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.