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Merck
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主要文件

401003

Sigma-Aldrich

(±)-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

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About This Item

经验公式(希尔记法):
C13H18O2
CAS号:
分子量:
206.28
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.77

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

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
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.

法律資訊

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

象形圖

Exclamation mark

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


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M Ouellet et al.
Proceedings of the National Academy of Sciences of the United States of America, 98(25), 14583-14588 (2001-11-22)
Both nonsteroidal anti-inflammatory drugs, such as ibuprofen, and the prototypical selective cyclooxygenase (Cox)-2 inhibitors DuP-697 and NS-398 block the inhibition of Cox-1 by aspirin in vitro. However, clinical studies have shown that the Cox-2 selective drugs (or coxibs) rofecoxib and
J A Mitchell et al.
Proceedings of the National Academy of Sciences of the United States of America, 90(24), 11693-11697 (1993-12-15)
Constitutive cyclooxygenase (COX-1; prostaglandin-endoperoxide synthase, EC 1.14.99.1) is present in cells under physiological conditions, whereas COX-2 is induced by some cytokines, mitogens, and endotoxin presumably in pathological conditions, such as inflammation. Therefore, we have assessed the relative inhibitory effects of
D Casper et al.
Neuroscience letters, 289(3), 201-204 (2000-08-29)
Non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of Alzheimer's disease, although the underlying mechanisms are unknown. Glutamate excitotoxicity has been implicated in Alzheimer's disease, Parkinson's disease, and others. We examined the effects of aspirin, acetaminophen, and ibuprofen on cultured primary
E M Boneberg et al.
Journal of clinical pharmacology, 36(12 Suppl), 16S-19S (1996-12-01)
Since the discovery of a cytokine-inducible isozyme of cyclooxygenase (COX-2), its pharmacologic inhibition has been the subject of recent investigations. These include tests for the selectivity of known nonsteroidal antiinflammatory drugs (NSAIDs) on the constitutive enzyme of cyclooxygenase (COX-1) compared
Ibuprofen, inflammation and Alzheimer disease.
T Wyss-Coray et al.
Nature medicine, 6(9), 973-974 (2000-09-06)

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