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Published on: May 1, 2015

A novel Bcl-2/Bcl-X(L)/Bcl-w inhibitor ABT-737 as therapy in multiple myeloma

D Chauhan1, M Velankar, M Brahmandam

  • 1The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.

Oncogene
|October 4, 2006
PubMed

Insights

ABT-737, a novel inhibitor of antiapoptotic proteins, effectively induces apoptosis in multiple myeloma (MM) cells, including drug-resistant types. This compound shows promise for overcoming chemotherapy resistance in MM patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Bcl-2 and Bcl-X(L) proteins are key regulators of apoptosis and contribute to chemotherapy resistance in multiple myeloma (MM).
  • Existing therapies for MM often face challenges due to drug resistance mediated by these antiapoptotic proteins.

Purpose of the Study:

  • To characterize the effects of ABT-737, a potent small-molecule inhibitor of Bcl-2, Bcl-X(L), and Bcl-w, on human multiple myeloma cells.
  • To evaluate the efficacy of ABT-737 in overcoming drug resistance and its potential combination therapy in MM.

Main Methods:

  • Treatment of human MM cell lines and purified patient MM cells with ABT-737.
  • Assessment of apoptosis induction, cell viability, and toxicity against normal cells.
  • Evaluation of ABT-737 in combination with standard MM therapies like bortezomib, melphalan, and dexamethasone.

Main Results:

  • ABT-737 effectively induced apoptosis in MM cells, including those resistant to conventional therapies and refractory to bortezomib, dexamethasone, and thalidomide.
  • The compound demonstrated minimal toxicity to normal peripheral blood mononuclear cells and bone marrow stromal cells.
  • ABT-737 abrogated MM cell growth stimulated by interleukin-6 or insulin-like growth factor-1 and activated caspases, leading to apoptosis.

Conclusions:

  • ABT-737 is a potent inducer of apoptosis in multiple myeloma cells and overcomes resistance mechanisms.
  • Combination therapy with ABT-737 and standard MM drugs (bortezomib, melphalan, dexamethasone) shows additive anti-MM activity.
  • These findings support clinical evaluation of ABT-737 for improving MM treatment outcomes.

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