, Volume 65, Issue 16, pp 2405–2427

Gemtuzumab Ozogamicin

A Review of its Use in Acute Myeloid Leukaemia
Adis Drug Evaluation



Gemtuzumab ozogamicin (Mylotarg®) is a conjugate of a monoclonal antibody and calicheamicin, which targets the membrane antigen CD33 in CD33-positive acute myeloid leukaemia (AML) and, after cell internalisation, releases a derivative of the cytotoxic calicheamicin component. In the US, it is approved as monotherapy in patients aged ≥60 years with a first relapse of AML who are ineligible for other cytotoxic therapy.

Monotherapy with gemtuzumab ozogamicin results in complete remission (CR) or CR with incomplete platelet recovery (CRp) in ≈25% of adults (including those aged ≥60 years) with CD33-positive AML in first relapse. Preliminary data indicate a potential role for gemtuzumab ozogamicin as a component of induction or consolidation regimens in adults and, based on an early study, in the treatment of children with AML, although randomised, controlled studies are needed. Serious adverse events, notably hepatotoxicity, characterise its tolerability profile, but gemtuzumab ozogamicin is comparatively well tolerated by most patients. Gemtuzumab ozogamicin is a valuable new treatment option for patients aged ≥60 years with CD33-positive AML in first relapse for whom other cytotoxic chemotherapy is not considered appropriate; patients with a first CR (CR1) of >12 months are likely to have the best outcome.

Pharmacological Properties

Gemtuzumab ozogamicin is a humanised monoclonal antibody conjugated to a cytotoxic calicheamicin derivative, which targets the CD33 antigen expressed by leukaemic blasts in most patients with AML. After internalisation by the leukaemic cell, the linker between the antibody and calicheamicin is hydrolysed, calicheamicin dimethyl hydrazide is released and reduced; the reduced species binds to DNA in the minor groove, causing site-specific double-stranded breaks and cell death.

In vitro, gemtuzumab ozogamicin displays good activity against certain CD33+ AML cell lines. At low concentrations (0.01–0.025 ng/mL), in vitro sensitivity of AML cells to gemtuzumab ozogamicin correlates with CD33 expression, but at high concentrations (1–10 μg/mL), CD33-independent uptake may occur. Various gemtuzumab ozogamicin resistance mechanisms have been suggested, including cell escape because of surface antigen expression or cell cycle phase, expression of proteins causing drug efflux, altered signalling pathways, antiapoptotic expression and patient antigen load. Sensitivity to gemtuzumab ozogamicin can be enhanced in vitro by ciclosporin, an inhibitor of p-glycoprotein-mediated drug efflux. In patients, a clinical response is inversely correlated with peripheral blood antigen load and drug efflux ratios, and is not predicted by pharmacokinetic parameters.

The maximum plasma concentrations of the CD33 antibody (hP67.6) and calicheamicin occur shortly after the end of the intravenous infusion of gemtuzumab ozogamicin. Distribution is mainly within plasma and antibody distribution in bone marrow, spleen and liver occurred in radiolabelling studies. The pharmacokinetic parameters of gemtuzumab ozogamicin differ after the first and second doses and vary widely between patients, particularly after the first dose; however, they do not depend on age or gender. The calicheamicin derivative remains conjugated in plasma and hP67.6 is believed to be eliminated from plasma mainly by binding to CD33 expressed on peripheral blast cells.

Therapeutic Efficacy

The clinical efficacy of gemtuzumab ozogamicin has been evaluated in noncomparative trials in adults. In a pooled analysis of three trials, one to three doses of gemtuzumab ozogamicin 9 mg/m2 monotherapy 14–28 days apart, each administered as a 2-hour intravenous infusion, resulted in CR in 13% of 277 patients with a first relapse of primary AML and CRp in another 13%, giving an overall remission (OR) rate of 26%. CR and CRp rates in patients aged ≥60 years, representing 57% of the trial population, were 12% and 12%. The OR rate was 34% in patients with a CR1 of ≥1 year and 11 % in those with a CR1 of ≤6 m onths. Median relapse-free survival for all those in OR was 5.2 months. Median overall survival was almost 5 months for the total patient population, and was >1 year in those patients achieving CR or CRp; overall survival was longer in patients in CR or CRp who proceeded to haematopoietic stem cell transplantation (HSCT) than in those receiving no further treatment.

In a dose-finding noncomparative trial in 29 children (median age 12 years) with relapsed or refractory AML, 14% achieved CR and 14% CRp after one or two gemtuzumab ozogamicin doses of 6–9 mg/m2, but dose-limiting toxicity occurred.

Early-phase trials of gemtuzumab ozogamicin in combination therapy regimens, usually with cytarabine and anthracyclines, resulted in CR rates of 35–83% in adults with primary and secondary AML, including those aged >60 years and, in a consolidation regimen, maintenance of remission in 32% of patients after 1 year.


One to three doses of gemtuzumab ozogamicin 9 mg/m2 were generally fairly well tolerated in adults with relapsed primary AML, although serious adverse events were reported. Patients receiving gemtuzumab ozogamicin monotherapy plus prior or subsequent HSCT had a 17% incidence of hepatic veno-occlusive disease (VOD) and a 10% VOD-associated fatality rate. VOD also occurred in patients who did not have HSCT; other severe hepatotoxicity has affected recipients of gemtuzumab ozogamicin.

Infusion-related events were common but generally transient and reversible. Gemtuzumab ozogamicin has, however, been associated with severe hypersensitivity reactions, including anaphylaxis, infusion reactions and pulmonary events. Almost all patients in phase II trials experienced severe neutropenia and thrombocytopenia, the latter associated with serious bleeding in 13% of patients. Other severe adverse effects had a relatively low incidence; grade 3 or 4 sepsis, pneumonia or nausea or vomiting affected 8–17% of patients. The overall incidence of early treatment-related mortality was 16%. Paediatric patients in a small dose-finding trial experienced similar adverse events, although there was less myelosuppression; VOD occurred at dosages of 6–9 mg/m2 in children and, as in adults, was more common in HSCT recipients, affecting 40%.


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© Adis Data Information BV 2005

Authors and Affiliations

  1. 1.Adis International LimitedMairangi Bay, AucklandNew Zealand

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