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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).

Sinonimo/i:

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

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1 G
CHF 63.00

CHF 63.00


Spedizione prevista il29 maggio 2025



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1 G
CHF 63.00

About This Item

Formula empirica (notazione di Hill):
C13H18O2
Numero CAS:
Peso molecolare:
206.28
Numero MDL:
Codice UNSPSC:
12352200
NACRES:
NA.77

CHF 63.00


Spedizione prevista il29 maggio 2025


Livello qualitativo

Descrizione

Merck USA index - 14, 4881

Saggio

≥98% (titration)

Stato

solid

Produttore/marchio commerciale

Calbiochem®

Condizioni di stoccaggio

OK to freeze
protect from light

Colore

white

Solubilità

ethanol: 1 mg/mL
DMSO: 5 mg/mL

Condizioni di spedizione

ambient

Temperatura di conservazione

10-30°C

Stringa SMILE

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)
HEFNNWSXXWATRW-UHFFFAOYSA-N

Descrizione generale

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).

Azioni biochim/fisiol

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

Attenzione

Toxicity: Harmful (C)

Ricostituzione

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

Altre note

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.

Note legali

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

Pittogrammi

Exclamation mark

Avvertenze

Warning

Indicazioni di pericolo

Classi di pericolo

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

Organi bersaglio

Respiratory system

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 1

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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Sigma-Aldrich

A7085

Acetaminofene

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.
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
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
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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