Turning the Tide on Cancer
Developing Onvansertib to Overcome Resistance, Extend Duration of Response and Increase Overall Survival
Targeting PLK1, a Key Regulatory Enzyme in Tumor Cell Division
Onvansertib Selectively Inhibits PLK1, a Proven Therapeutic Target that is Over-Expressed in Most Cancers
- Serine/threonine kinase, master regulator of cell-cycle progression
- Controls G2/Mitosis (G2/M) checkpoint
- Inhibition of PLK1 causes mitotic arrest and subsequent cell death
- Emerging data demonstrates PLK1 is also a key regulator of cellular functions beyond mitosis that are essential for tumor growth
- Biosynthesis of DNA
- DNA Damage Response
Synergistic in Combination
Onvansertib Works Synergistically in Combination with Chemotherapies and Targeted Therapeutics
KRAS-Mutated Metastatic Colorectal Cancer (mCRC)
Tumor Growth
Survival
Zytiga®-Resistant Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Onvansertib + Zytiga® (abiraterone) demonstrates synergy in mCRPC model (C4-2)1
Onvansertib + Zytiga® (abiraterone) significantly increase mitotic arrest1
Optimal Product Characteristics
Onvansertib is a First-In-Class, Third-Generation, Oral and Highly-Selective PLK1 Inhibitor
Advancing Clinical Programs
Zytiga-Resistant Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Adding onvansertib to daily Zytiga® to overcome resistance, extend treatment response and overall survival.
KRAS-Mutated Metastatic Colorectal Cancer (mCRC)
Combining onvansertib with FOLFIRI/Avastin® to improve efficacy by increasing duration of response and overall survival.
Relapsed/Refractory Acute Myeloid Leukemia (AML)
Combining onvansertib with decitabine to provide a new treatment option to improve efficacy and increase overalll survival.