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Merck
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Key Documents

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).

동의어(들):

(±)-Ibuprofen, [(±)-2-(4-Isobutylphenyl)-propionic Acid

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About This Item

실험식(Hill 표기법):
C13H18O2
CAS Number:
Molecular Weight:
206.28
MDL number:
UNSPSC 코드:
12352200
NACRES:
NA.77

Quality Level

분석

≥98% (titration)

형태

solid

제조업체/상표

Calbiochem®

저장 조건

OK to freeze
protect from light

색상

white

solubility

ethanol: 1 mg/mL
DMSO: 5 mg/mL

배송 상태

ambient

저장 온도

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 key

HEFNNWSXXWATRW-UHFFFAOYSA-N

일반 설명

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).

생화학적/생리학적 작용

Cell permeable: no
Primary Target
COX-1
Product competes with ATP.
Reversible: yes
Target IC50: 4.85 µM against COX-1

경고

Toxicity: Harmful (C)

재구성

Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

기타 정보

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.

법적 정보

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

픽토그램

Exclamation mark

신호어

Warning

유해 및 위험 성명서

Hazard Classifications

Acute Tox. 4 Oral - Eye Irrit. 2 - STOT SE 3

표적 기관

Respiratory system

Storage Class Code

11 - Combustible Solids

WGK

WGK 1

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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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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