pipeline

Advancing best-in-
class and first-in-class candidates

Discovery
IND-enabling
Phase 1

HER2, including oncogenic mutations

COVALENT ORTHOSTERIC INHIBITOR

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.

Candidate
IAM-H1
Target
HER2 wild type and mutants

CDK2/4

SELECTIVE DUAL INHIBITOR

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.

Candidate
IAM-C1
Target
CDK2/4

Protein-complex target for solid tumors

Allosteric inhibitor

Effector protein for solid tumors

Allosteric PPI modulator

Delivering development candidates years faster than industry norms

2 years
Iambic IAM-H1 program launch to IND
6 years
Industry average program launch to IND

Our platform expands possibilities for essential treatments

Therapeutic area

Broadly applicable platform capable of delivering value across diverse therapeutic areas

Protein classes

Demonstrated versatility for therapeutic leads across a wide array of protein classes

Mechanism of action

Demonstrated versatility across mechanisms, with orthosteric inhibitors, allosteric inhibitors, and protein-protein interaction modulators in our pipeline

Leverage our platform within your program

Imagine creating thousands of novel molecular designs and a read out of new biological data on a weekly cadence. By directing our powerful AI tools towards your high priority targets, we drive through chemical space to identify unique and highly differentiated development candidates on a time scale far faster than industry average.