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| Section2= | Section3= }} Seliciclib (roscovitine or CYC202) is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors that preferentially inhibit multiple enzyme targets including CDK2, CDK7 and CDK9, which alter the growth phase or state within the cell cycle of treated cells. Seliciclib is being developed by Cyclacel. Seliciclib is being researched for the treatment of non-small cell lung cancer (NSCLC), Cushing's disease, leukemia, HIV infection, herpes simplex infection, cystic fibrosis〔(),〕 and the mechanisms of chronic inflammation disorders. Seliciclib is a 2,6,9-substituted purine analog. Its structure in complex with CDK2 was determined in 1996. Seliciclib inhibits CDK2/E, CDK2/A, CDK7 and CDK9.〔(【引用サイトリンク】title=Cyclacel Begins a Phase IIb Randomized Trial of Seliciclib for Previously Treated Non-Small Cell Lung Cancer )〕 ==Uses== Seliciclib has been found to produce apoptosis in treated cancerous cells of non-small cell lung cancer (NSCLC) and other cancers. Seliciclib has previously undergone Phase IIa clinical trials, in 240 NSCLC patients as a combined dose with existing first- and second-line treatments.〔〔(【引用サイトリンク】title=Cyclacel Reports Interim Seliciclib Phase IIa Data at 2005 ASCO )〕 In the current ''APPRAISE'' trial, the research drug is undergoing Phase IIb clinical trial as a monotherapy for NSCLC in third-line patients.〔(【引用サイトリンク】title=Cyclacel Pharmaceuticals Reports Second Quarter 2006 Financial Results )〕 The side-effects reported in Phase I trials of seliciclib for NSCLC were "nausea, vomiting, transient elevations in serum creatinine and liver function parameters and transient hypokalemia".〔 Seliciclib is also in clinical trials for B-cell lymphomas, including multiple myeloma. Seliciclib has been shown to inhibit RNA polymerase II-dependent transcription and down-regulation of the protein MCL1. Seliciclib is also a possible antiviral agent. It causes the death of cells infected with HIV and preventing the replication of Herpes simplex virus. Seliciclib has been shown ''in vitro'' to induce apoptosis in neutrophil granulocytes. If this mechanism turns out to be safe, reliable and efficient ''in vivo'', the drug could improve treatment of chronic inflammation diseases such as cystic fibrosis and arthritis. These are usually treated with glucocorticoids which often have serious side effects. Seliciclib has been shown to cause parthogenetic egg activation. However it does create abnormal second polar bodies and therefore possible aneuploid zygotes. Egg activation usually involves calcium oscillations however this does not happen with seliciclib. Seciclib causes egg activation by inhibiting protein kinases which results in the inactivation of the maturation promoting factor (MPF).〔Doree M, Galas S. The cyclin-dependent protein kinases and the control of cell division. FASEB J 1994; 8:1114–1121〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Seliciclib」の詳細全文を読む スポンサード リンク
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