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首页-小分子抑制剂&激动剂-Immunology/Inflammation-NOD-like Receptor (NLR)-JT002
JT002

Chemical Structure : JT002

CAS No.: 2238820-43-2

JT002 (JT 002, JT-002)

货号: PC-21079Not For Human Use, Lab Use Only.

JT002 is a potent and selective inhibitor of NLRP3 inflammasome with IC50 of 6 nM (IL-1β production from hPBMCs), inhibits NLRP3 mediated cytokine production and pyroptosis.

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纯度 & COA & 质检文件 纯度: >98% (HPLC)

生物&药学活性

JT002 is a potent and selective inhibitor of NLRP3 inflammasome with IC50 of 6 nM (IL-1β production from hPBMCs), inhibits NLRP3 mediated cytokine production and pyroptosis.
JT002 potently inhibits IL-1α, IL-1β and IL-18 production with mean IC50 values of 3 nM, 4 nM and 4 nM, respectively, in human peripheral blood mononuclear cells (hPBMCs), with no effect on tumor necrosis factor alpha (TNFα) production up to 1 µM.
JT002 inhibits IL-1β production from human, mouse and rat PBMCs with mean IC50 values of 6, 25 and 159 nM, respectively.
JT002 potently inhibits IL-1β production under the alternative NLRP3 activating conditions with IC50 of 32 nM.
JT002 blocks canonical NLRP3-dependent IL-1β production activated downstream of ATP, nigericin, CHC or MSU with mean IC50 values of 5, 23, 2 and 3 nM, respectively and inhibits non-canonical induced IL-1β production with a mean IC50 value of 30 nM, with no inhibition of IL-1β production after NLRP1, NLRC4 or AIM2 activation at 10 uM.
JT002 blocks NLRP3 inflammasome complex formation and downstream pathway activation.
JT002 (30 mg/kg, oral) prevents disease progression in the Nlrp3A350V/+ knock-in murine model of Muckle Wells syndrome.
JT002 (25 mg/kg) attenuates airway inflammation and airway hyperresponsiveness in a mouse model of IL-17-dependent neutrophilic asthma.

物理化学性质&存储条件

分子量 432.50
分子式 C20H24N4O5S
外观性状 Solid
CAS No.
储存条件
固体粉末
-20°C 12 个月; 4°C 6 个月
配置液
-80°C 6 个月; -20°C 6 个月
Shipping
Solubility

10 mM in DMSO

Chemical Name/SMILES

O=S(C1=C2OC[C@@H](OC)CN2N=C1)(NC(NC3=C4CCCC4=CC5=C3CCC5)=O)=O

参考文献

1. Ambrus-Aikelin G, et al. Sci Rep. 2023 Aug 19;13(1):13524.

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