Seattle Genetics Highlights ADCETRIS® (Brentuximab Vedotin) Data In Relapsed Hodgkin Lymphoma And Other CD30-Positive Malignancies From Multiple Presentations At ASH Annual Meeting
Data highlights from the retrospective analysis of ADCETRIS treated patients age 60 and older were:
- Of the 40 patients evaluated, 33 patients (83 percent) had an objective response, including 18 (45 percent) complete remissions and 15 (38 percent) partial remissions.
- Of the 22 patients with sALCL and two patients with other CD30-positive malignancy, all 24 patients (100 percent) achieved an objective response. Of the 16 patients with HL, nine patients (56 percent) achieved an objective response.
- The incidence of adverse events was generally similar in older and younger patients, with peripheral sensory neuropathy, fatigue and anemia appearing to be more common among patients age 60 or older. Adverse events were manageable with dose modifications or delays.
- The most common adverse events of any grade with an incidence greater than 25 percent were peripheral sensory neuropathy (60 percent), fatigue (58 percent), nausea (38 percent), anemia (30 percent), fever (28 percent), diarrhea (25 percent) and neutropenia (25 percent).
- The most common Grade 3 or 4 adverse events were neutropenia (25 percent), anemia (20 percent), peripheral sensory neuropathy (15 percent), fatigue (10 percent) and thrombocytopenia (10 percent).
ADCETRIS is not approved for the treatment of all CD30-positive hematologic malignancies. A phase II clinical trial evaluating single-agent ADCETRIS as front-line therapy for HL patients age 60 and older is currently enrolling patients. For more information about this clinical trial, visit www.clinicaltrials.gov.
ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics’ proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.
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