HER2, including oncogenic mutations
IAM-H1 is a highly potent and irreversible tyrosine kinase inhibitor (TKI) that selectively targets HER2 and HER2 mutants, while sparing EGFR. Amplification and mutations of HER2 drive a wide range of human cancers. HER2 TKIs have had limited success due to a compensatory mechanism that increases the required therapeutic index beyond that of available pan-ERBB and HER2 inhibitors.
IAM-H1 exhibits over 1000-fold selectivity against EGFR, favorable PK and safety profiles, preferential tumor enrichment, and effective CNS penetrance. Together these make IAM-H1 a breakthrough molecule for realizing the full therapeutic potential of inhibiting HER2 signaling, while avoiding EGFR-driven toxicity. In vivo, IAM-H1 has demonstrated favorable efficacy and tolerability across a range of HER2 tumor models, including intracranial models, outperforming benchmark TKIs and antibody-drug conjugates (ADCs).
A multi-center Phase I trial is scheduled to commence patient dosing in early 2024.
IAM-C1 is a first-in-class small molecule inhibitor designed to specifically target CDK2 and CDK4, two cell-cycle kinases that are frequently dysregulated in various cancers. Through its selective inhibition of CDK2/4 while preserving other closely related CDKs including CDK1, CDK6, and CDK9, IAM-C1 has the potential to provide expanded therapeutic benefits compared to clinically approved CDK4/6 inhibitors.
IAM-C1 represents a promising new approach to address cell-cycle dysregulation in cancer, building upon the learnings from two decades of research and clinical experience. CDK4/6 inhibitors are the standard of care for patients with HR+/HER2- metastatic breast cancer (mBC) in both first- and subsequent-line settings. Despite the success of these agents, many patients demonstrate either intrinsic or acquired resistance to the approved CDK4/6 inhibitors. HR+/HER2- mBC remains a significant cause of morbidity and mortality, presenting extraordinary unmet patient need.
The more targeted approach of IAM-C1 offers a more favorable safety profile by reducing dose-limiting toxicities associated with non-CDK2/4 kinases, including CDK6.
Protein-complex target for solid tumors
Effector protein for solid tumors
Delivering development candidates years faster than industry norms
Our platform expands possibilities for essential treatments
Broadly applicable platform capable of delivering value across diverse therapeutic areas
Demonstrated versatility for therapeutic leads across a wide array of protein classes
Demonstrated versatility across mechanisms, with orthosteric inhibitors, allosteric inhibitors, and protein-protein interaction modulators in our pipeline
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