ECI830 (CDK2-IN-37) is an orally active, ATP-competitive and highly selective CDK2 inhibitor. ECI830 shows high selectivity over other CDK family members. ECI830 can be used for the study of HR+/HER2- breast cancer and CCNE1-amplified tumors (such as ovarian cancer and lung cancer ) [1].
In Vivo, In an HR+/HER2- breast cancer cell line (MCF7) xenograft model resistant to standard-of-care treatment, the combination of ECI830 and Ribociclib resulted in synergistic activity with deeper pathway suppression, enhanced biomarker modulation, and stronger tumor growth inhibition compared with either agent alone[1].
In Vitro, ECI830 demonstrated substantial antiproliferative activity in CCNE1-amplified ovarian (OVCAR3) and lung (H810) cancer cell lines[1].
References:
[1]. Karin Briner, et al. Cyclin-dependent kinase (cdk2) inhibitors. Patent WO2024/171094A1.
[2]. Ophelia Maertens, et al. Abstract 3099: Selective CDK2 inhibition with ECI830: preclinical characterization, efficacy, and on-target mechanism supported by biomarker and gene signature analysis. Cancer Res (2026) 86 (7_Supplement): 3099.
In Vivo, In an HR+/HER2- breast cancer cell line (MCF7) xenograft model resistant to standard-of-care treatment, the combination of ECI830 and Ribociclib resulted in synergistic activity with deeper pathway suppression, enhanced biomarker modulation, and stronger tumor growth inhibition compared with either agent alone[1].
In Vitro, ECI830 demonstrated substantial antiproliferative activity in CCNE1-amplified ovarian (OVCAR3) and lung (H810) cancer cell lines[1].
References:
[1]. Karin Briner, et al. Cyclin-dependent kinase (cdk2) inhibitors. Patent WO2024/171094A1.
[2]. Ophelia Maertens, et al. Abstract 3099: Selective CDK2 inhibition with ECI830: preclinical characterization, efficacy, and on-target mechanism supported by biomarker and gene signature analysis. Cancer Res (2026) 86 (7_Supplement): 3099.