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405268

Sigma-Aldrich

Indomethacin

≥98% (HPLC), powder, COX inhibitor, Calbiochem

Synonyme(s) :

Indomethacin, 1-( p-Chlorobenzoyl)-5-methoxy-2-methyl-1H-indole-3-acetic Acid, 1-(p-Chlorobenzoyl)-5-methoxy-2-methyl-1H-indole-3-acetic Acid

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About This Item

Formule empirique (notation de Hill):
C19H16ClNO4
Numéro CAS:
Poids moléculaire :
357.79
Numéro MDL:
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

product name

Indomethacin, A non-steroidal anti-inflammatory, cell permeable, antipyretic agent.

Niveau de qualité

Pureté

≥98% (by assay)

Forme

powder

Puissance

740 nM IC50

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze

Couleur

white to off-white

Solubilité

ethanol: 20 mg/mL

Conditions d'expédition

ambient

Température de stockage

10-30°C

InChI

1S/C19H16ClNO4/c1-11-15(10-18(22)23)16-9-14(25-2)7-8-17(16)21(11)19(24)12-3-5-13(20)6-4-12/h3-9H,10H2,1-2H3,(H,22,23)

Clé InChI

CGIGDMFJXJATDK-UHFFFAOYSA-N

Description générale

A cell-permeable, non-steroidal anti-inflammatory, anti-pyretic agent. Non-selective cyclooxygenase (COX) inhibitor (IC50 = 740 nM for COX-1; IC50 = 970 nM for COX-2). Inhibits phospholipase A2 (IC50 = 145 µM). Reported to reduce Aβ42 levels independently of COX activity.
A non-steroidal anti-inflammatory, cell permeable, antipyretic agent. Non-selective COX inhibitor (IC50 = 740 nM for COX-1; IC50 = 970 nM for COX-2). Inhibits phospholipase A2 (IC50 = 145 µM). Strongly inhibits insoluble transthyretin (TTR) amyloid fibril formation and suppresses production of Aβ-peptide and secreted form of APP by inhibition of APP mRNA levels in NG108-15 cells.

Actions biochimiques/physiologiques

Cell permeable: yes
Product does not compete with ATP.
Reversible: no

Avertissement

Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)

Autres remarques

Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.
Kodoyama, K., et al. 2001. Biochem. Biophys. Res. Commun.281, 483.
Weggen, S., et al. 2001. Nature414, 212.
Kalgutkar, A.S., et al. 2000. Proc. Natl. Acad. Sci. USA97, 925.
Klabunde, T., et al. 2000. Nat. Struct. Biol.7, 312.
Futaki, N., et al. 1994. Prostaglandins47, 55.
Futaki, N., et al. 1994. Prostaglandins47, 55.
Stevenson, K.M., and Lumbers, E.R. 1992. J. Dev. Physiol. 17, 257.
Oliw, E. 1980. Prostaglandins19, 271.

Informations légales

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

Pictogrammes

Skull and crossbones

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

Acute Tox. 1 Oral

Code de la classe de stockage

6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Les clients ont également consulté

T Klabunde et al.
Nature structural biology, 7(4), 312-321 (2000-03-31)
The human amyloid disorders, familial amyloid polyneuropathy, familial amyloid cardiomyopathy and senile systemic amyloidosis, are caused by insoluble transthyretin (TTR) fibrils, which deposit in the peripheral nerves and heart tissue. Several nonsteroidal anti-inflammatory drugs and structurally similar compounds have been
A S Kalgutkar et al.
Proceedings of the National Academy of Sciences of the United States of America, 97(2), 925-930 (2000-01-19)
All nonsteroidal antiinflammatory drugs (NSAIDs) inhibit the cyclooxygenase (COX) isozymes to different extents, which accounts for their anti-inflammatory and analgesic activities and their gastrointestinal side effects. We have exploited biochemical differences between the two COX enzymes to identify a strategy
S Weggen et al.
Nature, 414(6860), 212-216 (2001-11-09)
Epidemiological studies have documented a reduced prevalence of Alzheimer's disease among users of nonsteroidal anti-inflammatory drugs (NSAIDs). It has been proposed that NSAIDs exert their beneficial effects in part by reducing neurotoxic inflammatory responses in the brain, although this mechanism
E Oliw
Prostaglandins, 19(2), 271-284 (1980-02-01)
PGI2 and 6-keto-PGF1 alpha were converted to 6-methoxime-PGF1 alpha (6-MeON-PGF1 alpha) by treatment with methoxyamine HCl in acetate buffer. The formed 6-MeON-PGF1 alpha was measured by radioimmunoassay. Antisera were raised in rabbits after immunization against 6-MeON-PGF1 alpha-BSA conjugate. Diluted 1:20.000
K Kadoyama et al.
Biochemical and biophysical research communications, 281(2), 483-490 (2001-02-22)
Cyclooxygenase (COX) synthesizes bioactive prostaglandins from arachidonic acid, and there are COX-1 and COX-2 isoforms with distinct pathophysiological functions. Recent studies demonstrated that COX-2 expression was up-regulated in the brain of patients with Alzheimer's disease. We established mouse neuroblastoma x

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