Aprea Therapeutics Inc. (NASDAQ: APRE) has announced positive results from the phase II study evaluating eprenetapopt combination with azacitidine as a post-transplant management therapy in TP53 mutant MDS and AML patients.
The study attained a 58% relapse-free survival rate
The trial’s 33 patients had a 58% relapse-free survival rate at one-year post-transplant, with a median RFS of 12.1 months. Overall survival was 79% at one year after transplantation, with a median OS of 19.3 months. Previous clinical trials investigating post-transplant outcomes in patients with TP53 mutant MDS and AML have revealed around 30% RFS with a median OS of 5 to 8 months after transplantation. Furthermore, patients in the clinical trial tolerated the eprenetapopt and azacitidine post-transplant regimen well. In the second half of 2021, the company plans to meet with the US FDA to discuss the Phase 2 clinical study results, and it expects to share the findings at a future scientific or medical meeting.
Study principal investigator Asmita Mishra said, “The post-transplant RFS and OS data with eprenetapopt and azacitidine maintenance therapy in these very difficult-to-treat TP53 mutant MDS and AML patients are incredibly exciting. Although transplant is currently the only potentially curative treatment for patients with TP53 mutant MDS and AML, the risk of relapse with current standard of care remains unacceptably high and the median OS post-transplant is very limited at 8 months or less. Post-transplant maintenance therapy with eprenetapopt and azacitidine could, if approved, represent a new treatment paradigm that meaningfully improves outcomes for these patients with limited treatment options.”
Eprenetapopt reactivates inactive mutant p53 tumor suppressor gene.
Eprenetapopt (APR-246) is a small molecule the company is advancing that has shown the potential of reactivating the inactive and mutant P53 tumor suppressor gene often associated with around 50% of human cancers. APR-246 reactivates the protein by restoring wild-type P53 gene conformation and function, inducing programmed cell death in cancer cells.
