Program & Target
Preclinical
Early-Stage Clinical Development
Late-Stage Clinical Development
Partner
Rights
1Greater China includes People’s Republic of China, Hong Kong, Macau and Taiwan.
Science
At Avenzo, we are developing a pipeline of potentially best-in-class oncology therapies to fight cancers with high unmet medical needs. Our lead program selectively inhibits cyclin-dependent kinase 2, which are dysregulated in many cancers.
Our Programs
AVZO-021
We are developing a potential best-in-class selective CDK2 inhibitor, AVZO-021 (ARTS-021), for HR+ breast cancer, and other tumors which have elevated cyclin E expression such as ovarian cancer and small cell lung cancer.
AVZO-022
We are developing a potential best-in-class selective CDK4 inhibitor, AVZO-022 (ARTS-022), for HR+ breast cancer and other advanced solid tumors.
Mechanism of Action
FDA-approved CDK4/6 inhibitors target the cyclin D1-CDK4/6-pRb axis, which is dysregulated in HR+ breast cancer. Despite the impact of approved CDK4/6 inhibitors in HR+ breast cancer, patients develop resistance.
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The cyclin D1-CDK4/6-pRB axis acts as a checkpoint during the cell cycle transition from cell growth (G1) to DNA synthesis (S). Its deregulation or overexpression induces abnormal cell proliferation.1,2
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A key resistance mechanism to CDK4/6 agents is hyperactivation of CDK2 (through cyclin E elevation or other mechanisms).3
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The combination of CDK4/6i with a CDK2 inhibitor may lead to more durable responses and disease control in HR+/HER2- breast cancer, both in overcoming primary and acquired resistance to CDK4/6i and in the frontline and adjuvant settings.4,5
Note: Figured adapted from 1Bai et al., Cancer Bio & Med, 2017; 2VanArsdale et al., Clinical Cancer Research, 2015
3Turner et al., Clin Oncology, 2019
4Patel et al., Mol Cancer Research, 2018
5Al-Qasam et al., Nature Precision Oncology, 2022
Hyperactivation of CDK2 (through cyclin E elevation or other mechanisms) represents a key mechanism of breast cancer resistance to CDK4/6i (Alvarez-Fernandez and Malumbres, 2020). Inhibition of the CDK2 bypass mechanism may therefore block proliferation of CDK4/6i-resistant tumors. Furthermore, the combination of CDK 4/6 (or CDK4 selective) inhibitors with CDK2 may lead to more durable responses in HR+ breast cancer, overcoming primary and acquired resistance to CDK4/6i.
Clinical Trials
Study of AVZO-021 (ARTS-021) in Patients with Advanced Solid Tumors Phase 1/2, Status: Recruiting in the United States
AVZO-021 (ARTS-021) is being developed for the treatment of patients with solid tumors. Phase 1 is a dose-escalation phase aimed at assessing the safety and tolerability of AVZO-021 (ARTS-021) and determining the recommended Phase 2 dose. Phase 2 is a dose-expansion phase that will be conducted to assess the antitumor activity of AVZO-021 (ARTS-021) in patients with relapsed/refractory, unresectable locally advanced, or metastatic solid tumors. Learn more.
For questions about our clinical trials, please contact us via email at clinicaltrials@avenzotx.com.