We are pioneers in synthetic lethal approaches to precision oncology and are experts in MYC biology and cell division.
Making MYC-Driven Cancer Tractable
Why MYC Matters
MYC is one of the most important drivers of cancer aggressiveness. It contributes to therapeutic resistance and helps shape an immunosuppressive tumor microenvironment. Aberrant MYC expression or activity is implicated in up to 70% of human cancers. Despite its central role, MYC has long been considered biologically “undruggable” as a direct target. Prior direct or indirect attempts to shut down MYC biology have failed to deliver meaningful clinical benefit.
Our approach: MYC-SL
Rather than trying to inhibit MYC directly, we focus on the load-bearing dependencies required by MYC-high tumors to sustain growth. This strategy—MYC-SL—aims to eliminate MYC-driven tumor cells while sparing normal tissues with minimal MYC activity.
Our Proof Point: MKLP2
A MYC-SL Pillar Identified and Drugged
We discovered that MKLP2 is a critical dependency in MYC-driven tumors. MKLP2 regulates mitotic progression, multiple stress, and trafficking processes required by MYC-high tumor states. Blocking MKLP2 disrupts these functions and triggers MYC-SL. Using our SYMPLEX™ platform, we have developed a series of MKLP2 inhibitors with diverse chemical scaffolds and differentiated profiles.
With this platform, we are building a scalable MYC-SL pipeline advancing toward clinical development.
