product name MK-8745
Description: MK-8745 is a novel, potent and selective Aurora A inhibitor with IC50 of 0.6 nM, 450-fold more selective for Aurora A over Aurora B. MK-8745 is a novel Aurora-A specific inhibitor. MK8745 induced apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages. Exposure of p53 wild-type cells to MK8745 resulted in the induction of p53 phosphorylation (ser15) and an increase in p53 protein expression. p53-dependent apoptosis by MK8745 was further confirmed in HCT 116 p53(-/-) cells transfected with wild-type p53.
References: Leuk Lymphoma. 2012 Mar;53(3):462-71; Cell Cycle. 2012 Feb 15;11(4):807-17.
431.91
Formula
C20H19ClFN5OS
CAS No.
885325-71-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 86 mg/mL (199.1 mM)
Water: <1 mg/mL
Ethanol: 1 mg/mL (2.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19393590
| In Vitro |
In vitro activity: MK-8745 leads to cell cycle arrest at the G2/M phase with accumulation of tetraploid nuclei followed by cell death in non-Hodgkin lymphoma (NHL) cell lines. Treatment with MK-8745 induces p21(waf1/cip1) and CycB1, indicating cell cycle arrest and an increase in the G2/M phase cell population. Following MK-8745 treatment, Aurora-A substrates (TACC3, Eg5 and TPX2) are rapidly degraded following the reduction of phospho-Aurora-A. MK8745 induces apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages. Exposure of p53 wild-type cells to MK8745 results in the induction of p53 phosphorylation (ser15) and an increase in p53 protein expression. p53-dependent apoptosis by MK8745 is further confirmed in HCT 116 p53(-/-) cells transfected with wild-type p53. Kinase Assay: Cell Assay: When tested with p53-/+ cell lines, MK-8745 treatment induced apoptotic cell death in a p53-dependent manner through inhibiting Aurora A activity. In non-Hodgkin lymphoma (NHL) cell lines, MK-8745 treatment arrested cell cycle in G2/M phase and induced cell death via inhibiting Aurora A kinase. In HCT 116 Puma (-), HCT116 p21 (-), HCT116 Bax(-) and HCT116 Chk2(-) cell lines, MK-8745 treatment induced cell apoptosis with the percent of 25%, 22%, 25%, and 22%, respectively. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Leuk Lymphoma. 2012 Mar;53(3):462-71; Cell Cycle. 2012 Feb 15;11(4):807-17. |
Related Posts
product name MK-8745
Description: MK-8745 is a novel, potent and selective Aurora A inhibitor with IC50 of 0.6 nM, 450-fold more selective for Aurora A over Aurora B. MK-8745 is a novel Aurora-A specific inhibitor. MK8745 induced apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages. Exposure of p53 wild-type cells to MK8745 resulted in the induction of p53 phosphorylation (ser15) and an increase in p53 protein expression. p53-dependent apoptosis by MK8745 was further confirmed in HCT 116 p53(-/-) cells transfected with wild-type p53.
References: Leuk Lymphoma. 2012 Mar;53(3):462-71; Cell Cycle. 2012 Feb 15;11(4):807-17.
431.91
Formula
C20H19ClFN5OS
CAS No.
885325-71-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 86 mg/mL (199.1 mM)
Water: <1 mg/mL
Ethanol: 1 mg/mL (2.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19393590
| In Vitro |
In vitro activity: MK-8745 leads to cell cycle arrest at the G2/M phase with accumulation of tetraploid nuclei followed by cell death in non-Hodgkin lymphoma (NHL) cell lines. Treatment with MK-8745 induces p21(waf1/cip1) and CycB1, indicating cell cycle arrest and an increase in the G2/M phase cell population. Following MK-8745 treatment, Aurora-A substrates (TACC3, Eg5 and TPX2) are rapidly degraded following the reduction of phospho-Aurora-A. MK8745 induces apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages. Exposure of p53 wild-type cells to MK8745 results in the induction of p53 phosphorylation (ser15) and an increase in p53 protein expression. p53-dependent apoptosis by MK8745 is further confirmed in HCT 116 p53(-/-) cells transfected with wild-type p53. Kinase Assay: Cell Assay: When tested with p53-/+ cell lines, MK-8745 treatment induced apoptotic cell death in a p53-dependent manner through inhibiting Aurora A activity. In non-Hodgkin lymphoma (NHL) cell lines, MK-8745 treatment arrested cell cycle in G2/M phase and induced cell death via inhibiting Aurora A kinase. In HCT 116 Puma (-), HCT116 p21 (-), HCT116 Bax(-) and HCT116 Chk2(-) cell lines, MK-8745 treatment induced cell apoptosis with the percent of 25%, 22%, 25%, and 22%, respectively. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Leuk Lymphoma. 2012 Mar;53(3):462-71; Cell Cycle. 2012 Feb 15;11(4):807-17. |