ALLO-715 Found to Be Effective Against Multiple Myeloma

A pair of allogeneic chimeric antigen receptor (CAR) T-cell therapies, ALLO-715 and ALLO-647, may be safe and effective treatments for patients with multiple myeloma, according to a presentation at the 62^nd American Society of Hematology Annual Meeting and Exposition.

ALL0-715 is a genetically modified anti-BCMA AlloCAR T cell product in which the TCR alpha constant gene is disrupted in order to reduce the risk of graft-versus-host disease. The C52 gene is disrupted with Talen technology to the permit the use of ALLO-647, which is an anti-CD52 mAbm for selective and prolonged host lymphodepletion, according to the study.

The phase 1 open-label trial was made up of 19 patients who have received 3 or more prior lines of therapy, including a proteasome inhibitor, immunomodulator, and an anti-CD38 monoclonal antibody. All participants must be refractory to their last line of treatment. Patients received lymphodepletion followed by ALLO-715 at 1 of 4 dose levels in a 3+3 escalation design.

According to the study, a higher dose of ALLO-715 was associated with greater anti-cancer activity. Of the 19 patients, 15 received ALLO-715 at 3 dose levels. Eighty percent of responders were still in response at the time of data cutoff. Cytokine release syndrome was reported in 24% of patients. Over the course of the trial, 1 death occurred after the patient went into respiratory failure, but it was considered related to conditioning, according to the study.

Early data suggest that ALLO-715 and ALLO-647 have manageable safety profiles. Enrollment in ongoing cohorts with higher ALLO-715 and ALLO-647 are ongoing. According to the study, ALLO-715 showed evidence of clinical activity in the allogenic setting in patients with relapsed/refractory multiple myeloma.

REFERENCE

Mailankody, S. et al. 129 Universal: An Allogeneic First-in-Human Study of the Anti-Bcma ALLO-715 and the Anti-CD52 ALLO-647 in Relapsed/Refractory Multiple Myeloma [Abstract] December 5, 2020. Accessed December 14, 2020. https://ash.confex.com/ash/2020/webprogram/Paper140641.html.