Discovery of INCB159020, an Orally Bioavailable KRAS G12D Inhibitor

Qinda Ye1, Artem Shvartsbart1, Zhenwu Li1

  • 1Department of Discovery Chemistry, Incyte Research Institute, Incyte Corporation, Wilmington, Delaware 19803 United States.

PubMed

Insights

Researchers developed a new KRAS G12D inhibitor, INCB159020, demonstrating oral exposure in nonhuman primates. This breakthrough offers potential for treating KRAS G12D-driven cancers, expanding therapeutic options.

Area of Science:

  • Oncology
  • Medicinal Chemistry
  • Drug Discovery

Background:

  • KRAS-driven cancers represent a significant unmet medical need.
  • KRAS G12C inhibitors have shown clinical success, highlighting the therapeutic potential of targeting KRAS mutations.
  • KRAS G12D is the most prevalent KRAS mutation, offering a larger patient population for targeted therapies.

Purpose of the Study:

  • To discover and develop novel inhibitors targeting the KRAS G12D mutation.
  • To overcome the challenges associated with targeting KRAS G12D, particularly achieving sufficient potency and oral bioavailability.
  • To identify a KRAS G12D inhibitor with favorable ADME properties for potential clinical development.

Main Methods:

  • Structure-based drug design was employed to optimize a weakly potent hit compound.
  • Iterative medicinal chemistry efforts focused on enhancing molecular rigidity and balancing polarity.
  • Pharmacokinetic studies in nonhuman primates (NHP) were conducted to assess oral exposure.

Main Results:

  • Discovery of KRAS G12D inhibitor 23 (INCB159020) with significantly improved potency.
  • INCB159020 demonstrated successful oral exposure in nonhuman primate studies.
  • Optimization strategies successfully balanced potency with ADME properties required for oral administration.

Conclusions:

  • INCB159020 represents a promising KRAS G12D inhibitor with demonstrated oral bioavailability.
  • The development of INCB159020 validates structure-based drug design and focused optimization for targeting challenging mutant proteins.
  • This discovery holds potential for expanding treatment options for patients with KRAS G12D-mutant cancers.

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