Seattle Genetics, Inc. (Nasdaq: SGEN) today announced that its collaborator, Takeda Pharmaceutical Company Limited (Takeda), has received approval of ADCETRIS (brentuximab vedotin) from the Japanese Ministry of Health, Labour and Welfare (MHLW) for the treatment of patients with CD30-positive relapsed or refractory Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL). As a result, Seattle Genetics will receive two milestone payments from Takeda totaling $9 million upon final pricing agreement in Japan. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL and known to be expressed in some types of non-Hodgkin lymphoma, including ALCL.
“Until now, patients in Japan with relapsed or refractory Hodgkin lymphoma or ALCL had few therapeutic treatment options, and the approval of ADCETRIS represents a significant milestone in making this innovative targeted therapy available to these patients in need,” said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. “ADCETRIS is now approved in 39 countries, and we continue to work with our collaborator, Takeda, to expand regulatory approvals globally. Through both our regulatory activities and robust clinical development program, our goal is to establish ADCETRIS as the foundation of therapy worldwide for patients with CD30-positive malignancies.”
The approval of the new drug application was based on two global pivotal phase 2 clinical trials of ADCETRIS, as well as a phase 1/2 clinical trial conducted in Japan, for patients with relapsed or refractory CD30-positive HL and ALCL. In March 2012, the Japanese MHLW granted ADCETRIS orphan drug designation for the treatment of patients with HL and ALCL, which triggered priority review in Japan.
About ADCETRISADCETRIS (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.