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CDP323
CDP323 is a small-molecule prodrug antagonist of the vascular cell adhesion molecule 1 (VCAM-1) binding to α4-integrins. It was originally developed by the British biopharmaceutical company Celltech plc. (now UCB S.A.) and was a putative new drug for oral treatment of multiple sclerosis.〔Davenport RJ, Munday JR. ''Alpha4-integrin antagonism - an effective approach for the treatment of inflammatory diseases?'' Drug Discov Today 2007;12:569-76. PMID 17631252〕
In October 2006, UCB and Biogen Idec announced a collaboration to jointly develop and commercialize CDP323 for the treatment of multiple sclerosis and other potential indications.〔(Press Release UCB S.A. ) 2-Oct-2006; accessed 11-Sep-2007〕 In June 2009, development of CDP323 was discontinued due to discouraging results of a Phase II clinical trial.〔(''UCB: discontinuation of research concerning CDP323''. )〕
== Mechanism of action ==
The mechanism of action of CDP323 were believed to rely on preventing immune cells to migrate from blood vessels through the vessel walls to reach various inflamed tissues, including the brain. This mechanism is thought to prevent overshooting immune reactions and subsequent tissue damage as seen during uncontrolled immune cell migration as in multiple sclerosis. CDP323 has the same mechanism of action as the monoclonal antibody natalizumab.
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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