Seattle Genetics, Inc. has announced that it has initiated a second phase I clinical trial of SGN-35 in patients with Hodgkin lymphoma and other CD30-positive hematologic malignancies. SGN-35 is an antibody-drug conjugate (ADC) that utilizes Seattle Genetics’ proprietary technology to empower antibodies by linking them to potent cell-killing drugs.
“We are investing in a robust SGN-35 clinical program in order to fully explore the therapeutic potential of this first-in-class ADC,” said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer of Seattle Genetics.
“We are very encouraged by the multiple objective responses observed at well-tolerated doses in our ongoing phase I trial of SGN-35 utilizing an every three week dosing schedule, and we look forward to reporting additional data at the American Society of Clinical Oncology meeting in early June. In addition, we are initiating this second phase I trial to evaluate the tolerability, antitumor activity and pharmacokinetic profile of more frequent SGN-35 dosing, followed by an exploration of SGN-35 in combination with Gemzar, a chemotherapy agent commonly used in the treatment of Hodgkin lymphoma. During 2008, we are planning to move forward rapidly to define our development pathway for SGN-35, including late-stage clinical trials and registration strategy.”
The phase I study will initially evaluate escalating single-agent doses of SGN-35 administered weekly to patients with relapsed or refractory CD30-positive hematologic malignancies, including Hodgkin lymphoma. Following the monotherapy portion of the study, the trial will continue with an investigation of SGN-35 in combination with Gemzar (gemcitabine). The trial is expected to enroll up to approximately 40 patients at multiple centers in the United States.
SGN-35 is an ADC comprising an anti-CD30 antibody attached by an enzyme cleavable linker to a potent, synthetic drug payload, monomethyl auristatin E (MMAE), using Seattle Genetics’ proprietary technology. The ADC is designed to be stable in the bloodstream, but to release MMAE upon internalization into CD30-expressing tumor cells, resulting in a targeted cell-killing effect.