Send to:

Choose Destination
See comment in PubMed Commons below
Expert Opin Biol Ther. 2012 Jul;12(7):965-79. doi: 10.1517/14712598.2012.683522. Epub 2012 May 8.

Belatacept : a new biological agent for maintenance immunosuppression in kidney transplantation.

Author information

  • 1Allegheny General Hospital, Division of Nephrology and Hypertension, Department of Medicine, Pittsburgh, PA 15212, USA.



Over the past decades, calcineurin inhibitors (CNIs) have become the cornerstone of transplant immunosuppression. CNIs can exert negative effects on chronic allograft function along with cardiovascular (CV) and metabolic adverse effects. Belatacept , a selective co-stimulation blocker of T cells, is the first US FDA (06/2011) and EMEA (06/2011) approved biologic agent for maintenance immunosuppression in renal transplantation.


The authors critically reviewed the literature over the last few years comparing belatacept with current standard of maintenance immunosuppression including CNIs in kidney transplantation.


Despite the increased incidence and severity of acute rejection with belatacept in Phase II and III studies, a better preservation of GFR and reduced incidence of chronic allograft nephropathy was observed as compared with CNIs. Patient and graft survivals were similar over 3- and 5-year follow-up post-transplantation. Incidence of adverse events were similar between the groups, but the risk of post-transplant lymphoproliferative disorder, predominantly involving CNS, was higher in Epstein-Barr virus seronegative recipients on belatacept, especially with a more intensive regimen. CV and metabolic end points were more favorable in belatacept versus CNI groups with similar incidences of diabetes after transplantation. Belatacept seems to be a promising drug for the future, but long-term outcomes are awaited.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Write to the Help Desk