merck
CN

SML1741

TH1020

≥95% (HPLC)

别名:

4-((4-苄基-5-(吡啶-4-基)-4H-1,2,4-三唑-3-基)硫基]吡啶基[3 ′,2′,4, 5]-噻吩并[3,2-d]嘧啶, 4-[[4-(苯甲基)-5-(4-吡啶基)-4H-1,2,4-三唑-3-基]硫基]-吡啶基[3′,2′:4 ,5]噻吩并[3,2-d]嘧啶

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关于此项目

经验公式(希尔记法):
C23H15N7S2
化学文摘社编号:
分子量:
453.54
UNSPSC Code:
51111800
PubChem Substance ID:
NACRES:
NA.77
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InChI key

CBBXTGWSGPEJEE-UHFFFAOYSA-N

InChI

1S/C23H15N7S2/c1-2-5-15(6-3-1)13-30-20(16-8-11-24-12-9-16)28-29-23(30)32-22-19-18(26-14-27-22)17-7-4-10-25-21(17)31-19/h1-12,14H,13H2

SMILES string

C1(C2=CC=NC=C2)=NN=C(SC3=NC=NC4=C3SC5=C4C=CC=N5)N1CC6=CC=CC=C6

assay

≥95% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 3 mg/mL, clear (warmed)

storage temp.

2-8°C

Quality Level

Application

TH1020已用于抑制猪肠单层上皮细胞和小鼠中的toll样受体5(TLR5)。

Biochem/physiol Actions

TH1020介导肿瘤坏死因子-α(TNF-α)相关信号传导的抑制,它通过结合TLR5二聚体之间的分子界面以破坏四聚体复合物的形成。
TH1020是一种无细胞毒性的无细胞毒性toll样受体5(TLR5)/鞭毛蛋白复合物抑制剂。
TH1020是一种无细胞毒性的无细胞毒性toll样受体5(TLR5)/鞭毛蛋白复合物抑制剂。TH1020可选择地阻止鞭毛蛋白诱导的TLR5信号转导,而不影响配体诱导的TLR2、TLR3、TLR4、TLR7或TLR8的激活。

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Yu Luo et al.
Veterinary research, 50(1), 48-48 (2019-06-22)
Enterotoxigenic Escherichia coli (ETEC) are an important cause of post-weaning diarrhea (PWD) in piglets. The IL-17 cytokine family is well known to play important roles in the host defense against bacterial infections at the mucosa. Previously, we reported the potential
Lei Yan et al.
ChemMedChem, 11(8), 822-826 (2015-12-05)
Protein-protein interactions have been regarded as "undruggable" despite their importance in many biological processes. The complex formed between host toll-like receptor 5 (TLR5) and flagellin, a globular protein that is the main component of a bacterial flagellum, plays a vital role
Norimitsu Morioka et al.
Journal of neurochemistry, 150(6), 738-758 (2019-07-06)
Intrathecal treatment with recombinant high-mobility group box-1 (rHMGB1) in naïve mice leads to a persistent and significantly decreased hind paw withdrawal threshold to mechanical stimuli, suggesting that spinal HMGB1 evokes abnormal pain processing. By contrast, repeated intrathecal treatment with anti-HMGB1

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