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).
Szinonimák:
(±)-Ibuprofen, [(±)-2-(4-Isobutylphenyl)-propionic Acid
Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez
Összes fotó(1)
About This Item
Tapasztalati képlet (Hill-képlet):
C13H18O2
CAS-szám:
Molekulatömeg:
206.28
MDL-szám:
UNSPSC kód:
12352200
NACRES:
NA.77
Javasolt termékek
Minőségi szint
Teszt
≥98% (titration)
Forma
solid
gyártó/kereskedő neve
Calbiochem®
tárolási körülmény
OK to freeze
protect from light
szín
white
oldhatóság
ethanol: 1 mg/mL
DMSO: 5 mg/mL
kiszállítva
ambient
tárolási hőmérséklet
10-30°C
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)
Nemzetközi kémiai azonosító kulcs
HEFNNWSXXWATRW-UHFFFAOYSA-N
Általános leírás
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).
Biokémiai/fiziológiai hatások
Cell permeable: no
Primary Target
COX-1
COX-1
Product competes with ATP.
Reversible: yes
Target IC50: 4.85 µM against COX-1
Figyelmeztetés
Toxicity: Harmful (C)
Feloldás
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Egyéb megjegyzések
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.
Jogi információk
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Figyelmeztetés
Warning
Figyelmeztető mondatok
Óvintézkedésre vonatkozó mondatok
Veszélyességi osztályok
Acute Tox. 4 Oral - Eye Irrit. 2 - STOT SE 3
Célzott szervek
Respiratory system
Tárolási osztály kódja
11 - Combustible Solids
WGK
WGK 1
Lobbanási pont (F)
Not applicable
Lobbanási pont (C)
Not applicable
Analitikai tanúsítványok (COA)
Analitikai tanúsítványok (COA) keresése a termék sarzs-/tételszámának megadásával. A sarzs- és tételszámok a termék címkéjén találhatók, a „Lot” vagy „Batch” szavak után.
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Az ügyfelek ezeket is megtekintették
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.
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
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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