What happened to anti-CD33 therapy for acute myeloid leukemia?

Curr Hematol Malig Rep. 2012 Mar;7(1):65-73. doi: 10.1007/s11899-011-0103-0.


CD33, a 67-kDa glycoprotein expressed on the majority of myeloid leukemia cells as well as on normal myeloid and monocytic precursors, has been an attractive target for monoclonal antibody (mAb)-based therapy of acute myeloid leukemia (AML). Lintuzumab, an unconjugated, humanized anti-CD33 mAb, has modest single-agent activity against AML but failed to improve patient outcomes in two randomized trials when combined with conventional chemotherapy. Gemtuzumab ozogamicin, an anti-CD33 mAb conjugated to the antitumor antibiotic calicheamicin, improved survival in a subset of AML patients when combined with standard chemotherapy, but safety concerns led to US marketing withdrawal. The activity of these agents confirms that CD33 remains a viable therapeutic target for AML. Strategies to improve the results of mAb-based therapies for AML include antibody engineering to enhance effector function, use of alternative drugs and chemical linkers to develop safer and more effective drug conjugates, and radioimmunotherapeutic approaches.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aminoglycosides / therapeutic use*
  • Antibodies, Monoclonal, Humanized / therapeutic use*
  • Antigens, CD / immunology*
  • Antigens, Differentiation, Myelomonocytic / immunology*
  • Antineoplastic Agents / therapeutic use*
  • Gemtuzumab
  • Humans
  • Leukemia, Myeloid, Acute / therapy*
  • Radioimmunotherapy / methods*
  • Sialic Acid Binding Ig-like Lectin 3


  • Aminoglycosides
  • Antibodies, Monoclonal, Humanized
  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • Antineoplastic Agents
  • CD33 protein, human
  • Sialic Acid Binding Ig-like Lectin 3
  • Gemtuzumab
  • lintuzumab