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2-(2-(2,4-dioxopentan-3-ylidene)hydrazineyl)benzonitrile as novel inhibitor of receptor tyrosine kinase and PI3K/AKT/mTOR signaling pathway in glioblastoma

Дата публикации в реестре: 2021-08-05T19:44:02Z

Аннотация:
Ключевые слова:
2 [2 (2,4 dioxopentan 3 ylidene)hydrazineyl]benzonitrile, antimitotic agent, benzonitrile, caspase 3, caspase 7, cisplatin, cyclin D, cyclin dependent kinase 6, cyclin E, hydrazine derivative, mammalian target of rapamycin, neurotrophin, phosphatidylinositol 3 kinase, protein kinase B, protein kinase Mer, protein p53, protein serine threonine kinase inhibitor, protein tyrosine kinase A, protein tyrosine kinase inhibitor, reactive oxygen metabolite, transcription factor E2F, unclassified drug, antineoplastic agent, benzonitrile, nitrile, phosphatidylinositol 3 kinase, protein kinase B, protein kinase inhibitor, protein tyrosine kinase, target of rapamycin kinase, Akt signaling, antiproliferative activity, Article, binding affinity, cell cycle progression, cell proliferation, cell viability, comparative study, controlled study, cytotoxicity, diazotization, DNA repair, down regulation, drug protein binding, drug receptor binding, drug synthesis, enzyme active site, enzyme activity, enzyme inhibition, G1 phase cell cycle checkpoint, gene expression, glioblastoma, glioblastoma cell line, human, human cell, IC50, LN-229 cell line, molecular docking, neuroapoptosis, oxidation reduction potential, oxidative stress, protein expression, S phase cell cycle checkpoint, u87 cell line, antagonists and inhibitors, apoptosis, cell survival, chemistry, drug effect, gene expression regulation, glioblastoma, metabolism, pathology, signal transduction, tumor cell line, Antineoplastic Agents, Apoptosis, Cell Line, Tumor, Cell Proliferation, Cell Survival, G1 Phase Cell Cycle Checkpoints, Gene Expression Regulation, Neoplastic, Glioblastoma, Humans, Nitriles, Phosphatidylinositol 3-Kinases, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Receptor Protein-Tyrosine Kinases, S Phase Cell Cycle Checkpoints, Signal Transduction, TOR Serine-Threonine Kinases

Тип: Article

Права: open access

Источник: European Journal of Medicinal Chemistry


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