On June 20, 2023 Accutar Biotechnology, Inc., a biotechnology company focusing on artificial intelligence (AI)-empowered drug discovery, reported the dosing of the first patient in a Phase 1 study of AC0676, an orally bioavailable, chimeric degrader molecule designed to target and degrade Bruton’s Tyrosine Kinase (BTK) with high potency, selectivity, and broad mutant coverage (Press release, Accutar Biotechnology, JUN 20, 2023, View Source [SID1234632807]).
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"The initiation of this study distinguishes Accutar as the first company to successfully bring oral chimeric degraders against three different targets into the clinic," said Jie Fan, Ph.D., Chief Executive Officer of Accutar Biotechnology, Inc. "Leveraging our protein crystallography and AI-empowered PPI-TAC (Protein-Protein Interaction Targeting Chimera) platforms, AC0676 was designed to potently and selectively degrade both wildtype BTK and BTK mutations that confer drug resistance to both covalent and non-covalent BTK inhibitors, including but not limited to C481S and kinase dead mutations such as L528W. We are excited about the differentiated therapeutic profile of AC0676 and its broad potential to treat patients with B-cell malignancies."
The purpose of the Phase 1 multi-center, open-label study is to assess the safety, tolerability, pharmacokinetics, and preliminary anti-tumor activity of AC0676 treatment in patients with relapsed/refractory B-cell malignancies, including Chronic Lymphocytic Leukemia (CLL), Small Lymphocytic Lymphoma (SLL), non-GCB Diffuse Large B-cell Lymphoma (DLBCL), Mantle Cell Lymphoma (MCL), Follicular Lymphoma (FL), , Marginal Zone Lymphoma (MZL), or Waldenström Macroglobulinemia (WM). Additional information on this clinical trial can be found on www.clinicaltrials.gov (NCT05780034).
About AC0676
AC0676 is an investigational orally bioavailable, chimeric degrader of Bruton’s Tyrosine Kinase (BTK) for the potential treatment of relapsed/refractory B-cell malignancies. In preclinical studies, AC0676 has demonstrated potent and selective BTK protein degradation with broad coverage of BTK wildtype and mutants (including C481S, L528W, and others), favorable pharmacological properties, as well as promising anti-tumor activity in animal models.