1. Apoptosis NF-κB Metabolic Enzyme/Protease Immunology/Inflammation
  2. Ferroptosis Keap1-Nrf2 FOXO NO Synthase Quinone Reductase
  3. NPB-1575

NPB-1575 是一种强效的,口服有效的并且能通过血脑屏障的抗炎剂。NPB-1575 通过激活 IRS2/Nrf2/NF-κB 来减轻神经炎症并抵抗铁死亡 (ferroptosis)。NPB-1575 对脑缺血损伤具有保护作用并改善神经功能预后。NPB-1575 可用于局部缺血性中风的研究。

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NPB-1575 Chemical Structure

NPB-1575 Chemical Structure

CAS No. : 161984-54-9

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

NPB-1575 is a potent, orally active and brain-penetrant anti-inflammatory agent. NPB-1575 mitigates neuroinflammation and resists ferroptosis by activating the IRS2/Nrf2/NF-κB axis. NPB-1575 shows protective effect against cerebral ischemic injury and improve the neurological functional prognosis. NPB-1575 can be used for the study of ischemic stroke[1].

体外研究
(In Vitro)

NPB-1575 (1-10 μM, 2 h) 通过 IRS2/Akt 信号通路激活 Nrf 2 并抑制 FOXO 1,在 LPS 刺激的 BV2 细胞中具有显著的体外抗炎效应[1]
NPB-1575 (1-10 μM) 通过上调 IRS2 减弱了原代小胶质细胞中的炎症反应[1]
NPB-1575 (1-10 μM) 在原代神经元和小胶质细胞共培养模型中通过上调 IRS2 抑制了缺血性中风中的铁死亡[1]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: LPS (HY-D1056) (1 μg/mL)-stimulated BV2 microglial cells
Concentration: 1, 3, 10 μM
Incubation Time: Cultured for 6 h and then stimulated with LPS for 6 h
Result: Significantly reduced iNOS and Iba1 protein expression dose-dependently.
Significantly increased IRS2 and phosphorylation of AKT.
Increased the levels of Nrf2, HO-1 and NQO-1 concentration-dependently.
Markedly reduced the levels of total FOXO1 and nucleus FOXO1.
Be blocked by IRS2 knockout, FOXO1 overexpression, LY294002(HY-10108) and ML385 (HY-100523).
Reduced NO and TNF-α releases.

Western Blot Analysis[1]

Cell Line: Primary neuron-microglia transwell cell, following LPS stimulation
Concentration: 1, 3, 10 μM
Incubation Time: 12 h
Result: Reversed the ferroptosis of neurons.
Regulated the levels of TFR1, ACSL4, SLC7A11 and GPX4.
体内研究
(In Vivo)

NPB-1575 (25 mg/kg, p.o.,术后单次给药) 在 pMCAO 大鼠中通过 IRS2 可以减轻脑缺血时的神经炎症,抵抗铁死亡[1]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Permanent occlusion of middle cerebral artery (pMCAO) model established in Male Sprague-Dawley rats with a weight of 260–280 g[1]
Dosage: 25 mg/kg
Administration: Oral gavage (p.o.), 5 min to 4 h after surgery (pMCAO), and behavioral recovery (limb-placing test, rotarod) at 3, 7, and 28 days post-pMCAO.
Result: Reduced the cerebral infarction volume of rats at 3 and 7 days after pMCAO.
Showed significant improvement in behavioral recovery up to 28 days after pMCAO.
Significantly increased level of IRS2 and the protein expression in the brain tissue.
Significantly reduced the levels of CD68, iNOS and NF-κB.
Persistent suppression of microglial activation (Iba1) and pro-inflammatory cytokines (TNF-α, IL-6).
Promoted AKT phosphorylation, raised Nrf2, HO-1, and NQO-1 levels and reduced FOXO1 expression.
Improved TFR1, ACSL4 and SLC7A11 and GPX4 levels via IRS2 and the effects were reversed by IRS2 knockdown.
分子量

314.38

Formula

C19H22O4

CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

纯度 & 产品资料
参考文献
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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