产品
编 号：F204489
分子式：C21H23ClFNO2
分子量：375.86
分子式：C21H23ClFNO2
分子量：375.86
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 1704801-24-0
产品详情
生物活性：
AX-024 hydrochloride is an orally available, first-in-class inhibitor of the TCR-Nck interaction that selectively inhibits TCR-triggered T cell activation with an IC50 ~1 nM. AX-024 hydrochloride modulates cell signaling by targeting SH3 domains. AX-024 hydrochloride has low-acute toxicity and high potency and selectivity, and strongly inhibit the production of IL-6, TNF-α, IFN-γ, IL-10 and IL-17A.
体内研究：
The AX-024 hydrochloride-treated group presents less scales and reduces skin thickening compare to the vehicle group. AX-024 hydrochloride significantly reduces thickening of both skin layers, but more effectively of the dermis, which rather resembles that of mice treated with a control cream lacking imiquimod (IMQ). AX-024 hydrochloride significantly diminishes the number of airway inflammatory cells in both assays. Mice receiving AX-024 hydrochloride rapidly recovers from neurological impairment and weight loss, becoming symptom-free by day 30, unlike mice that receives the vehicle, in which ataxia and loss of the righting reflex persist.
体外研究：
AX-024 hydrochloride is >10,000-fold more potent than the AX-000 hit in terms of inhibition of TCR-triggered T cell proliferation. The IC50 of AX-024 hydrochloride in this assay is 1 nM, although it shows inhibitory effects at a concentration of 1 pM or less. AX-024 hydrochloride is also a much more potent inhibitor of cytokine release by human peripheral blood mononuclear cells stimulated with anti-CD3 than AX-000, strongly hindering interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ), IL-10, and IL-17A production at a concentration of 10 nM. In CD8+ T cells of OT1 TCR transgenic (OT1Tg) mice bearing wild-type (WT) AX-024 hydrochloride strongly inhibits T cell proliferation at a concentration of 0.1 nM when OT1Tg T cells are WT for the PRS mutation. Coimmunoprecipitation experiments in these cells show that Nck recruitment to the TCR is induced upon stimulation in the absence of drug but is inhibited in the presence of AX-024 hydrochloride in a dose-dependent manner at concentrations starting from 1 nM.
AX-024 hydrochloride is an orally available, first-in-class inhibitor of the TCR-Nck interaction that selectively inhibits TCR-triggered T cell activation with an IC50 ~1 nM. AX-024 hydrochloride modulates cell signaling by targeting SH3 domains. AX-024 hydrochloride has low-acute toxicity and high potency and selectivity, and strongly inhibit the production of IL-6, TNF-α, IFN-γ, IL-10 and IL-17A.
体内研究：
The AX-024 hydrochloride-treated group presents less scales and reduces skin thickening compare to the vehicle group. AX-024 hydrochloride significantly reduces thickening of both skin layers, but more effectively of the dermis, which rather resembles that of mice treated with a control cream lacking imiquimod (IMQ). AX-024 hydrochloride significantly diminishes the number of airway inflammatory cells in both assays. Mice receiving AX-024 hydrochloride rapidly recovers from neurological impairment and weight loss, becoming symptom-free by day 30, unlike mice that receives the vehicle, in which ataxia and loss of the righting reflex persist.
体外研究：
AX-024 hydrochloride is >10,000-fold more potent than the AX-000 hit in terms of inhibition of TCR-triggered T cell proliferation. The IC50 of AX-024 hydrochloride in this assay is 1 nM, although it shows inhibitory effects at a concentration of 1 pM or less. AX-024 hydrochloride is also a much more potent inhibitor of cytokine release by human peripheral blood mononuclear cells stimulated with anti-CD3 than AX-000, strongly hindering interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ), IL-10, and IL-17A production at a concentration of 10 nM. In CD8+ T cells of OT1 TCR transgenic (OT1Tg) mice bearing wild-type (WT) AX-024 hydrochloride strongly inhibits T cell proliferation at a concentration of 0.1 nM when OT1Tg T cells are WT for the PRS mutation. Coimmunoprecipitation experiments in these cells show that Nck recruitment to the TCR is induced upon stimulation in the absence of drug but is inhibited in the presence of AX-024 hydrochloride in a dose-dependent manner at concentrations starting from 1 nM.
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