Mechanism of action Like the related drugs palbociclib and ribociclib,<unk>  inhibits the enzymes cyclin-dependent kinase 4 (CDK4) and cyclin-dependent kinase 6 (CDK6). These enzymes are responsible for phosphorylating and thus deactivating the retinoblastoma protein, which plays a role in cell cycle progression from the G1 (first gap) to the S (synthesis) phase. Blocking this pathway prevents cells from progressing to the S phase, thereby inducing apoptosis (cell death). In vitro analysis using cancer cell lines, it is reported that<unk>  induces non‐apoptotic cell death characterized by formation of cytoplasmic vacuoles derived from lysosomes. This result suggest that there may be a mechanism of action other than inhibition of a cyclin-dependent kinase. Pharmacokinetics N-desethylabemaciclib (M2), the main metabolite After oral intake, absolute bioavailability is 45%. Highest blood plasma concentrations are reached after 8 hours on average (range: 4.1–24.0 hours). When in the circulation, 96.3% of<unk>  is bound to plasma proteins. The substance is mainly metabolized by the liver enzyme CYP3A4 to N-desethylabemaciclib (M2), and to a lesser extent to hydroxy derivatives (M18, M20) and another oxidative metabolite (M1). These metabolites have high plasma protein binding rates similar to the parent substance.<unk>  is excreted mainly via the feces (81%) and to a small extent via the urine (3%). Its elimination half-life is 18.3 hours on average.
Abemaciclib
Trilaciclib
Cemiplimab
Nirsevimab
Regdanvimab
Lirentelimab
Obiltoxaximab
Sotrovimab