Molecular Formula | C33H39N2O2.Cl |
Molar Mass | 531.136 |
Solubility | DMSO: ≥ 27 mg/mL |
Appearance | powder |
Color | white to beige |
Storage Condition | 2-8°C |
In vitro study | TAK-779 is a potent and selective nonpeptide antagonist of CCR5, with a K i of 1.1 nM, and effectively and selectively inhibits R5 HIV-1, with EC 50 and EC 90 of 1.2 nM and 5.7 nM, respectively, in MAGI-CCR5 cells. TAK-779 less potently blocks the binding of [ 125 I]-monocyte chemotactic protein 1 to CCR2b in CHO/CCR2b cells, with an IC 50 for CCR2b of 27 nM. TAK-779 also completely inhibits the binding of [ 125 I]-RANTES to CHO/CCR5 cells with an IC 50 of 1.4 nM. TAK-779 (20 nM) selectively inhibits CCR5-mediated Ca 2+ -signaling. In addition, TAK-779 shows no inhibition on X4 HIV-1 strains. TAK-779 is an antagonist of CXCR3, and inhibits the migration of T cells but not T cell proliferation. |
In vivo study | TAK-779 (10 mg/kg per day, s.c.) significantly prolongs the allograft survival of the rat intestinal transplantation model. TAK-779 also decreases the number of CD4 + as well as CD8 + T cells in spleen, blood and recipient mesenteric lymph nodes (MLN). TAK-779 (150 µg per mouse, s.c.) supppresses the development of experimental autoimmune encephalomyelitis (EAE) in myelin oligodendrocyte glycoprotein (MOG)-immunized C57BL/6 mice. TAK-779 decreases the infiltration of CXCR3 and CCR5 bearing leukocytes into the spinal cord. TAK-779 does not alter myelin oligodendrocyte glycoprotein (MOG)-specific immune responses or affect the potential of MOG-specific T cells to transfer experimental autoimmune encephalomyelitis (EAE). |
WGK Germany | 3 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 1.883 ml | 9.414 ml | 18.828 ml |
5 mM | 0.377 ml | 1.883 ml | 3.766 ml |
10 mM | 0.188 ml | 0.941 ml | 1.883 ml |
5 mM | 0.038 ml | 0.188 ml | 0.377 ml |