An orally active proteasome inhibitor induced apoptosis in multiple myeloma (MM) cells

06-21-2006

According to recent research from the United States, "Bortezomib therapy has proven successful for the treatment of relapsed and/or refractory MM; however, prolonged treatment is associated with toxicity and development of drug resistance. Here, we show that the novel proteasome inhibitor NPI-0052 induces apoptosis in MM cells resistant to conventional and Bortezomib therapies."

"NPI-0052 is distinct from Bortezomib in its chemical structure, effects on proteasome activities, mechanisms of action, and toxicity profile against normal cells. Moreover, NPI-0052 is orally bioactive. In animal tumor model studies, NPI-0052 is well tolerated and prolongs survival, with significantly reduced tumor recurrence. Combining NPI-0052 and Bortezomib induces synergistic anti-MM activity," explained D. Chauhan and colleagues, Harvard University.

The researchers concluded, "Our study therefore provides the rationale for clinical protocols evaluating NPI-0052, alone and together with Bortezomib, to improve patient outcome in MM."

Chauhan and colleagues published their study in Cancer Cell (A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib. Cancer Cell, 2005;8(5):407-419).

For additional information, contact K.C. Anderson, Harvard University, School of Medicine, Dana Farber Cancer Institute, Dept. Med Oncology, Jerome Lipper Multiple Myeloma Center, Boston, MA 02115, USA.

Publisher contact information for the journal Cancer Cell is: Cell Press, 1100 Massachusetts Avenue, Cambridge, MA 02138, USA.