C-DIM8 is a para-phenyl-substituted diindolylmethane (C-DIM) and an antagonist of the orphan receptor nuclear receptor-related protein 77 (Nur77).{49136} It inhibits reporter gene expression induced by the Nur77 agonist C-DIM5 (Item No. 27980) in PANC-28 cells when used at a concentration of 20 µM. C-DIM8 (10, 15, and 20 µM) reduces expression of BIRC5, the gene encoding survivin, in PANC-1 pancreatic cancer cells.{57162} In vivo, C-DIM8 (30 mg/kg) induces tumor cell apoptosis and reduces tumor volume in an L3.6pl pancreatic carcinoma mouse xenograft model.
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A Nur77 antagonist; inhibits C-DIM5-induced reporter gene expression in PANC-28 cells at 20 µM; reduces expression of BIRC5 in PANC-1 cells at 10, 15, and 20 µM; induces tumor cell apoptosis and reduces tumor volume in an L3.6pl pancreatic carcinoma mouse xenograft model at 30 mg/kg
Formal name: 4-(di-1H-indol-3-ylmethyl)-phenol
Synonyms: 1,1-bis-(3’-indolyl)-1-(p-hydroxyphenyl)methane|DIM-C-pPhOH
Molecular weight: 338.4
CAS: 151358-47-3
Purity: ≥95%
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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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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