Paris (France), October 22, 2020 – 6 pm CEST – Onxeo S.A. (Euronext Paris, NASDAQ Copenhagen: ONXEO), hereafter “Onxeo” or “the Company”, a clinical-stage biotechnology company specializing in the development of innovative drugs targeting tumor DNA Damage response (DDR), in particular against rare or resistant cancers, today announced that it has received from the European Patent Office (EPO) a notice of intent to grant a patent which strengthens the protection in Europe of AsiDNA™, its first-in-class inhibitor of tumor DNA repair in combination with PARP inhibitors (PARPi). This patent protects in particular the method of use of AsiDNA™ in combination with PARP inhibitors in the treatment of certain cancers for which the DNA repair pathway via homologous recombination (HR) is not impaired or deficient, these HR-proficient cancers being mostly insensitive to treatment with PARP inhibitors.

This patent will provide a term of protection until 2036. It completes the already robust set of patent families protecting AsiDNA™ and its related compounds, alone or in combination.

“To be fully effective, PARPi are dependent on the presence of mutations such as BRCA mutations that inactivate DNA repair via the homologous recombination pathway. The granted patent is based on the fact that AsiDNA™ is able, through its original mechanism of action, to block all DNA repair pathways, including the homologous recombination pathway. AsiDNA™ thus recreates a context of “HR deficiency” allowing PARPi to be effective on tumors that are normally not sensitive to PARPi,” commented Françoise Bono, Chief Scientific Officer of Onxeo.

“This activity reinforces AsiDNA™’s range of potential indications and particularly its interest in association with a PARPi. We have shown in preclinical studies and started the clinical demonstration that AsiDNA™ has the ability to reverse the resistance acquired to a PARP inhibitor in patients eligible for these treatments. Now, another complementary application of AsiDNA™ appears, in combination with PARP inhibitors in HR-proficient patients with little or no sensitivity to PARPi alone.” added Olivier de Beaumont, Chief Medical Officer of Onxeo.

The DNA repair pathways, BRCA-dependent homologous recombination pathway and PARP pathway, are complementary and essential for tumor cell survival and proliferation. If one pathway is deficient (homologous recombination by BRCA mutation) and the other is blocked by a PARP inhibitor, the cell dies (synthetic lethality).  PARPi have demonstrated a real clinical benefit[1], particularly in the treatment of ovarian cancer with BRCA mutations, but this benefit is much reduced, or even insignificant, when homologous recombination remains active in about 50% of patients[2]. Extending the efficacy of PARP inhibitors to this important group would represent a major therapeutic opportunity for these patients whose options are currently limited.

[1] Moore et al. N Engl J Med 2018; 379:2495-2505

[2] Zeimet, A.G., Wieser, V., Knoll, K. et al. PARP inhibitors in the treatment of ovarian cancer. memo (Magazine of European Medical Oncology) 13, 198–201 (2020).