1374743-00-6
基本信息
骨髓保護(hù)劑
曲拉西利 (NMN)
化合物 T13202L
G1T28
G1T-28
G1T 28
TRILACICLIB.
2'-[[5-(4-甲基哌嗪-1-基)吡啶-2-基]氨基}-7',8'-二氫-6'H-螺環(huán)[環(huán)己烷-1,9'-吡嗪[1',2':1,5]吡咯[2,3-D]嘧啶]-6'-酮
2'-((5-(4-methylpiperazin-1-yl) yridine-2-yl)amino)-7',8'-dihydro-6'H-spiro[cyclohexane-1,9'-pyrazino[1',2':1,5]pyrrolo[2,3-d]pyrimidin]-6'-one
Spiro[cyclohexane-1,9'(6'H)-pyrazino[1',2':1,5]pyrrolo[2,3-d]pyrimidin]-6'-one, 7',8'-dihydro-2'-[[5-(4-methyl-1-piperazinyl)-2-pyridinyl]amino]-
物理化學(xué)性質(zhì)
常見問題列表
Target | Value |
CDK4/cyclin D1
(Cell-free assay) | 1 nM |
CDK6/cyclin D3
(Cell-free assay) | 4 nM |
Incubation with Trilaciclib (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 causes a transient, and reversible G 1 arrest. A transient Trilaciclib-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.
Trilaciclib (G1T28) treatment results in a robust and dose-dependent suppression of proliferation in HSPCs at 12 hours, with 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 can produce reversible cell-cycle arrest in HSPCs in a dose-dependent manner in vivo . Mice given 100 mg/kg Trilaciclib 30 minutes prior to etoposide treatment, exhibits only background levels of caspase-3/7 activity. These data demonstrate that Trilaciclib can protect the bone marrow from chemotherapy-induced apoptosis in vivo . The data demonstrate that treatment with Trilaciclib prior to 5-FU likely decreases 5-FU-induced damage by chemotherapy in HSPCs, thus accelerating blood count recovery after chemotherapy.