Aspirin(Synonyms: 阿司匹林; Acetylsalicylic Acid; ASA)

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Aspirin (Synonyms: 阿司匹林; Acetylsalicylic Acid; ASA) 纯度: 99.92%

Aspirin是非选择性和不可逆的 COX-1COX-2 抑制剂,IC50 分别为5,210 μg/mL。

Aspirin(Synonyms: 阿司匹林; Acetylsalicylic Acid;  ASA)

Aspirin Chemical Structure

CAS No. : 50-78-2

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10 mM * 1 mL in DMSO ¥500 In-stock
500 mg ¥400 In-stock
1 g ¥500 In-stock
5 g ¥800 In-stock
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生物活性

Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL.

IC50 & Target[1]

COX-1

27.75 μM (IC50)

COX-2

1.17 mM (IC50)

体外研究
(In Vitro)

Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever[2]. Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation. This mechanism of action accounts for the effect of aspirin on prevention of coronary artery and cerebrovascular thrombosis. Aspirin is less effective in inhibiting COX-2 activity. Aspirin and salicylate inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer[3]. Aspirin inhibits the activation of NF-κB. This inhibition prevents the degradation of the NF-κB inhibitor, 1κB, and therefore NF-κB is retained in the cytosol. Aspirin also inhibits NF-κB-dependent transcription from the lgκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells[4]. Aspirin inhibits COX-1 and COX-2 with IC50 values of 3.57 μM and 29.3 μM, respectively in human articular chondrocytes[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Clinical Trial

分子量

180.16

Formula

C9H8O4

CAS 号

50-78-2

中文名称

阿司匹林;乙酰水杨酸;邻乙酰水杨酸

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 : 400 mg/mL (2220.25 mM; Need ultrasonic)

H2O : 0.1 mg/mL (0.56 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 5.5506 mL 27.7531 mL 55.5062 mL
5 mM 1.1101 mL 5.5506 mL 11.1012 mL
10 mM 0.5551 mL 2.7753 mL 5.5506 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: ≥ 10 mg/mL (55.51 mM); Clear solution

    此方案可获得 ≥ 10 mg/mL (55.51 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 100.0 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% (20% SBE-β-CD in saline)

    Solubility: ≥ 10 mg/mL (55.51 mM); Clear solution

    此方案可获得 ≥ 10 mg/mL (55.51 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 100.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中,混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
  • 3.

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

    Solubility: ≥ 10 mg/mL (55.51 mM); Clear solution

    此方案可获得 ≥ 10 mg/mL (55.51 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 100.0 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 上海金畔生物科技有限公司 网站选购。
参考文献
  • [1]. Mitchell JA, et al. Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and induciblecyclooxygenase. Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):11693-7.

    [2]. Vane JR, et al. The mechanism of action of aspirin. Thromb Res. 2003 Jun 15;110(5-6):255-8.

    [3]. Wu KK, et al. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3(2):107-12.

    [4]. Kopp E, et al. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12;265(5174):956-9.

    [5]. Blanco FJ, et al. Effect of antiinflammatory drugs on COX-1 and COX-2 activity in human articular chondrocytes. J Rheumatol. 1999 Jun;26(6):1366-73.

Cell Assay
[5]

Chondrocytes are isolated from articular cartilage of donors with no articular disease. Unstimulated and interleukin 1 (IL-1) stimulated chondrocytes are used as models to study the effects of drugs on COX-1 and COX-2. Cells are incubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in each sample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by different concentrations of the test substance by linear regression analysis[5].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

参考文献
  • [1]. Mitchell JA, et al. Selectivity of nonsteroidal antiinflammatory drugs as inhibitors of constitutive and induciblecyclooxygenase. Proc Natl Acad Sci U S A. 1993 Dec 15;90(24):11693-7.

    [2]. Vane JR, et al. The mechanism of action of aspirin. Thromb Res. 2003 Jun 15;110(5-6):255-8.

    [3]. Wu KK, et al. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin Vasc Med. 2003 May;3(2):107-12.

    [4]. Kopp E, et al. Inhibition of NF-kappa B by sodium salicylate and aspirin. Science. 1994 Aug 12;265(5174):956-9.

    [5]. Blanco FJ, et al. Effect of antiinflammatory drugs on COX-1 and COX-2 activity in human articular chondrocytes. J Rheumatol. 1999 Jun;26(6):1366-73.

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