Onxeo to Present Data supporting Lead Asset AsiDNA in 5 Poster Presentations at 2019 American Association for Cancer Research Annual Meeting

Regulatory News:

Onxeo S.A. (Euronext Paris, NASDAQ Copenhagen: ONXEO), (“Onxeo” or “the Company”), a clinical-stage biotechnology company specializing in the development of innovative drugs targeting tumor DNA Damage response (DDR) in oncology, in particular against rare or resistant cancers, today provides details on the presentation of data from five studies supporting the company’s lead drug candidate, AsiDNA, in poster sessions at the upcoming American Association for Cancer Research (AACR) Annual Meeting being held March 29 - April 3, 2019, in Atlanta, GA, USA.

Françoise Bono, PhD, Chief Scientific Officer, commented: “We are very pleased to have five studies accepted and presented at the prominent AACR meeting as it reflects the interest, the quality and the diversity of our current translational research on AsiDNA. Through these data, we further demonstrate the uniqueness of our lead compound in terms of mechanism of action and its related unique properties, especially on preventing the occurrence of resistance to treatment, one of the major issues in oncology today. All these data complement and reinforce our rationale for the continued clinical development of AsiDNA expected to start in the coming weeks, now that we have identified the active doses that trigger target engagement and confirmed the favorable safety profile in our phase I DRIIV study. We look forward to presenting and discussing our very exciting findings during the conference."

Details of the sessions on April 1 and 2, 2019 include:

Abstract 2095 / Poster 2 – AsiDNA, a targeted therapy with no acquired resistance

Session: PO.ET03.03. Drug Resistance 3
Date: Monday, April 1
Time: 1:00 p.m. – 5:00 p.m. ET
Location: Section 11

AsiDNA is the first antitumor drug with an agonist activity. This study demonstrates that long term exposure of cancer cells to the strong alarm signal, generated by AsiDNA does not promote resistance emergence. It induces a stable new state characterized by the down regulation of the targeted pathways that persists for months after treatment. This property is due to the original mechanism of action of AsiDNA, which acts by over-activating a “false” signaling of DNA damage through DNA-PK and PARP enzymes. Such property is not observed with other DNA repair inhibitors such as the PARP inhibitors olaparib and talazoparib. Long term treatment with AsiDNA induces the occurrence of an “alarm down” state in the tumor cells that increases product’s efficacy. These results suggest that agonist drugs such as AsiDNA could promote a state-dependent tumor cell evolution by lowering their ability to respond to damage signal.