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Treatment with the CD3 x CD123 bispecific antibody APVO436 plus venetoclax and azacitidine led to durable remissions in patients with relapsed/refractory acute myeloid leukemia who had not received prior venetoclax.
Treatment with the CD3 x CD123 bispecific antibody APVO436 plus venetoclax (Venclexta) and azacitidine (Vidaza) led to durable remissions in patients with relapsed/refractory acute myeloid leukemia (AML) who had not received prior venetoclax, according to data from the dose-escalation portion of a phase 1/2 trial (NCT03647800).1
Among 11 treated patients, 9 (82%) experienced a favorable response and were evaluable for duration of remission (DOR). The median DOR was not reached. Three patients underwent stem cell transplant after achieving a sufficient response. Notably, 1 patient experienced a complete response and received the maximum of 8 cycles of treatment, leading to a DOR of at least 8 months.
“This DOR data adds to a growing body of clinical evidence [safety, tolerability, efficacy and now durability] that provides strong support for the further development of APVO436 in combination therapy for patients with AML,” Aptevo Therapeutics wrote in a news release announcing the data.
Previously reported data from the dose-escalation portion of the study showed that APVO436 plus venetoclax and azacitidine produced a clinical benefit rate of 91% in venetoclax-naïve patients with AML.
APVO436 was considered safe and well tolerated. Less than 25% of patients experienced cytokine release syndrome (CRS), and most instances of CRS were mild or moderate at grade 1 or 2.
The dose-escalation portion of the study enrolled patients at least 18 years of age with histologically confirmed AML or myelodysplastic syndromes (MDS).2 Patients with AML needed to have relapsed or refractory disease and refused or were not candidates for intensive chemotherapy or allogeneic transplant. All patients were required to have an ECOG performance status of 0 to 2 and a life expectancy of more than 2 months in the opinion of the investigator.
Key exclusion criteria included any central nervous system disease related to the underlying malignancy, a history of seizures, acute promyelocytic leukemia, prior treatment with an anti-CD123 therapy, any clinically significant graft-vs-host disease secondary to prior allogenic stem cell transplant, or any therapy or experimental treatment for MDS or AML within 7 days of the first dose of study drug.
Dose escalation started with 3 single-patient cohorts, with the next cohort enrolling only after a patient completed the first 4-week cycle of treatment without experiencing grade 2 or higher adverse effects. In any cohorts where grade 2 or higher AEs were reported, they were expanded to a 3+3 design. Cohort 4 and subsequent cohorts were 3+3, and these started after patients in the prior cohort who completed the first cycle of treatment were evaluated for AEs and dose-limiting toxicities. Patients received intravenous APVO436 in 6, 28-day cycles, unless they experienced disease progression, had intolerable toxicity, or withdrew consent. Notably, starting in cohort 5, step-up dosing was introduced to mitigate infusion-related reactions and CRS.
Determining the maximum tolerated dose was the primary end point of dose escalation. Secondary end points included frequency and severity of AEs, pharmacokinetics and pharmacodynamics, and immunogenicity.
The phase 2 program for APVO436 will include trials enrolling patients with AML both in the frontline and relapsed/refractory settings who are naïve to venetoclax. The first trial enrolling patients with relapsed/refractory AML is expected to begin in the second half of 2023, and the frontline trial is slated to start in the first half of 2024.