2. Metabolic Enzyme/Protease Neuronal Signaling NF-κB Immunology/Inflammation Stem Cell/Wnt MAPK/ERK Pathway
  3. Glycosidase Amyloid-β NF-κB COX ERK NO Synthase Interleukin Related
  4. K284-6111

K284-6111 是一种高亲和力且口服活性的 CHI3L1 抑制剂，可抑制 CHI3L1 的表达。K284-6111 抑制 ERK 和 NF-κB 信号通路。K284-6111 抑制 p50 和 p65 的核转位以及 IκB 的磷酸化。K284-6111 通过减轻淀粉样生成和神经炎症改善记忆功能障碍，同时降低炎症蛋白 (如 iNOS、COX-2、GFAP 和 Iba-1) 的水平。K284-6111 减少类特应性皮炎的皮肤炎症，并抑制 LPS (HY-D1056) 诱导的肝损伤。K284-6111 可用于阿尔茨海默症和脓毒症样肝损伤的研究。

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K284-6111

K284-6111 Chemical Structure

CAS No. : 702668-62-0

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10 mg ￥3720
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K284-6111 相关抗体

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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COX COX-1 COX-2 COX-3

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ERK ERK1 ERK2 ERK5 ERK8

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nNOS iNOS eNOS

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IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

K284-6111 is a high-affinity and orally active CHI3L1 inhibitor, and inhibits CHI3L1 expression. K284-6111 inhibits ERK and NF-κB pathway. K284-6111 suppresses nuclear translocation of p50 and p65, and phosphorylation of IκB. K284-6111 improves memory dysfunction by alleviating amyloidogenesis and neuroinflammation, with the reduction of inflammatory proteins (eg: iNOS, COX-2, GFAP, and Iba-1). K284-6111 reduces atopic-like skin inflammation and inhibits LPS (HY-D1056) -induced liver injury. K284-6111 can be used for the study of Alzheimer's diseases and sepsis like hepatic injury[1][2][3][4].

体外研究
(In Vitro)

K284-6111 (0.5-2 μM, 24 h) 降低 Aβ 或 LPS (HY-D1056) 在 BV-2 细胞和星形胶质细胞中诱导的 NO 浓度[1][2]。
K284-6111 (5 μM, 26 h) 降低 CHI3L1 过表达所引起的 BV-2 细胞的神经炎症[1]。
K284-6111 (5 μM, 26 h) 抑制 Aβ 诱导的 BV-2 细胞中 PTX3 的表达[1]。
K284-6111 (0.5-2 μM, 26 h) 阻止 LPS 刺激的 BV-2 细胞和星形胶质细胞中以及 TNF-α/IFN-γ 激活的 HaCaT 细胞的 p50 和 p65 的核转位[2][3] 。
K284-6111 (0.5-2 μM, 26 h) 阻止 LPS 诱导的神经炎症、淀粉样生成以及 Aβ1-42 诱导的 BV-2 细胞和星形胶质细胞凋亡[1][2] 。
K284-6111 (0.5-2 μM, 4-6 h) 抑制 TNF-α/IFN-γ 组合处理的 HaCaT 细胞中 CHI3L1、IL-1β、IL-4、IL-6 TSLP 和 LTF 的水平[3]。
K284-6111 (2 μM, 6 days) 减轻特应性皮炎重建的人类皮肤 (RHS) 模型中的炎症[3]。
K284-6111 (0.5-22 μM，1 h) 降低 LPS 诱导的肝细胞中 CHI3L1、CXCL3 的表达以及细胞因子的释放[4]。
K284-6111 (2 μg/mL，25 h) 降低经人重组 CXCL3 和 LPS 处理的 THLE-2 细胞以及 CXCL3 敲除 THLE-2 细胞经 LPS 处理后的 IL-10 和 IL-4 水平[4]。

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

K284-6111 相关抗体:

Western Blot Analysis[1]

Cell Line: Aβ-induced BV2 cells and CHI3L1 overexpressing BV-2 cells
Concentration: 5 μM
Incubation Time: 26 h
Result: Reduced Aβ-induced expression of inflammatory proteins such as iNOS, COX-2, and IBA-1.

Real Time qPCR[1]

Cell Line: Aβ-induced BV2 cells and CHI3L1 overexpressing BV-2 cells
Concentration: 5 μM
Incubation Time: 26 h
Result: Reduced the mRNA expression level of pro-inflammatory cytokines such as Tnf, Il1b, Il6, and Cd86.

ELISA Assay[3]

Cell Line: HaCaT cells treated with TNF-α/IFN-γ combination
Concentration: 0.5, 1, 2 μM
Incubation Time: 4 h
Result: Decreased the level of CHI3L1, IL-1β, IL-4, IL-6 and TSLP.

Western Blot Analysis[3]

Cell Line: HaCaT cells treated with TNF-α/IFN-γ combination
Concentration: 0.5, 1, 2 μM
Incubation Time: 6 h
Result: Inhibited the nuclear translocation of p50 and p65 and p-IκBα.

Real Time qPCR[4]

Cell Line: LPS-induced hepatic cells
Concentration: 0.5, 1, 2 μM
Incubation Time: 1 h
Result: Reduced the mRNA levels of M1 macrophage protein and cytokines (iNOS, CD86, TNF-α, and IL-6) and M2 macrophage cytokines (MRC1, Arg 1, IL-10, and IL-4).
体内研究
(In Vivo)

K284-6111 (3 mg/kg，灌胃给药，每天一次，持续四周) 缓解了Tg2576 AD小鼠模型中的记忆障碍[1]。
K284-6111 (3 mg/kg，灌胃给药，每日一次，4 周) 预防 Aβ1-42 灌注小鼠的记忆障碍[2]。
K284-6111 (1-2 mg/mL (10-20 μg/cm2)，局部给药，每周 3 次，4 周) 抑制 Phthalic anhydride (HY-I0815) 诱导的特应性皮炎[3]。
K284-6111 (0.25-1 mg/kg，腹腔注射，每三天一次，持续 2 周) 对 LPS 诱导的肝损伤表现出保护作用[4]。

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

Animal Model: Twelve-month-old Tg2576 mice[1]
Dosage: 3 mg/kg
Administration: i.g. once daily for 4 weeks
Result: Increased the mean time spent in the target quadrant.
Showed higher an average step-through latency.
Inhibited the accumulation of Aβ in Tg2576 mouse brain.
Reduced the number of iNOS and COX-2-reactive cells.
Decreased the expression of GFAP, IBA-1, iNOS, and COX-2.
Decreased the expression levels of the markers M1 microglia (Tnf, Il1b, Il6, and Cd86).
Did not affect M2 microglia markers such as Arg1, Mrc1, Tgfb, and Il10.
Reduced the levels of p-IκBα, p-ERK1/2, and p-JNK.
Reduced the levels of PTX3.
Animal Model: Aggregated Aβ1-42 (300 pmol) was unilaterally infused into the brains of 8- to 10-week-old male ICR mice over 14 days[2]
Dosage: 3 mg/kg
Administration: i.g. once daily for 4 weeks
Result: Showed a great reduction in escape latency on day 6.
Showed a shorter escape distance compared to Aβ1-42-infused mice.
Spent much more time in the quadrant zone.
Increased step-through latency.
Reduced the expression of CHI3L1, inflammatory proteins (iNOS and COX-2), and GFAP and Iba-1.
Decreased Aβ-induced mRNA levels of CHI3L1, TNF-α, IL-1β, and IL-6 in brain tissues.
Prevented amyloidogenesis and neuronal cell death in Aβ1-42-infused mice brain.
Decreased the expression of p50 p65 and p-IκBα.
Animal Model: C57BL/6J mice (8-week-old) applied with 5% Phthalic anhydride (PA) solution was spread on the back skin 3 times a week for 4 weeks[3]
Dosage: 1 mg/mL and 2 mg/mL (10 μg or 20 μg/cm2)
Administration: Topical administration 3 times a week for 4 weeks
Result: Reduced epidermal thickness.
Reduced the number of infiltrating mast cells in the skin.
Decreased the serum IgE concentration.
Reduced the lymph node weight.
Reduced the levels of CHI3L1, IL-1β, IL-4, IL-6 and TSLP.
Reduced the mRNA expression of AD-related genes such as TNF-α, IL-1β, IL-4, IL-5, IL-6, IL-13, IL-31, IL-33, and CCL17.
Inhibited the nuclear translocation of p50 and p65 in a dose-dependent manner.
Reduced LTF expression in PA-induced skin tissues.
Animal Model: C57BL/6J mice (8-week-old) were injected with LPS (i.p., 30 mg/kg)[4]
Dosage: 0.25, 0.5, 1 mg/kg
Administration: i.p. once every three days for 2 weeks
Result: Showed the induction of significant liver damage.
Reduced CHI3L1 expression and cytokine release (iNOS, COX-2) in LPS-induced liver injury.
分子量

535.70

Formula

C30H37N3O4S
CAS 号
性状

固体

颜色

White to off-white

运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
细胞实验： 

DMSO 中的溶解度 : 2 mg/mL (3.73 mM; 超声助溶 (<60°C); 吸湿的 DMSO 对产品的溶解度有显著影响，请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.8667 mL 9.3336 mL 18.6672 mL
5 mM --- --- ---
查看完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
=
浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物实验：

以下溶解方案，请直接配制工作液。建议现用现配，在短期内尽快用完。 以下溶剂前显示的百分比是指该溶剂在您配制终溶液中的体积占比； 如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶。

  • 方案 一

    请依序添加每种溶剂： 15% Cremophor EL    85% Saline

    Solubility: 1.67 mg/mL (3.12 mM); 悬浊液; 超声助溶

动物溶解方案计算器
请输入动物实验的基本信息：

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

只
由于实验过程有损耗，建议您多配一只动物的量
计算结果
工作液所需浓度 : mg/mL
纯度 & 产品资料

纯度: 99.94%

COA (285 KB) HNMR (272 KB) LCMS (97 KB)

产品使用指南 (1538 KB)
参考文献

K284-6111 相关分类

完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.8667 mL 9.3336 mL 18.6672 mL 46.6679 mL
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.

Keywords:

K284-6111702668-62-0GlycosidaseAmyloid-βNF-κBCOXERKNO SynthaseInterleukin Relatedβ-amyloid peptideAβAbetaNuclear factor-κBNuclear factor-kappaBCyclooxygenaseExtracellular signal regulated kinasesNitric oxide synthasesNOSILAlzheimer’s diseaseNeuroinflammationCHI3L1LactoferrinAtopic dermatitisInhibitorinhibitorinhibit

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