Nisoldipine-d6 is intended for use as an internal standard for the quantification of nisoldipine (Item No. 20998) by GC- or LC-MS. Nisoldipine is a calcium channel inhibitor.{33001} It binds to calcium channels in isolated rat ventricular membranes (Kd = 0.04 nM) and inhibits calcium uptake by smooth muscle cells.{33001,59310} Nisoldipine inhibits acetylcholine-induced contraction of isolated rabbit coronary arteries (IC50 = 0.03 nM).{33001} In vivo, nisoldipine (3 mg/kg) reduces ventricular tachycardia and fibrillization and increases survival in a rat model of ventricular arrhythmias induced by myocardial ischemia.{59311} Dietary administration of nisoldipine (50-100 mg/kg) reduces systolic blood pressure in spontaneously hypertensive rats.{33005} Formulations containing nisoldipine have been used in the treatment of hypertension.
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An internal standard for the quantification of nisoldipine by GC- or LC-MS
Formal name: 3-methyl 5-(2-(methyl-d3)propyl-3,3,3-d3) 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
Synonyms:
Molecular weight: 394.5
CAS: 1285910-03-3
Purity: ≥99% deuterated forms (d1-d6)
Formulation: A solid
1,2-Dipalmitoyl-sn-glycero-3-PC (DPPC) is a zwitterionic glycerophospholipid commonly used in the formation of lipid monolayers, bilayers, and liposomes for use in a variety of applications.{14480,24261,14478,14479} It has been used in the formation of proteoliposomes for implantation of γ-glutamyl transpeptidase into human erythrocyte membranes.{14478} Incorporation of glycosphingolipid antigens into DPPC-containing liposomes increases the immunogenicity of the antigens in mice.{14479}
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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 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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