401003
(±)-Ibuprofen
A nonsteroidal anti-inflammatory drug (NSAID) that acts as a reversible and competitive inhibitor of cyclooxygenase 1 (COX-1) (IC50 = 4.85 µM).
别名:
(±)-Ibuprofen, [(±)-2-(4-Isobutylphenyl)-propionic Acid
登录 查看组织和合同定价。
选择尺寸
关于此项目
经验公式（希尔记法）:
C13H18O2
化学文摘社编号:
分子量:
206.28
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
Assay:
≥98% (titration)
Form:
solid
Quality level:
Storage condition:
OK to freeze
protect from light
protect from light
产品名称
(±)-Ibuprofen, A nonsteroidal anti-inflammatory drug (NSAID) that acts as a reversible and competitive inhibitor of cyclooxygenase 1 (COX-1) (IC50 = 4.85 µM).
SMILES string
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 key
HEFNNWSXXWATRW-UHFFFAOYSA-N
description
Merck USA index - 14, 4881
assay
≥98% (titration)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
white
solubility
ethanol: 1 mg/mL
DMSO: 5 mg/mL
shipped in
ambient
storage temp.
10-30°C
Quality Level
Biochem/physiol Actions
Cell permeable: no
Primary Target
COX-1
COX-1
Product competes with ATP.
Reversible: yes
Target IC50: 4.85 µM against COX-1
Disclaimer
Toxicity: Harmful (C)
General description
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).
Other Notes
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.
Preparation Note
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - Eye Irrit. 2 - STOT SE 3
target_organs
Respiratory system
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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.
Z Lambat et al.
Metabolic brain disease, 15(4), 249-256 (2001-06-01)
There is increasing evidence suggesting a protective role for anti-inflammatory medications in neurological disorders such as Alzheimer's disease (AD). While there has not been any direct evidence for this, a number of clinical studies indicate that those patients who have
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
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持