Alemtuzumab (Campath)

Targets CD52 which may be present on B-cells, T-cells and natural killer cells.

Mechanism of action on B-cell CLL cells includes antibody dependent cytotoxicity, complement mediated cell lysis, and induction of apoptosis in chronic lymphocytic cell leukemia.

Active in several B and T cell lymphomas including peripheral T cell lymphoma, cutaneous T cell lymphoma and follicular lymphoma.

Subcutaneous administration associated with fewer flu-like symptoms than intravenous administration.

Capable of inducing a remission in some patients with CLL who have relapsed following fludarabine treatment.

When used as a first-line treatment in chronic lymphocytic leukemia the effect on enlarged lymph nodes is more significant then when used in refractory disease.

Anti-infective prophylactic therapy should be initiated at the onset of chemotherapy and continued for 2 months after the completion of treatment or until CD4 count is greater or equal to 200 cells/microL.

Rapidly depletes malignant lymphocytes as well as CD52 expressing B lymphocytes and T lymphocytes, natural killer cells and monocytes.

Pulsed treatment causes prolonged T-cell depletion and modulation of lymphocyte function.

Depletion in lymphocytes associated with increased susceptibility to opportunistic infection, particularly in immunocompromised patients associated a result of disease or prior treatment.

CMV reactivation is most common opportunistic infection in CLL patients treated with alemtuzumab.

When used in multiple sclerosis associated with autoimmunity, most seriously ITP.

Antibody induction therapy includes rabbit anti-thymocyte globulin which is a lymphocyte depleting polyclonal antibody, and basiliximab, a non-lymphocyte depleting monoclonal antibody targeting the interleukin-2-receptor.

Alemtuzumab antibody induction therapy decreases acute kidney rejetion compared to conventional therapy in renal transplant patients (Hanaway MJ et al).

In a phase 2 study of CLL patients who had failed fludarabine this agent achieved a 33% overall response and 16 month median overall survival (Keating M et al).

Recommended as use as a single agent or combined with fludarabine as first line therapy and advanced CLL for patients with poor prognostic cytogenetics, such as 17p.

Presently the only drug approved that has activity for patients with leukemia cells that lack p53 function.

Tradename Lamtrada.

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