Kadcyla To be more specific, DM1-containing catabolites are released.

Kadcyla is a HER2- targeted
antibody drug conjugate (ADC). It works directly inside cancerous cells however
Avastin does not. When Trastuzumab emtansine (T-DM1) binds to HER2 on the
plasmas membrane, using a stable linker it creates a complex of HER2-TDM1 which
inserts itself into the cell by receptor-mediated endocytosis. Avastin however,
does not form a complex on the plasma membrane. The adopted endocytic vesicles then
produce premature endosomes. These can either be reutilized and put back to the
cell membrane or they can develop to form a lysosome. Proteolytic deterioration
of the antibody fragment of T-DMI in the lysosomes instigates the release of DM1
(emtansine). To be more specific, DM1-containing catabolites are released. This
constrains microtubule congress resulting in cell apoptosis. When DM1 binds to
tubulin, it disorders microtubule networks in the cell. (Barok, Joensuu, Isola 2014) Subsequently, at the G2-M phase cell
cycle arrest happens and thus cell death occurs. In human breast cancer cells
that overexpress HER2, Trastuzumab emtansine impedes HER2 receptor signalling, reconciles
antibody-dependent cell-mediated cytotoxicity, and hinders shedding of the HER2
extracellular field. (Google Books 2018)
Both Kadcyla and Avastin cause cell apoptosis. Trastuzumab is the predominant
therapy used for HER2-positive breast cancer. Kadcyla is clinically proven to
be the most effective with metastatic breast cancer (MBC) and early breast
cancer (EBC). In both breast cancers, there has been improvement in survival
rate. (Dubel, Reichert 2014)