Ethosuximide-d5 is intended for use as an internal standard for the quantification of ethosuximide (Item No. 23947) by GC- or LC-MS. Ethosuximide is an anticonvulsant.{36303,36304,36305,36306,36307} It increases glucose, fructose-1,6-bisphosphate, and pyruvate levels in rat brain when administered at a dose of 200 mg/kg.{36303} Ethosuximide (400 mg/kg) reduces the severity of audiogenic seizures in a rat model of barbiturate withdrawal-induced convulsions.{36304} It also inhibits tonic hindlimb extension induced by pentylenetetrazole (PTZ; Item No. 18682) or brainstem stimulation (ED50s = 35 and 70 mg/kg, respectively), as well as leptazol-induced clonic seizures (ED50 = 230 mg/kg), in rats.{36305,36306} Ethosuximide reduces resting tremor by 60% in a macaque model of Parkinson’s disease induced by MPTP when administered at a dose of 150 mg/animal for 5 days.{36307} Formulations containing ethosuximide have been used in the treatment of petit mal seizures.
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An internal standard for the quantification of ethosuximide by GC- or LC-MS
Formal name: 3-(ethyl-1,1,2,2,2-d5)-3-methyl-2,5-pyrrolidinedione
Synonyms: CI-366-d5|NSC 64013-d5
Molecular weight: 146.2
CAS: 1989660-59-4
Purity: ≥99% deuterated forms (d1-d5)
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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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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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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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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