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Belatacept: A worthy alternative to cyclosporine?

Journal of Pharmacology and Pharmacotherapeutics
Medknow Publications
Publication Date
DOI: 10.4103/0976-500x.92499
  • Molecules Of The Millennium
  • Medicine
  • Pharmacology


INTRODUCTION Renal transplant is the definitive therapy in patients with end-stage renal disease (ESRD) and offers the only solace for such patients who have no alternative other than frequent hemodialysis, a process which contributes to sufficient morbidity.[1] Recent developments in the field of renal transplant including novel drugs have contributed immensely to the improvement in 1-year graft survival rates which approach almost 90%.[2] The pharmacotherapy of organ transplantation for immunosuppression consists primarily of an induction regimen comprising a monoclonal antibody such as basiliximab followed by maintenance immunosuppression consisting of calcineurin inhibitors (CNI) like cyclosporine or tacrolimus, and antiproliferative agents (mycophenolate mofetil) and low-dose corticosteroids. Long-term benefits of these drugs have not been as satisfactory, with the 5-year graft survival falling as low as 72%. Allograft dysfunction is a common cause for allograft loss. Several factors contribute to allograft dysfunction such as interstitial fibrosis, tubular atrophy and chronic toxicity of CNIs.[3] By the end of 2 years as many as 50% of patients on CNIs develop nephrotoxicity. The increased incidence of cardiovascular diseases in these group of patients have also been attributed to CNI owing to the drug's propensity to worsen hypertension, diabetes and dyslipidemia.[4–7] An active search for a better alternative to alleviate the suffering of patients on long-term immunosuppressive post renal transplant has led to the development of a new drug belatacept, recently approved by USFDA in June 2011. MECHANISM OF ACTION Belatacept is a selective T-cell costimulation blocker. It compises of a recombinant extracellular domain of human cytotoxic T lymphocyte antigen-4 (CTLA-4) and a fragment of a modified Fc portion of human IgG1. The drug binds to CD 80/86 ligands of antigen-stimulating cells and thereby inhibits the CD-28-mediated T-cell costimulation. T-cells activation requ

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