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Author Notes:

Correspondence: Robert Bray, Email: bray@emory.edu

Disclosures: The authors of this manuscript have conflicts of interest to disclose as described by the American Journal of Transplantation.

M. Roberts, M. Polinsky, and L. Yang are salaried employees of and own stock in Bristol‐Myers Squibb.

R. Townsend and H.‐U. Meier‐Kriesche were salaried employees of Bristol‐Myers Squibb at the time that these analyses undertaken and still own stock in Bristol‐Myers Squibb.

C. P. Larsen has received grants from Bristol‐Myers Squibb.

R. Bray and H. Gebel have no conflicts of interest to disclose.


Research Funding:

The BENEFIT and BENEFIT‐EXT studies were sponsored by Bristol‐Myers Squibb

Support for third‐party writing assistance for this manuscript was provided by Tiffany DeSimone, PhD, of CodonMedical, an Ashfield Company, part of UDG Healthcare plc, and was funded by Bristol‐Myers Squibb.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Surgery
  • Transplantation
  • antibody biology
  • belatacept
  • clinical research
  • practice
  • clinical trial
  • cyclosporin A (CsA)
  • immunosuppressant - calcineurin inhibitor
  • immunosuppressant - fusion proteins and monoclonal antibodies
  • kidney transplantation
  • nephrology

De novo donor-specific antibodies in belatacept-treated vs cyclosporine-treated kidney-transplant recipients: Post hoc analyses of the randomized phase III BENEFIT and BENEFIT-EXT studies


Journal Title:

American Journal of Transplantation


Volume 18, Number 7


, Pages 1783-1789

Type of Work:

Article | Final Publisher PDF


Donor-specific antibodies (DSAs) are associated with an increased risk of antibody-mediated rejection and graft failure. In BENEFIT and BENEFIT-EXT, kidney-transplant recipients were randomized to receive belatacept more intense (MI)–based, belatacept less intense (LI)–based, or cyclosporine-based immunosuppression for up to 7 years (84 months). The presence/absence of HLA-specific antibodies was determined at baseline, at months 6, 12, 24, 36, 48, 60, and 84, and at the time of clinically suspected episodes of acute rejection, using solid-phase flow-cytometry screening. Samples from anti-HLA-positive patients were further tested with a single-antigen bead assay to determine antibody specificities, presence/absence of DSAs, and mean fluorescence intensity (MFI) of any DSAs present. In BENEFIT, de novo DSAs developed in 1.4%, 3.5%, and 12.1% of belatacept MI-treated, belatacept LI-treated, and cyclosporine-treated patients, respectively. The corresponding values in BENEFIT-EXT were 3.8%, 1.1%, and 11.2%. Per Kaplan-Meier analysis, de novo DSA incidence was significantly lower in belatacept-treated vs cyclosporine-treated patients over 7 years in both studies (P <.01). In patients who developed de novo DSAs, belatacept-based immunosuppression was associated with numerically lower MFI vs cyclosporine-based immunosuppression. Although derived post hoc, these data suggest that belatacept-based immunosuppression suppresses de novo DSA development more effectively than cyclosporine-based immunosuppression.

Copyright information:

© 2018 The Authors. American Journal of Transplantation published by Wiley Periodicals, Inc. on behalf of The American Society of Transplantation and the American Society of Transplant Surgeons

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/).

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