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Naproxen sodium_Molecular_structure_CAS_26159-34-2)
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Naproxen sodium

Catalog No. S1626 Name Selleck Chemicals
CAS Number 26159-34-2 Website http://www.selleckchem.com
M. F. C14H13NaO3 Telephone (877) 796-6397
M. W. 252.24099 Fax (832) 582-8590
Purity Email sales@selleckchem.com
Storage -20°C Chembase ID: 72768

SYNONYMS

IUPAC name
sodium (2S)-2-(6-methoxynaphthalen-2-yl)propanoate
IUPAC Traditional name
naproxen sodium
Synonyms
Anaprox
Naposin
Naprelan
Miranax

DATABASE IDS

CAS Number 26159-34-2

PROPERTIES

Salt Data Sodium
Storage Condition -20°C

DETAILS

Description (English)
Research Area
Description Neurological Disease
Biological Activity
Description Naproxen (Aleve, Anaprox) is a COX inhibitor for COX-1 and COX-2 with IC50 of 2.2 μg/mL and 1.3 μg/mL, respectively.
Targets COX-1 COX-2
IC50 2.2 μg/mL 1.3 μg/mL [1]
In Vitro Naproxen is approximately equipotent inhibitor of COX-1 and COX-2 in intact cells with IC50 of 2.2 μg/mL and 1.3 μg/mL, respectively. [1] Naproxen decreases the in vitro LPS-induced PGE2 and TXB2 production in rats and humans with IC50 of 30.7 μM and 79.5 μM for PGE2 inhibition, 72.4 μM and 48.3 μM for TXB2 inhibition, respectively. [2] Naproxen produces concentration-related inhibition of TXB2 production from human platelets and LPS-induced TXB2 production from human mononuclear cells with plC50 values (-log concentration inhibiting TXB2 by 50%) of 5.7 and 6.4, respectively, and exhibits slightly inhibitory selectivity for constitutive and induced COX-2 with IC50 COX-1/IC50 COX-2 of 6.3. [3] Only high concentration of Naproxen can significantly induce apoptosis at 48 hours in HCA-7 colon cancer cells with IC50 of 1.45 mM. [4]
In Vivo Administration of Naproxen reduces the LPS-induced PGE2 and TXB2 production in vivo in rats with IC50 values of 12.8 μM and 5.9 μM, respectively, which represents that Naproxen is a nonselective COX inhibitor with the log IC50 ratio (COX-2/COX-1) of 0.34. [2] Naproxen displays IC50 of 27 μM for analgesia in a rat model with carrageenan-induced arthritis and IC50 of 40 μM for antipyretics in a yeast-induced fever rat model, while exhibits inhibition of PGE2 with IC50 of 13 μM and TXB2 with IC50 of 5 μM. [5]
Clinical Trials Phase IV completed in testing the effect on blood pressure of sumatriptan and Naproxen sodium combination tablets, tablets containing only sumatriptan, and tablets containing only Naproxen sodium when these drugs are taken to treat migraine headaches that occur during a 6-month period.
Features Naproxen displays approximately equipotent inhibitory selectivity for COX-1 and COX-2 in intact cells.
Protocol
Kinase Assay [1]
COX-1 and COX-2 activities in intact cells For the determination of COX-1 and COX-2 inhibition, bovine aortic endothelial cells (BAEC) are incubated for 30 minutes with Naproxen (0.1 ng/mL to 1 mg/mL), and cultured J774.2 macrophages are treated with endotoxin at 1 μg/mL for 12 hours to induce COX-2 followed by incubated for 30 minutes with Naproxen (0.1 ng/mL to 1 mg/mL), respectively. Arachidonic acid (30 μM) is then added, and the cells are incubated for a further 15 minutes at 37 °C. The medium is then removed, and radioimmunoassay is used to measure the formation of 6-keto-PGF1α, PGE2, thromboxane B2, or PGF for the assessment of IC50 for COX-1 and COX-2.
Cell Assay [4]
Cell Lines Human colon cancer HCA-7 cell lines
Concentrations Dissolved in culture medium, final concentration ~20 mM
Incubation Time 24 and 48 hours
Methods Cells are exposed to Naproxen for 24 and 48 hours, respectively. At the end of incubation, cells are harvested by trypsinization, stained with trypan blue solution (0.04% wt/vol) and counted in a Neubauer haemocytometer chamber for the determination of cell viability.
Animal Study [2]
Animal Models Male Sprague-Dawley rats
Formulation Dissolved in 0.9% NaCl
Doses 2.5, 10 or 25 mg/kg
Administration Intravenously (i.v.) infusion or intraperitoneal (i.p.) injection
References
[1] Mitchell JA, et al. Proc Natl Acad Sci, 1993, 90(24), 11693-11697.
[2] Huntjens DR, et al. Br J Pharmacol, 2006, 148(4), 396-404.
[3] Grossman CJ, et al. Inflamm Res, 1995, 44(6), 253-257.
[4] Tavolari S, et al. Carcinogenesis, 2008, 29(2), 371-380.
[5] Krekels EH, et al. Pharm Res, 2011, 28(7), 1561-1576.