Trilaciclib hydrochloride (G1T28 hydrochloride) is a CDK4/6 inhibitor with IC 50 s of 1 nM and 4 nM for CDK4 and CDK6 , respectively In Vitro Incubation with Trilaciclib hydrochloride (G1T28) for 24 hours induces a robust G 1 cell-cycle arrest (time=0). By 16 hours after Trilaciclib hydrochloride washout, cells have reentered the cell cycle and demonstrate cell-cycle kinetics similar to untreated control cells. These results demonstrate that Trilaciclib hydrochloride causes a transient, and reversible G 1 arrest. A transient Trilaciclib hydrochloride-mediated G 1 cell-cycle arrest in CDK4/6-sensitive cells decreases the in vitro toxicity of a variety of commonly used cytotoxic chemotherapy agents associated with myelosuppression. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Trilaciclib hydrochloride (G1T28) treatment results in a robust and dose-dependent suppression of proliferation in HSPCs at 12 hours, with 5-ethynyl-2′-deoxyuridine (EdU) incorporation returning near baseline levels in a dose-dependent manner by 24 hours after administration. These data demonstrate that a single oral dose of Trilaciclib hydrochloride can produce reversible cell-cycle arrest in HSPCs in a dose-dependent manner in vivo . Mice given 100 mg/kg Trilaciclib hydrochloride 30 minutes prior to etoposide treatment, exhibits only background levels of caspase-3/7 activity. These data demonstrate that Trilaciclib hydrochloride can protect the bone marrow from chemotherapy-induced apoptosis in vivo . The data demonstrate that treatment with Trilaciclib hydrochloride prior to 5-fluorouracil (5-FU) likely decreases 5-FU-induced damage by chemotherapy in HSPCs, thus accelerating blood count recovery after chemotherapy . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid IC50& Target:Cdk4/cyclin D1 1 nM (IC 50 ) cdk6/cyclin D3 4 nM (IC 50 )