NEWTOWN, PA — Onconova Therapeutics, Inc (NASDAQ: ONTX)., a renowned biopharmaceutical company, recently shared preclinical data on narazaciclib’s effectiveness in treating Bruton’s kinase inhibitor (BTKi)-resistant mantle cell lymphoma (MCL). The data was presented at the 65th Annual Meeting of the American Society for Hematology in San Diego.
Steve Fruchtman, M.D., President and CEO of Onconova, expressed his satisfaction with the data, which demonstrates that narazaciclib significantly inhibits tumor growth, even when used as a single agent. Moreover, when combined with ibrutinib, narazaciclib showed synergy in both ibrutinib-sensitive and -resistant settings.
“These data are significant as they provide further evidence for the potential use of narazaciclib in cancers with cyclin over-expression,” said Dr. Fruchtman. He emphasized the compound’s ability to promote G1 cell cycle blockade, a mechanism critical in halting cancer cell proliferation.
The study also highlighted narazaciclib’s multi-kinase activity and its ability to target resistance pathways missed by other CDK4/6 inhibitors. Notably, it demonstrated that the combination of narazaciclib and ibrutinib triggers metabolic reprogramming alongside DNA damage.
Titled “Narazaciclib, a differentiated CDK4/6 antagonist, prolongs cell cycle arrest and metabolomic reprogramming, enabling restoration of ibrutinib sensitivity in BTKi-resistant mantle cell lymphoma,” the study aimed to evaluate narazaciclib’s activity and mechanism of action in MCL models.
Key findings included narazaciclib’s safety and efficacy in reducing cell viability in MCL models, including those resistant to ibrutinib. Furthermore, the combination of narazaciclib and ibrutinib showed greater synergy in ibrutinib-resistant models, inducing a superior G1 cell cycle blockade.
In instances of ibrutinib resistance, the synergy between narazaciclib and ibrutinib triggered metabolic reprogramming alongside DNA damage, mediated by the USP24 and P53 axis.
Collectively, these preclinical data suggest that narazaciclib has significant single agent activity and the potential to restore ibrutinib sensitivity in BTKi-resistant models. The full details of the study are available on the Onconova website under “Scientific Presentations.”
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