405268
Indomethacin
≥98% (HPLC), powder, COX inhibitor, Calbiochem
Synonim(y):
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
Zaloguj sięWyświetlanie cen organizacyjnych i kontraktowych
About This Item
Wzór empiryczny (zapis Hilla):
C19H16ClNO4
Numer CAS:
Masa cząsteczkowa:
357.79
Numer MDL:
Kod UNSPSC:
12352200
NACRES:
NA.77
Polecane produkty
product name
Indomethacin, A non-steroidal anti-inflammatory, cell permeable, antipyretic agent.
Poziom jakości
Próba
≥98% (by assay)
Postać
powder
siła działania
740 nM IC50
producent / nazwa handlowa
Calbiochem®
warunki przechowywania
OK to freeze
kolor
white to off-white
rozpuszczalność
ethanol: 20 mg/mL
Warunki transportu
ambient
temp. przechowywania
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)
Klucz InChI
CGIGDMFJXJATDK-UHFFFAOYSA-N
Opis ogólny
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.
Działania biochem./fizjol.
Cell permeable: yes
Product does not compete with ATP.
Reversible: no
Ostrzeżenie
Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)
Inne uwagi
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.
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.
Informacje prawne
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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Hasło ostrzegawcze
Danger
Zwroty wskazujące rodzaj zagrożenia
Zwroty wskazujące środki ostrożności
Klasyfikacja zagrożeń
Acute Tox. 1 Oral
Kod klasy składowania
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
Klasa zagrożenia wodnego (WGK)
WGK 3
Temperatura zapłonu (°F)
Not applicable
Temperatura zapłonu (°C)
Not applicable
Certyfikaty analizy (CoA)
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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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