Currently Enrolling Trials
Campath, a humanized monoclonal antibody, has been approved as an injectable treatment for B-cell chronic lymphocytic leukemia (B-CLL). Campath is designed for use in B-CLL patients who have been treated with alkylating agents and have failed fludarabine therapy. This drug gives refractory B-CLL patients a new hope for treatment, as there are no other approved therapeutic options.
Chronic lymphocytic leukemia is the most prevalent form of leukemia in adults and affects approximately 120,000 patients in the United States and Europe. B-CLL is characterized by an accumulation of leukemic lymphocytes in the bone marrow, blood, and other body tissues. This accumulation leads to bone marrow dysfunction and enlargement of the lymph nodes, liver, and spleen. Related symptoms of the disease include fatigue, bone pain, night sweats, decreased appetite, and weight loss.
Campath was evaluated in a multi-center, open-label, noncomparative study of 93 B-CLL patients previously treated with alkylating agents, who had failed fludarabine treatment. There were also two supportive, multi-center, open-label, noncomparative trials of Campath enrolling a total of 56 B-CLL patients. Results were determined by objective tumor response rates and duration of response, as defined by the NCI Working Group Response Criteria.
In the largest of the three trials, an overall response rate of 33 percent was observed, with a median duration of seven months. A 30 percent mortality rate was recorded, either during the study or within six months of its completion. Half of these deaths were due to progression of the disease, while the other half were related to Campath therapy. Adverse events associated with Campath therapy included infusion-related events, infections, and hematological toxicity.
Adverse events associated with the use of Campath therapy may include (but are not limited to) the following:
- Fever and rigors
Mechanism of Action
Campath (alemtuzumab) works by binding to the CD52 antigen that is present on the surface of the malignant lymphocytes. After binding, the drug induces antibody-dependent lysis, or killing. This causes the removal of malignant lymphocytes from the blood, bone marrow, and other affected organs.
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