Abatacept in the treatment of rheumatoid arthritis

Abstract

T-cell biology has regained importance in the pathogenesis of rheumatoid arthritis. Despite the significant improvements associated with the introduction of tumor necrosis factor-alpha blockade, reasonable proportions of failures and suboptimal responses have been reported, necessitating a search for alternative targeted therapies. This has included drug therapy designed to interrupt T-cell activation via the co-stimulation pathway. Abatacept is a recombinant fusion protein that blocks the co-stimulatory signal mediated by the CD28-CD80/86 pathway, which is required for T-cell activation. Several clinical trials have confirmed the safety and efficacy of this drug in the treatment of rheumatoid arthritis. This review summarizes the clinical data supporting this line of treatment and considers the safety and efficacy data from phase II and III trials.

Figure 1

Mean SF-36 (a) physical (PCS) and (b) mental (MCS) component summary score by treatment group and visit (*P < 0.05; ^†P < 0.01; ^‡P < 0.001). Treatment groups are 'Abatacept' = abatacept + MTX and 'Placebo' = placebo + MTX. Reproduced from Ann Rheum Dis 2007, 66: 189–194 [32] with permission from the BMJ Publishing Group.

Figure 2

Mean (a) Fatigue VAS score and (b) HAQ-DI score by treatment group and visit (*P < 0.05; ^†P < 0.01; ^‡P < 0.001). Treatment groups are 'Abatacept' = abatacept + MTX and 'Placebo' = placebo + MTX. Reproduced from Ann Rheum Dis 2007, 66: 189–194 [32] with permission from the BMJ Publishing Group.