Mefenamic acid-d4 is intended for use as an internal standard for the quantification of mefenamic acid (Item No. 23650) by GC- or LC-MS. Mefenamic acid is a non-steroidal anti-inflammatory drug (NSAID) and a COX-2 inhibitor.{41197} It binds to COX-2 (Kd = 4 nM) and inhibits COX-2-dependent oxygenation of arachidonic acid (Item Nos. 90010 | 90010.1 | 10006607) in vitro (Ki = 10 µM). Mefenamic acid (30 mg/kg) reduces acetic acid-induced writhing in rats.{41198} It inhibits increases in skin thickness in a mouse model of delayed-type hypersensitivity induced by dinitrochlorobenzene (DNBC).{41198} Mefenamic acid also reduces the antibody response to sheep red blood cells in mice.
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An internal standard for the quantification of mefenamic acid by GC- or LC-MS
Formal name: 6-[(2,3-dimethylphenyl)amino]-benzoic-2,3,4,5-d4 acid
Synonyms: C.I. 473-d4
Molecular weight: 245.3
CAS: 1216745-79-7
Purity: ≥99% deuterated forms (d1-d4)
Formulation: A solid
The PtdIn phosphates play an important role in the generation and transduction of intracellular signals.{8344,4096,14518} PtdIns-(3,4,5)-P3-biotin is an affinity probe which allows the PIP3 to be detected through an interaction with the biotin ligand. This design allows PtdIns-(3,4,5)-P3-biotin to serve as a general probe for any protein with a high affinity binding interaction with inositol-(3,4,5)-triphosphate phospholipids, such as phosphatidylinositol 3-kinase, PTEN, or PH-domain-containing proteins.
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The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
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The PtdIn phosphates play an important role in the generation and transduction of intracellular signals.{8344,4096,14518} PtdIns-(3,4,5)-P3-biotin is an affinity probe which allows the PIP3 to be detected through an interaction with the biotin ligand. This design allows PtdIns-(3,4,5)-P3-biotin to serve as a general probe for any protein with a high affinity binding interaction with inositol-(3,4,5)-triphosphate phospholipids, such as phosphatidylinositol 3-kinase, PTEN, or PH-domain-containing proteins.
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Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression and are therefore promising targets for cancer therapy. (R)-Roscovitine is a potent inhibitor of Cdk2/cyclin E with an IC50 value of 0.1 µM.{14988} It also inhibits Cdk7/cyclin H, Cdk5/p35, and cell division cycle (cdc)/cyclin B with IC50 values of 0.49, 0.16, and 0.65 µM, respectively.{14987,14988,14991} (R)-Roscovitine inhibits the growth of rapidly proliferating cells with an average IC50 value of 15.2 µM against a panel of 19 human tumor cell lines.{14988} In murine models of polycystic kidney disease, (R)-roscovitine effectively inhibited disease progression at doses of 50-100 mg/kg.{14564}
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