Turning the Tide on Cancer
Developing Onvansertib to Overcome Resistance, Extend Duration of Response and Increase Overall Survival
PLK1 is a Proven Therapeutic Target that is Overexpressed in Most Cancers
PLK1 is a Proven Therapeutic Target that is Overexpressed in Most Cancers
- PLK1 is a serine/threonine kinase and master regulator of cell-cycle progression
- PKL1 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 such as DNA damage response
Inhibition of PLK1 Causes Mitotic Arrest and Subsequent Cell Death¹
Optimal Product Characteristics
Onvansertib Overcomes the Shortcomings of Prior PLK Inhibitors
Prior generation PLK inhibitors demonstrated clinical activity but had
less than optimal drug properties.
Synergistic in Combination
Onvansertib Works Synergistically in Combination with Chemotherapies and Targeted Therapeutics
- Preclinical models indicate that onvansertib can synergize with targeted and chemo-therapies
- The underlying mechanism for many of these synergies is due to PLK1’s function in:
- Repair of DNA damage
- Mitotic processes
- Synergy suggests that lower doses can be used for both onvansertib and the targeted or chemotherapy; potentially decreasing AEs
Mechanism of Therapeutic Synergy Between DNA Damaging Agents and Onvansertib
Our Clinical Programs
KRAS-Mutated Metastatic Colorectal Cancer (mCRC)
Combining onvansertib with FOLFIRI/Avastin® to improve efficacy by increasing duration of response and overall survival.
Metastatic Pancreatic Ductal Adenocarcinoma (PDAC)
Leveraging the synergy of onvansertib to increase duration and response of overall survival.
Zytiga-Resistant Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Adding onvansertib to daily Zytiga® to overcome resistance, extend treatment response and overall survival.