Alemtuzumab for Cytolytic Induction of Immunosuppression in Heart Transplant Recipients

Abstract

Although alemtuzumab may be a practical option for inducing immunosuppression, data are insufficient to recommend its routine use in deference to more established agents. Large, randomized clinical trials with extended durations of follow-up must be conducted to characterize its efficacy and safety further.

Immunosuppressive therapies after heart transplantation — The balance between under- and over-immunosuppression

“…These initial results were then confirmed in a larger case control series by Teuteberg et al [43][44][45][46][47]. Further studies on alemtuzumab are, however, needed before its routine use can be considered [48].…”

Impact of induction immunosuppression on survival in heart transplant recipients: a contemporary analysis of agents

“…In our analysis of the UNOS/STAR database, we found that the use of antibody based induction immunosuppression in heart transplant recipients, in general, is not associated with significant differences in overall survival. Previously published reports have demonstrated an accepted improvement in general outcomes with antibody based induction therapy .…”

“…In our analysis of the UNOS/STAR database, we found that the use of antibody based induction immunosuppression in heart transplant recipients, in general, is not associated with significant differences in overall survival. Previously published reports have demonstrated an accepted improvement in general outcomes with antibody based induction therapy (5)(6)(7)(8)(9)(10)(11)(12). The agents used in these reports have been variedranging from the IL-2 receptor antibodies (basiliximab or daclizumab), T-cell depleting agents (anti-thymocyte globulin [ATG], anti-lymphocyte globulin [ALG], and thymoglobulin), CD52 monoclonal antibody (alemtuzumab), to monoclonal anti-CD3 agent OKT3.…”

Immune Checkpoint Inhibitor-Associated Cardiotoxicity: Current Understanding on Its Mechanism, Diagnosis and Management

“…Alemtuzumab, a monoclonal antibody that binds to CD52, can result in destruction of complement-mediated peripheral immune cells (monocytes, lymphocytes, macrophages, natural killer cells, and dendritic cells). Although the use of alemtuzumab in the context of cardiac allograft rejection has previously been evaluated, data on its use in patients with irAEs is limited (Cahoon et al, 2012). A recent report has indicated that 30 mg of alemtuzumab led to rapid T-cell depletion and was associated with the resolution of cardiac immunotoxic effects (Esfahani et al, 2019).…”