dexketoprofen and Neoplasms

dexketoprofen has been researched along with Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for dexketoprofen and Neoplasms

Article	Year
Structure-activity relationships and cancer-cell selective toxicity of novel inhibitors of glioma-associated oncogene homologue 1 (Gli1) mediated transcription. Journal of medicinal chemistry, 2009, Jul-23, Volume: 52, Issue:14 We report novel inhibitors of Gli1-mediated transcription as potential anticancer agents. Focused chemical libraries were designed and assessed for inhibition of functional cell-based Gli1-mediated transcription and selective toxicity toward cancer cells. The SAR was revealed, and the selectivity of the lead compounds' inhibition of Gli1-mediated transcription over that of Gli2 was determined. Compound 63 (NMDA298-1), which inhibited Gli1-mediated transcription in C3H10T1/2 cells with an IC(50) of 6.9 muM, showed 3-fold selectivity for inhibiting transcription mediated by Gli1 over that by Gli2. Cell-viability assays were performed to evaluate the chemical library in a normal cell line and a panel of cancer cell lines with or without up-regulated expression of the Gli1 gene. These compounds decreased the viability of several cancer cell lines but were less active in the noncancerous BJ-hTERT cells. Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Genes, Reporter; Humans; Inhibitory Concentration 50; Neoplasms; Oncogene Proteins; Pyrazoles; Structure-Activity Relationship; Trans-Activators; Transcription, Genetic; Tyramine; Zinc Finger Protein GLI1	2009

Article

Year

Structure-activity relationships and cancer-cell selective toxicity of novel inhibitors of glioma-associated oncogene homologue 1 (Gli1) mediated transcription.

Journal of medicinal chemistry, 2009, Jul-23, Volume: 52, Issue:14

We report novel inhibitors of Gli1-mediated transcription as potential anticancer agents. Focused chemical libraries were designed and assessed for inhibition of functional cell-based Gli1-mediated transcription and selective toxicity toward cancer cells. The SAR was revealed, and the selectivity of the lead compounds' inhibition of Gli1-mediated transcription over that of Gli2 was determined. Compound 63 (NMDA298-1), which inhibited Gli1-mediated transcription in C3H10T1/2 cells with an IC(50) of 6.9 muM, showed 3-fold selectivity for inhibiting transcription mediated by Gli1 over that by Gli2. Cell-viability assays were performed to evaluate the chemical library in a normal cell line and a panel of cancer cell lines with or without up-regulated expression of the Gli1 gene. These compounds decreased the viability of several cancer cell lines but were less active in the noncancerous BJ-hTERT cells.

Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Genes, Reporter; Humans; Inhibitory Concentration 50; Neoplasms; Oncogene Proteins; Pyrazoles; Structure-Activity Relationship; Trans-Activators; Transcription, Genetic; Tyramine; Zinc Finger Protein GLI1

2009