Aprea Therapeutics has enrolled its first patients in Phase II of an ongoing clinical study of APR-246, a potential treatment of high-grade serous ovarian cancer.
The biopharmaceutical company has been developing novel anticancer therapies targeting the tumour suppressor protein p53.
Aprea Therapeutics president and chief executive officer Christian S. Schade said: "The initiation of the Phase II clinical study marks an important milestone for Aprea.
"We are committed to developing and advancing therapies targeting p53 and, together with upcoming clinical studies of APR-246 in other tumour types, this Phase II study in ovarian cancer affirms the progress Aprea is making toward the development of next-generation anticancer treatments."
For the Phase II clinical study, Aprea will enrol up to 400 relapsed, p53-mutated, high-grade ovarian cancer patients in Europe and the US.
Patients will be randomly given carboplatin and pegylated liposomal doxorubicin with or without APR-246; the primary endpoint for the study is progression-free survival.
This trial comes after the successful completion of Phase Ib clinical studies showing that APR-246 is generally well-tolerated while showing robust signals of efficacy in patients with serious disease.
Aprea senior vice president and chief medical officer Dr. Mikael von Euler said: "APR-246 is an exciting new agent because it targets tumours with mutant forms of p53, the gene most frequently altered in human cancers.
"The Phase Ib portion of this study demonstrated not only that APR-246 can be safely combined with standard chemotherapy for relapsed ovarian cancer but also that a favourable impact on progression-free survival could be achieved with the combination regimen in this difficult-to-treat population.
"We are pleased to continue development of this drug candidate and look forward to validating these Phase Ib findings in the randomised Phase II part of the study."
The p53 tumour suppressor gene is a frequently mutated gene in human cancer, occurring in approximately 50% of all human tumours.
These mutations are often associated with resistance to anti-cancer drugs.
APR-246 has been shown to convert the mutant p53 into a wild-type p53 form, thereby inducing programmed cell death in human cancer cells.