Our Pipeline

Small Molecule Therapies Targeting a Broad Spectrum of Tumor Types

Portfolio of Validated Oncogenic Drivers with Clear Paths to Early Clinical Signals

Our deep expertise in small molecule, structure-guided oncology drug discovery enables us to develop mutation and isoform-selective inhibitors against validated oncogenes. Our sense of urgency and commitment to patient benefit pave a clear path to early clinical signals.


Expertise in Small Molecule Drug Discovery

Structure & physics-based drug design

Validated Oncogenic Alterations

KRAS MutationS

Maximizing Therapeutic Index

Mutation & isoform-selective strategies

AKT1 E17K Mutant-Selective Inhibitor

The PTEN/PI3K/AKT pathway controls essential cellular processes spanning growth, survival, and metabolism. Pathway alterations lead to a variety of malignancies. Among these alterations is AKT1 E17K, a clinically validated oncogene that drives ~2% of all cancers, including breast, endometrial, and prostate cancers. Precision therapy options for AKT1 E17K cancer patients have limited durability. We developed ALTA-2618, an orally bioavailable, mutant-selective, and covalent allosteric inhibitor of AKT1 E17K.

ATP-Competitive Inhibitors of AKT1

Oncogenic AKT1 E17K is kept “open” by the E17K alteration. ATP-competitive inhibitors target the activated kinase domain requiring high concentrations to compete with cellular ATP. These concentrations inhibit wild type AKT, leading to unintended toxicities.

Covalent Allosteric Inhibitors of AKT1 E17K

ALTA-2618 overcomes these limitations through covalent capture of the disease-driving E17K. This strategy avoids inhibition of wild type AKT and spares patients on-target toxicities. This mutant-selective approach enables complete target coverage.

KRAS Isoform Selective

KRAS is a central regulator of multiple cellular signal transduction pathways and is mutated in >20% of all cancers. KRAS was once considered an “undruggable” target, but first-generation medicines achieved a breakthrough by targeting the OFF state of the KRAS G12C mutant. The narrow scope of mutational coverage and suboptimal properties of first-generation medicines have limited durability and poor tolerability for patients. We developed ALTA-3263, a KRAS isoform selective compound with improved drug-like properties and ON state inhibition to target >90% of KRAS mutations.

Defining KRAS Inhibition

We have overcome multiple KRAS drug design hurdles to deliver a highly differentiated KRAS isoform-selective profile:


Improved drug-like properties and oral bioavailability to enable complete target coverage in tumors.


Exquisite activity against slow-cycling mutations (G12V) requires inhibition of the KRAS(ON) state.


High potency against >90% of all KRAS mutations found in cancer, including G12V and G12D.


Maximized tolerability and safety by sparing NRAS & HRAS to preserve normal cell function.