1、Product Data SheetAspirinCat. No.: HY-14654CAS No.: 50-78-2分式: CHO分量: 180.16作靶點(diǎn): COX; Autophagy; Mitophagy; Virus Protease作通路: Immunology/Inflammation; Autophagy; Anti-infection儲(chǔ)存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn) DMSO : 100 mg/mL (555.06 mM; Need ultrasoni

2、c)H2O : 0.1 mg/mL (0.56 mM; Need ultrasonic)SolventMass1 mg 5 mg 10 mgConcentration制備儲(chǔ)備液1 mM 5.5506 mL 27.7531 mL 55.5062 mL5 mM 1.1101 mL 5.5506 mL 11.1012 mL10 mM 0.5551 mL 2.7753 mL 5.5506 mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲(chǔ)備液；旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存式和期限：-80C, 6 months; -20C, 1 month。-80C 儲(chǔ)存時(shí)，請(qǐng)?jiān)?/p>

3、 6 個(gè)內(nèi)使，-20C 儲(chǔ)存時(shí)，請(qǐng)?jiān)?1 個(gè)內(nèi)使。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥式選擇適當(dāng)?shù)娜芙獍?。以下溶解案都?qǐng)先按照 In Vitro 式配制澄清的儲(chǔ)備液，再依次添加助溶劑：為保證實(shí)驗(yàn)結(jié)果的可靠性，澄 的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使； 以下溶劑前顯的百分 指該溶劑在您配制終溶液中的體積占；如在配制過(guò)程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過(guò)加熱和/或超聲的式助溶1. 請(qǐng)依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (13.88 mM); Clear sol

4、ution此案可獲得 2.5 mg/mL (13.88 mM，飽和度未知) 的澄清溶液。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 400 L PEG300 中，混合均勻；向上述體系中加50 L Tween-80，混合均勻；然后繼續(xù)加 450 L 理鹽定容 1 mL。2. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (13.88 mM); Clear solutionPage 1 of 2 www.MedChemE此案可獲得 2.5 mg/mL (13.88

5、 mM，飽和度未知) 的澄清溶液。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 900 L 20% 的 SBE-CD 理鹽溶液中，混合均勻。3. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (13.88 mM); Clear solution此案可獲得 2.5 mg/mL (13.88 mM，飽和度未知) 的澄 溶液，此案不適于實(shí)驗(yàn)周 期在半個(gè)以上的實(shí)驗(yàn)。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 900 L 油中，混合均勻。BIOLOGIC

6、AL ACTIVITY物活性 Aspirin選擇性和不可逆的 COX-1 和 COX-2 抑制劑，IC50 分別為5，210 g/mL。IC & Target COX-1 COX-227.75 M (IC50) 1.17 mM (IC50)體外研究 Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to theformation of prostaglandins (PGs) that cause inflammation,

7、 swelling, pain and fever2. Aspirin acetylates serine-530 ofcyclooxygenase-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 cerebrovascularthrombosis. As

8、pirin is less effective in inhibiting COX-2 activity. Aspirin and salicylate inhibit COX-2 protein expressionthrough interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2promoter/enhancer3. Aspirin inhibits the activation of NF-B. This inhibition p

9、revents the degradation of the NF-Binhibitor, 1B, and therefore NF-B is retained in the cytosol. Aspirin also inhibits NF-B-dependent transcription fromthe lg enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells4.Aspirin inhibits COX-1 and COX-2 with

10、IC50 values of 3.57 M and 29.3 M, respectively in human articularchondrocytes5.PROTOCOLCell 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

11、 COX-1 and COX-2. Cells areincubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in eachsample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by differentconcentrations of the test substance by linear

12、 regression analysis5.MCE has not independently confirmed the accuracy of these methods. They are for reference only.戶使本產(chǎn)品發(fā)表的科研獻(xiàn) Cancer Res. 2018 Oct 1;78(19):5586-5599. Cell Death Dis. 2018 Aug 28;9(9):847.See more customer validations on HYPERLINK www.MedChemE www.MedChemEPage 2 of 3 www.MedChemER

13、EFERENCES1. 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

14、 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.McePdfHe