Tolmetin sodium
Based on 1 publication(s) in Google Scholar
Tolmetin sodium is an orally active and potent COX inhibitor with IC50s of 0.35 μM and 0.82 μM human COX-1 and COX-2, respectively. Tolmetin sodium is a non-steroidal anti-inflammatory drug (NSAID).
For research use only. We do not sell to patients.
- CAS No.: 35711-34-3
- Formula: C15H14NNaO3
- Molecular Weight:279.27
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Tolmetin sodium
More
Biological Activity
Description
IC50 & Target
[1]|
Human COX-1 0.35 μM (IC50) |
Human COX-2 0.82 μM (IC50) |
In Vitro
Tolmetin sodium (0.25 mM) does not attenuate lipid peroxidation in rat brain homogenate. Tolmetin (0.25, 0.5, 0.75, 1 mM) shows radical scavenging properties but without superoxide anion generation in rat brain homogenat[3].
Tolmetin sodium (0.001-100 μM) shows anticancer activity againts HT-29 colon cancer cell line in a dose-dependent manner[4].
Tolmetin sodium (0-100 μM) shows no effect on osteoblast growth[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Tolmetin sodium (5 mg/kg twice a day for 5 days) pre-treatment considerably attenuates quinolinic acid (QA)-induced neurotoxicity[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
-
CAS No. 35711-34-3
-
Molecular Weight 279.27
-
Formula C15H14NNaO3
-
SMILES
O=C(CC1=CC=C(N1C)C(C2=CC=C(C)C=C2)=O)O[Na]
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
-
Journal Impact Factor
-
Most Recent
Protocols
-
Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
[1]. T D Warner, et al. Nonsteroid drug selectivities for cyclo-oxygenase-1 rather than cyclo-oxygenase-2 are associated with human gastrointestinal toxicity: a full in vitro analysis. Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7563-8. [Content Brief]
[2]. Etcheverry SB, et al. Three new vanadyl(IV) complexes with non-steroidal anti-inflammatory drugs (Ibuprofen, Naproxen and Tolmetin). Bioactivity on osteoblast-like cells in culture. J Inorg Biochem. 2002 Jan 1;88(1):94-100. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)