On March 8, 2024 Onconova Therapeutics, Inc. (NASDAQ: ONTX), ("Onconova" or "the Company"), a clinical-stage biopharmaceutical company focused on discovering and developing novel products for patients with cancer, reported that the Company will present an abstract related to preclinical studies conducted by the Company and its collaborators to further characterize the mechanism of rigosertib at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2024 (AACR 2024), taking place April 5-10, 2024 in San Diego, CA (Press release, Onconova, MAR 8, 2024, View Source [SID1234640971]).
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"The ability to impact multiple targets is an important characteristic of Onconova’s two lead clinical programs, rigosertib and narazaciclib. We are pleased to present new preclinical studies that explore the molecular targets for rigosertib, in clinical development through a series of investigator initiated studies (IIS)," commented Steven Fruchtman, M.D., President and Chief Executive Officer of Onconova. "The studies provide additional prospective on the main cellular pathways impacted by rigosertib, including RAS-MAPK signaling and reactive oxygen species (ROS)-related proteins. In addition, the studies highlight rigosertib’s impact on the tumor microenvironment through the activation of inflammation–related targets, such as an NLRP3. We hope to apply this translational science to help guide the clinical program to enable the potential use of rigosertib in difficult-to-treat cancers."
Poster Information:
Poster Title:
Rigosertib promotes anti-tumor activity of cancer cells via CETSA revealed novel targets and activates NLRP3-dependent inflammatory responses (2033/16)
Session: Microenvironment, Immunity, and DNA Repair in Therapeutic Response (PO.ET05.02)
Date/Time: Monday, April 8 9:00a-12:30p PT
Brief Overview: Onconova and its collaborators conducted a series of biochemistry and molecular and cell biology assays to study rigosertib’s molecular and inflammation-based targets. The team used a specialized mass spectrometry assay (a Cellular Thermal shift Assay or CETSA-MS) as one of the tools to identify new targets which were then validated as novel targets of rigosertib.
Conclusions: This work identified a series of cellular and inflammatory targets that may be affected by rigosertib. In particular, the research highlighted target activity through RAS-MAPK signaling, ROS-mediation JNK activation, and tumor microenvironment reprogramming through NLRP3 activation, which may contribute to preclinical and clinical synergistic effects with checkpoint inhibitors. The identification of these targets and signaling pathways may be helpful in the design of clinical trials to address difficult-to-treat cancers.