AMD-3465-hexahydrobromide-GENZ-644494-hexahydrobromide-DataSheet-生命科学试剂-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEAMD 3465 hexahydrobromideCat. No.: HY-15971CAS No.: 185991-07-5Synonyms: GENZ-644494 hexahydrobromide分式: CHBrN分量: 896.07作靶点: CXCR; HIV作通路: GPCR/G Protein; Immunology/Inflammation; Anti-infection储存式: Powder -20C 3 years4C 2 years

2、In solvent -80C 6 months-20C 1 month溶解性数据体外实验 H2O : 38 mg/mL (42.41 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制备储备液1 mM 1.1160 mL 5.5799 mL 11.1598 mL5 mM 0.2232 mL 1.1160 mL 2.2320 mL10 mM 0.1116 mL 0.5580 mL 1.1160 mL请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液，并请注意储备液的保存

3、式和期限。BIOLOGICAL ACTIVITY物活性 AMD 3465 hexahydrobromide种有效的 CXCR4 拮抗剂，在 SupT1 细胞中，能够抑制 2G5mAb，CXCL12AF647 与 CXCR4 的结合，IC50 值分别为 0.75 nM 和 18 nM；AMD 3465 同时可有效抑制 X4HIV 的复制 (IC50，1-10 nM)，但对 R5 HIV 病毒作。IC50 & Target 2G5 mAb-CXCR4 CXCL12AF647- X4 HIV-1 (NL4.3) X4 HIV-1 (RF)1/3 Master of Small Molecules 您

4、边的抑制剂师www.MedChemE0.75 nM (IC50, in SupT1 CXCR4 6.1 nM (IC50, in MT-4 7.4 nM (IC50, in MT-4cells) 18 nM (IC50, in cells) cells)SupT1 cells)X4 HIV-1 (HE) X4 HIV-1 (IIIB) X4 HIV-1 HIV-2 (ROD)9.8 nM (IC50, in MT-4 12.3 nM (IC50, in MT- (NL4.3AMD3100) 12.3 nM (IC50, in MT-cells) 4 cells) 2822 nM (IC50,

5、in MT- 4 cells)4 cells)HIV-2 (EHO)12.3 nM (IC50, in MT-4cells)体外研究 AMD 3465 hexahydrobromide is a potent antagonist of CXCR4, inhibits binding of 12G5 mAb andCXCL12AF647 to CXCR4, with IC50s of 0.75 nM and 18 nM in SupT1 cells. AMD 3465 (50 nM) totally blocksCXCL12-induced calcium mobilization, with

6、 an IC50 of 17 nM, but shows no effect on the intracellularcalcium fluxes elicited by the CCR5 ligands RANTES, LD78 and MIP-1 in U87.CD4.CCR5 cells. AMD3465 also potently inhibits the replication of X4 HIV strains (IC50: 1-10 nM), but has no effect on CCR5-using(R5) viruses. AMD3465 is cytotoxic to

7、the X4 HIV-1 strains IIIB, NL4.3, RF and HE with an IC50 ranging from6 to 12 nM. The IC50 for suppression of the HIV-2 strains ROD and EHO is 12.3 nM 1. AMD 3465 inhibitsCXCL-12-induced growth in U87 and Daoy cells. AMD 3465 treatment stimulates the phosphorylation ofErk1/2 in U87 and Daoy cells 2.体

8、内研究 AMD 3465 (2.5 mg/kg/d, s.c. for 5 weeks) significantly blocks the growth of U87 GBM and Daoy xenografts2.PROTOCOLCell Assay 2 Following serum starvation for 24 h, astrocytes, granule cells, U87 cells, and Daoy cells are treated with 1 g/mL CXCL12, 2.5 ng/mL AMD 3465, 200 M rolipram, or 10 M fors

9、kolin. Daoy and U87 cell growth inculture is measured by trypan blue exclusion after 24 and 48 h of treatment, respectively 2.MCE has not independently confirmed the accuracy of these methods. They are for reference only.Animal Mice 2Administration 2 Mice are imaged at least twice after implantation

10、 of cells to identify those with equivalent tumor growth rates.Two weeks after tumor cell implantation, cohorts of mice with approximately equivalent tumorbioluminescence are divided into equal control and treatment groups. Animals in AMD 3465 experimentsreceive s.c. osmotic pumps loaded with 10 mg/

11、mL AMD 3465 in sterile PBS or PBS alone. The infusion rateis 0.25 L/h (50 g/d). For the experiments with rolipram or caffeine, mice in the treatment groups receiveoral administration of rolipram (5 g/g/d) or caffeine (100 g/g/d). The concentration of drug in the water isdetermined from daily measure

12、ments of water consumption by each animal over the course of 7 days.Concentrations are adjusted based on water consumption to provide the prescribed dose 2.MCE has not independently confirmed the accuracy of these methods. They are for reference only.2/3 Master of Small Molecules 您边的抑制剂师www.MedChemE

13、户使本产品发表的科研献 J Labelled Comp Radiopharm. 2018 May 15;61(5):438-446. Patent. US20180263995A1.See more customer validations on HYPERLINK / www.MedChemEREFERENCES1. Hatse S, et al. AMD3465, a monomacrocyclic CXCR4 antagonist and potent HIV entry inhibitor. Biochem Pharmacol. 2005 Sep1;70(5):752-61.2. Yang L, et al. Blocking CXCR4-mediated cyclic AMP suppression inhibits brain tumor growth in vivo. Cancer Res. 2007 Jan15;67(2):651-8.