Inotuzumab ozogamicin was able to eliminate residual disease among adult patients with B-cell acute lymphoblastic leukemia (ALL), leading to improved long-term overall survival outcomes, according to findings from a single-center phase II trial published in Blood Cancer Journal.
“Our results show that inotuzumab is highly effective at clearing residual disease in patients already in remission, with durable responses and encouraging survival,” said principal investigator Elias Jabbour, MD, Professor of Leukemia, The University of Texas MD Anderson Cancer Center. “This approach has the potential to deepen remissions and change how we manage patients at high risk of relapse.”
Background and Study Methods
Inotuzumab ozogamicin is a targeted anti-CD22 antibody-drug conjugate that has already induced high response rates in patients with ALL.
In the single-center phase II study, the investigators evaluated the use of inotuzumab ozogamicin at 0.6 mg/m2 day 1 and 0.3 mg/m2 day 8 (cycle 1) followed by 0.3 mg/m2 days 1 and 8 (cycles 2–6) for adults with B-cell ALL who were in morphologic remission with detectable measurable residual disease (n = 37).
Key Findings
Twenty-six patients (70%) achieved measurable residual disease negativity, including 76% of the patients with Philadelphia chromosome (Ph)-negative ALL (n = 17), and 65% of the Ph-positive patients. The measurable residual disease negativity rate on next-generation sequencing was 73%.
Patients were followed for a median of 50 months. The median overall survival was 61 months, with a median relapse-free survival of 40 months.
Patients who were in their first remission had a median overall survival that was not yet reached vs 14 months for patients in their second remission or beyond (P = .056).
Three cases (8%) of nonfatal sinusoidal obstructive syndrome were reported, but treatment was otherwise considered safe.
DISCLOSURES: This research was supported by the University of Texas MD Anderson institutional funds and Pfizer. For full disclosures of the study authors, visit nature.com.
