Our team brings decades of experience in targeted oncology drug development, with a unique blend of expertise in computational and quantum chemistry, medicinal chemistry, and translational biology. We excel at rapidly applying next-generation drug discovery technologies to cancers’ most challenging driver mechanisms.
This synergy of human experience and computational power has enabled us to efficiently develop a pipeline of precision small molecule therapies targeting a broad spectrum of clinically validated oncogenic targets.
AKT, part of the PI3K/AKT/mTOR signaling pathway, controls cell growth, survival, and metabolism and contributes to the development and progression of many cancers. (Mutations that lock AKT in a permanently “ON” [activated] state drive uncontrolled tumor cell proliferation.) Roughly 27,000 people in the US are diagnosed with AKT-driven cancers each year, including approximately 5% of people with breast cancer, 3% with endometrial cancer, and 1.5% with prostate cancer.
Historic approaches involve targeting all three AKT isoforms (AKT1, AKT2, AKT3) in their active states to block activation. This approach is associated with significant side effects and a poor therapeutic index. We’re advancing ALTA2618, our first-in-class, mutation-specific AKT1 E17K inhibitor designed to precisely target the oncogenic driver while sparing wild-type AKT. By avoiding the toxicities of pan-AKT inhibition, we hope to deliver safer, more effective options to patients with AKT-driven cancers, including subsets of breast, endometrial, and prostate cancers.
KRAS plays a central role in regulating cell growth, division, and survival, and, when mutated, becomes a powerful driver of cancer. It is one of the most commonly mutated oncogenes and is present in >20% of cancers (including non-small cell lung, pancreatic, and colorectal), representing approximately >180,000 people annually in the US.
KRAS has long been a compelling target for small molecule drug development, and first-generation mutation-specific KRAS inhibitors have proven that it is druggable – paving the way for the next generation. We’re building on this progress with ALTA3263, our first-in-class, pan-KRAS inhibitor designed to shut down KRAS activity in both ON and OFF states. By expanding mutational coverage (e.g., to G12D and G12V) and improving durability, we aim to bring effective treatment to more people across more KRAS-driven cancers.
