405268
Indomethacin
≥98% (HPLC), powder, COX inhibitor, Calbiochem
Synonym(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
Empirical Formula (Hill Notation):
C19H16ClNO4
CAS Number:
Molecular Weight:
357.79
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
product name
Indomethacin, A non-steroidal anti-inflammatory, cell permeable, antipyretic agent.
Quality Level
assay
≥98% (by assay)
form
powder
potency
740 nM IC50
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
color
white to off-white
solubility
ethanol: 20 mg/mL
shipped in
ambient
storage temp.
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)
InChI key
CGIGDMFJXJATDK-UHFFFAOYSA-N
General description
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.
Biochem/physiol Actions
Cell permeable: yes
Product does not compete with ATP.
Reversible: no
Warning
Toxicity: Highly Toxic & Carcinogenic / Teratogenic (I)
Other Notes
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.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 1 Oral
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Customers Also Viewed
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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