Discovery of GDC-0853: A Potent, Selective, and Noncovalent Bruton's Tyrosine Kinase Inhibitor in Early Clinical Development.
James J CrawfordAdam R JohnsonDinah L MisnerLisa D BelmontGeorgette M CastanedoRegina ChoyMelis CoraggioLiming DongCharles EigenbrotRebecca EricksonNico GhilardiJonathan HauArna KatewaPawan Bir KohliWendy LeeJoseph W LubachBrent S McKenzieDaniel F OrtwineLeah SchuttSuzanne TayBinQing WeiKarin ReifLichuan LiuHarvey WongXiaojing WangPublished in: Journal of medicinal chemistry (2018)
Bruton's tyrosine kinase (Btk) is a nonreceptor cytoplasmic tyrosine kinase involved in B-cell and myeloid cell activation, downstream of B-cell and Fcγ receptors, respectively. Preclinical studies have indicated that inhibition of Btk activity might offer a potential therapy in autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus. Here we disclose the discovery and preclinical characterization of a potent, selective, and noncovalent Btk inhibitor currently in clinical development. GDC-0853 (29) suppresses B cell- and myeloid cell-mediated components of disease and demonstrates dose-dependent activity in an in vivo rat model of inflammatory arthritis. It demonstrates highly favorable safety, pharmacokinetic (PK), and pharmacodynamic (PD) profiles in preclinical and Phase 2 studies ongoing in patients with rheumatoid arthritis, lupus, and chronic spontaneous urticaria. On the basis of its potency, selectivity, long target residence time, and noncovalent mode of inhibition, 29 has the potential to be a best-in-class Btk inhibitor for a wide range of immunological indications.
Keyphrases
- tyrosine kinase
- cell therapy
- systemic lupus erythematosus
- rheumatoid arthritis
- epidermal growth factor receptor
- disease activity
- small molecule
- single cell
- bone marrow
- high throughput
- acute myeloid leukemia
- oxidative stress
- ankylosing spondylitis
- stem cells
- signaling pathway
- human health
- immune response
- risk assessment
- climate change
- chemotherapy induced