Psoralidin(Synonyms: 补骨脂定)

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天然产物 天然产物苯丙素类 Phenylpropanoids

Psoralidin (Synonyms: 补骨脂定) 纯度: 99.90%

Psoralidin 是 COX-2 和 5-LOX 的双重抑制剂。具有抗癌，抗菌和抗炎作用。Psoralidin 显著下调 NOTCH1 信号传导。Psoralidin 还极大地诱导 ROS 产生。

Psoralidin(Synonyms: 补骨脂定)

Psoralidin Chemical Structure

CAS No. : 18642-23-4

规格 价格 是否有货 数量
5 mg ￥600 In-stock
10 mg ￥1080 In-stock
50 mg   询价  
100 mg   询价  

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Psoralidin 相关产品

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生物活性

Psoralidin is a dual inhibitor of COX-2 and 5-LOX, regulates ionizing radiation (IR)-induced pulmonary inflammation.Anti-cancer, anti-bacterial, and anti-inflammatory properties[1]. Psoralidin significantly downregulates NOTCH1 signaling. Psoralidin also greatly induces ROS generation[2].

IC50 & Target[1]

COX-2

 

5-LOX

 

体外研究
(In Vitro)

Three breast cancer cell (BCC)populations (ALDH– cells, ALDH+ cells, and commercial BSCSs) are sensitive to Psoralidin treatment (10, 15, 20, and 25 μM; 24 hours) with IC50s ranging from 18 to 21 μM; however, the MCF-12A cells were resistant to Psoralidin[2].
Psoralidin (30 μM; 24 hours) results in a significant induction of apoptosis for ALDH– cells, ALDH+ cells, and commercial BCSCs[2].
Psoralidin treatment also downregulates NOTCH1 expression in both ALDH– and ALDH+ cells[2].

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

Cell Viability Assay[2]

Cell Line: ALDH– cells, ALDH+ cells, commercial breast cancer stem cells (BSCSs), and normal breast epithelial cells (MCF-12A)
Concentration: 10, 15, 50, and 25 μM
Incubation Time: 24 hours
Result: IC50s of 18 to 21 μM for ALDH– cells, ALDH+ cells, commercial BCSCs.

Apoptosis Analysis[2]

Cell Line: ALDH– cells, ALDH+ cells, and commercial BCSCs
Concentration: 20 and 30 μM
Incubation Time: 24 hours
Result: No significant induction of apoptosis was observed for any of the three cell types following treatment at 20 μM. However, 53.60%, 44.1%, and 45.9% of cells were apoptotic at 30 μMin ALDH– cells, ALDH+ cells, and commercial BCSCs, respectively.

体内研究
(In Vivo)

Psoralidin (5 mg/kg) regulates expression of pro-inflammatory cytokines that play an important role in inflammatory diseasesin IR-irradiated lung of BALB/c mouse[1].

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

Animal Model: BALB/c mice[1]
Dosage: 5 mg/kg
Administration: Intraperitoneal application; 30 min before and 1 h after IR irradiation (20 Gy).
Result: Anti-inflammatory effect in IR-irradiated mice.

分子量

336.34

Formula

C20H16O5
CAS 号

18642-23-4
中文名称

补骨脂定；补骨脂次素
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
In Vitro: 

DMSO : 50 mg/mL (148.66 mM; ultrasonic and warming and heat to 60°C)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.9732 mL 14.8659 mL 29.7318 mL
5 mM 0.5946 mL 2.9732 mL 5.9464 mL
10 mM 0.2973 mL 1.4866 mL 2.9732 mL

*

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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: 2.08 mg/mL (6.18 mM); Suspended solution; Need ultrasonic

    此方案可获得 2.08 mg/mL (6.18 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (6.18 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.18 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Yang HJ, et al. Psoralidin, a dual inhibitor of COX-2 and 5-LOX, regulates ionizing radiation (IR)-induced pulmonary inflammation.Biochem Pharmacol. 2011 Sep 1;82(5):524-34.

    [2]. Suman S, et al. Silencing NOTCH signaling causes growth arrest in both breast cancer stem cells and breast cancer cells.Br J Cancer. 2013 Nov 12;109(10):2587-96.