Autophagy inhibitor
Azithromycin is an antibiotic by inhibiting protein synthesis, used for the treatment of bacterial infections.
Azithromycin 10mM (1mL in DMSO)
£129.00
Target: Protein synthesis
Chemical name: (2R,3S,4R,5R,8R,10R,11R,12S,13S,14R)-13-[(2,6-dideoxy-3-C-methyl-3-O-methyl-α-L-ribo-hexopyranosyl)oxy]-2-ethyl-3,4,10-trihydroxy-3,5,6,8,10,12,14-heptamethyl-11-[[3,4,6-trideoxy-3-(dimethylamino)-β-D-xylo-hexopyranosyl]oxy]-1-oxa-6-azacyclopentadecan-15-one
Size: 10mM (1mL in DMSO)
Formula: C38H72N2O12
Molecular weight: 748.98
Purity: 100 %
Solubility: 100 mg/mL (DMSO), 100 mg/mL (ethanol)
Storage: 3 years -20°C powder, 2 years -80°C in solvent
In vitro:
Azithromycin reduces about 40% of IL-8 mRNA and protein expression in cystic fibrosis (CF) cells reaching the levels of non-CF cells. Azithromycin results in 50% and 70% reduction of NF-kappaB and AP-1 DNA binding, respectively, leading to levels of non-CF cells. [1] Azithromycin significantly enhances the intensity of a co-stimulatory molecule, CD80, on DCs but not CD86 and CD40 in dendritic cells (DCs). Azithromycin significantly increases the production of IL-10 and Clarithromycin (CAM) significantly inhibits the production of IL-6 by DCs. Azithromycin increases IL-10 and CAM decreases IL-2 productions significantly, when naive T cells derived from spleen are co-cultured with DCs treated in advance with LPS and these macrolides. [2] Azithromycin selectively inhibits fluid-phase endocytosis of horseradish peroxidase and lucifer yellow in J774 mouse macrophages. Azithromycin delays sequestration of receptor-bound transferrin and peroxidase-anti-peroxidase immune complexes into cell-surface endocytic pits and vesicles. Azithromycin down-regulates cell surface transferrin receptors, but not Fc gamma receptors, by causing a major delay in the accessibility of internalized transferrin receptors to the recycling route, without slowing down subsequent efflux, resulting in redistribution of the surface pool to an intracellular pool. [3] Azithromycin inserts into the DOPC lipid bilayer, so as to decrease its cohesion and to facilitate the merging of DPPC into the DOPC fluid matrix. [4]
References:
[1] Cigana C, et al. P Biochem Biophys Res Commun, 2006, 350(4), 977-982.
[2] Sugiyama K, et al. Clin Exp Immunol, 2007, 147(3), 540-546.
[3] Tyteca D, et al. Exp Cell Res, 2002, 281(1), 86-100.
[4] Fa N, et al. Biochim Biophys Acta, 2007, 1768(7), 1830-1838.