推薦產品
品質等級
化驗
≥98% (titration)
形狀
solid
製造商／商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
white
溶解度
ethanol: 1 mg/mL
DMSO: 5 mg/mL
運輸包裝
ambient
儲存溫度
10-30°C
SMILES 字串
OC(=O)C(C)c1ccc(cc1)CC(C)C
InChI
1S/C13H18O2/c1-9(2)8-11-4-6-12(7-5-11)10(3)13(14)15/h4-7,9-10H,8H2,1-3H3,(H,14,15)
InChI 密鑰
HEFNNWSXXWATRW-UHFFFAOYSA-N
一般說明
A nonsteroidal anti-inflammatory drug (NSAID) that acts as a reversible and competitive inhibitor of cyclooxygenase 1 (COX-1) (IC50 = 4.85 µM). Inhibits COX-2 at higher concentrations (IC50 = 223 µM). Blocks aspirin inactivation of COX-1 (EC50 antagonism of 200 µM aspirin = 290 nM). Shown to reduce the total Aβ secretion (Amyloid β40 and 42) in human neuronal cells and offers neuroprotection against glutamate-, nitric oxide-, and superoxide-induced damage. Reported to activate peroxisome proliferator-activated receptors (PPAR) α and γ in both CV-1 and C3H10T1/2 cells (~100 µM-500 µM).
A nonsteroidal anti-inflammatory drug (NSAID) that acts as a reversible, competitive, non-selective cyclooxygenase (COX) inhibitor (IC50 = 4.85 µM for purified COX-1 and 223 µM for purified COX-2). Also reported to inhibit COX-1 and COX-2 activity in intact bovine aortic endothelial cells (BAEC) (IC50 = 7 µM for COX-1 and 72.7 µM for COX-2). Potently blocks aspirin inactivation of COX-1 (EC50 antagonism of 200 µM aspirin ~290 nM for ovine COX-1). Decreases the secretion of total Aβ (Amyloid β40&42) by human neuronal cells and offers neuroprotection against glutamate-, nitric oxide- and superoxide-induced damage. Activates peroxisome proliferator activated receptors α and γ in both CV-1 and C3H10T1/2 cells (~100 µM - 500 µM).
生化／生理作用
Cell permeable: no
Primary Target
COX-1
COX-1
Product competes with ATP.
Reversible: yes
Target IC50: 4.85 µM against COX-1
警告
Toxicity: Harmful (C)
重構
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他說明
Asanuma, M., et al. 2001. J. Neurochem.76, 1895.
Blasko, I., et al. 2001. Neurobiol. Dis.8, 1094.
Ouellet, M., et al. 2001. Proc. Natl. Acad. Sci. USA98, 14583.
Casper, D., et al. 2000. Neurosci. Lett.289, 201.
Lambat, Z., et al. 2000. Metab. Brain Dis.15, 249.
Lim, G.P., et al. 2000. J. Neurosci.20, 5709.
Ogawa, O., et al. 2000. Eur. J. Pharmacol.408, 137.
Wyss-Coray, T., and Mucke, L. 2000. Nat. Med.6, 973.
Lehmann, J.M., et al. 1997. J. Biol. Chem.272, 3406.
Boneburg, E.M., et al. 1996. J. Clin. Pharmacol.36, 16S.
Mitchell, J.A., et al. 1994. Proc. Natl. Acad. Sci. USA90, 11693.
Blasko, I., et al. 2001. Neurobiol. Dis.8, 1094.
Ouellet, M., et al. 2001. Proc. Natl. Acad. Sci. USA98, 14583.
Casper, D., et al. 2000. Neurosci. Lett.289, 201.
Lambat, Z., et al. 2000. Metab. Brain Dis.15, 249.
Lim, G.P., et al. 2000. J. Neurosci.20, 5709.
Ogawa, O., et al. 2000. Eur. J. Pharmacol.408, 137.
Wyss-Coray, T., and Mucke, L. 2000. Nat. Med.6, 973.
Lehmann, J.M., et al. 1997. J. Biol. Chem.272, 3406.
Boneburg, E.M., et al. 1996. J. Clin. Pharmacol.36, 16S.
Mitchell, J.A., et al. 1994. Proc. Natl. Acad. Sci. USA90, 11693.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
訊號詞
Warning
危險聲明
危險分類
Acute Tox. 4 Oral - Eye Irrit. 2 - STOT SE 3
標靶器官
Respiratory system
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 1
閃點（°F）
Not applicable
閃點（°C）
Not applicable
分析證明 (COA)
輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號，寫有 ‘Lot’或‘Batch’.。
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J M Lehmann et al.
The Journal of biological chemistry, 272(6), 3406-3410 (1997-02-07)
Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) and cyclooxygenase inhibitor that is frequently used as a research tool to study the process of adipocyte differentiation. Treatment of various preadipocyte cell lines with micromolar concentrations of indomethacin in the presence of
O Ogawa et al.
European journal of pharmacology, 408(2), 137-141 (2000-11-18)
Recent studies show that a mononuclear phagocyte lineage, including microglia, plays a possible role in the pathogenesis of Alzheimer's disease through nitric oxide (NO)-mediated neurotoxicity. Epidemiological studies show that nonsteroidal anti-inflammatory drugs (NSAIDs) have a protective effect against Alzheimer's disease.
I Blasko et al.
Neurobiology of disease, 8(6), 1094-1101 (2001-12-14)
Trying to decrease the production of Amyloid beta (Abeta) has been envisaged as a promising approach to prevent neurodegeneration in Alzheimer's disease (AD). A chronic inflammatory reaction with activated microglia cells and astrocytes is a constant feature of AD. The
G P Lim et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 20(15), 5709-5714 (2000-07-26)
The brain in Alzheimer's disease (AD) shows a chronic inflammatory response characterized by activated glial cells and increased expression of cytokines and complement factors surrounding amyloid deposits. Several epidemiological studies have demonstrated a reduced risk for AD in patients using
M Asanuma et al.
Journal of neurochemistry, 76(6), 1895-1904 (2001-03-22)
Recently, it has been reported that inflammatory processes are associated with the pathophysiology of Alzheimer's disease and that treatment of non-steroidal anti-inflammatory drugs reduce the risk for Alzheimer's disease. In the present study, we examined nitric oxide radical quenching activity
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