Glipizide-d11 is intended for use as an internal standard for the quantification of glipizide (Item No. 11579) by GC- or LC-MS. Glipizide is a hypoglycemic agent.{46791} It inhibits ATP-sensitive potassium (KATP) channels in primary mouse pancreatic β cells (IC50 = 6.4 nM). Glipizide induces insulin release from isolated rat pancreatic tissue with an EC50 value of 40 nM.{46792} Dietary administration of glipizide (5 mg/kg per day for 10 days) increases the number of insulin receptors on isolated and purified mouse liver plasma membranes.{46793} It reduces plasma glucose and triglyceride, but not total cholesterol, levels and increases plasma insulin levels in a rat model of diabetes induced by a high-fat diet and streptozotocin (STZ; Item No. 13104) when administered orally at a dose of 5 mg/kg.{46794} Formulations containing glipizide have been used in the treatment of type 2 diabetes.
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An internal standard for the quantification of glipizide by GC- or LC-MS
Formal name: N-[2-[4-[[[(cyclohexyl-1,2,2,3,3,4,4,5,5,6,6-d11-amino)carbonyl]amino]sulfonyl]phenyl]ethyl]-5-methyl-2-pyrazinecarboxamide
Synonyms: CP 28720|K 4024|TK 1320
Molecular weight: 456.6
CAS: 1189426-07-0
Purity: ≥98% deuterated forms (d1-d11)
Formulation: A solid
The maintenance of embryonic stem cells in culture typically requires feeder cells and various exogenous factors found in serum. Murine embryonic stem (mES) cells can be maintained in the absence of feeder cells and serum but require the leukemia inhibitor factor (LIF) and bone morphogenic protein (BMP) to prevent differentiation and promote self-renewal. SC-1 is a small molecule activator of stem cell renewal that allows the propagation of OG2 mES cells for at least 10 passages in an undifferentiated state.{14533} The activity of SC-1 is mediated by the combined inhibition of RasGAP and ERK1 with Kd values of 98 and 212 nM, respectively.{14533} Inhibition of RasGAP increases Ras signaling via the PI3-kinase pathway which promotes self-renewal, whereas inhibition of ERK blocks differentiation.
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The nuclear factor-κB (NF-κB) regulates the expression of numerous genes involved in immunity and inflammation, cellular stress responses, growth, and apoptosis. Resveratrol, a polyphenolic trans-stilbene, is a known inhibitor of the activation of NF-κB and exhibits activity against a wide variety of cancer cells. CAY10512 is a substituted trans-stilbene analog of resveratrol that is 100-fold more potent as measured by antioxidant activity. The IC50 value for inhibition of TNFα-induced activation of NF-κB by CAY10512 is 0.15 µM compared to 20 µM by resveratrol.{14545}
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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 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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