Catalog No.S1457 Synonyms: BMS-232632
Molecular Weight(MW): 802.93
Atazanavir Sulfate is a HIV protease inhibitor with Ki of 2.66 nM in a cell-free assay.
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Protease inhibitors induce macroautophagy. JEG3 were seeded on glass chamber slides (1 x 104 cell per chamber; 8-well μ slides; Ibidi, Martinsried, Germany), grown for 24 h under cell culture conditions, and treated for 24 h with 0-10 ug/ml of either lopinavir/ritonavir or atazanavir. Cells were then incubated for 30 min with the blue-green fluorescent autophagy marker monodansylcadaverine and viewed under a fluorescence microscope.
Reprod Toxicol 2014 50, 122-8. Atazanavir Sulfate purchased from Selleck.
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Choose Selective HIV Protease Inhibitors
|Description||Atazanavir Sulfate is a HIV protease inhibitor with Ki of 2.66 nM in a cell-free assay.|
|Features||Atazanavir is generally more potent than other HIV-1 Prt inhibitors, including IDV, SQV, RTV, NFV, and APV.|
Atazanavir inhibits the proteolytic cleavage of the viral gag precursor p55 polyprotein with IC50 of ~47 nM in virus-infected H9 cells. Atazanavir exhibits potent antiviral activity with EC50 of 3.89 nM in RF/MT-2 strains. . Atazanavir is shown to be an inhibitor of bilirubin glucuronidation with IC50 of 2.4 μM. Atazanavir inhibits recombinant UGT1A1 with Ki of 1.9 μM.  Atazanavir inhibits cell growth in U251, T98G, and LN229 glioblastoma cell lines, with strikingly increased GRP78 and CHOP protein levels. Atazanavir causes a prominent increase of polyubiquitinated proteins of various different sizes in U251 glioblastoma cells.  Atazanavir also inhibits human 20S proteasome with IC50 of 26 μM. Atazanavir (30 μM) changes the magnitudes of ER stress and UPR gene expression in HepG2 cells.  Atazanavir (30 mM) causes a 2.5-fold increase in immunoreactive P-gp expression with decreased intracellular Rh123 in LS180V cells. 
Protease assays:To determine the inhibition constants (Ki) for each Prt inhibitor, purified HIV-1 RF wild-type Prt (2.5 nM) is incubated at 37 ℃ with 1 μM to 15 μM fluorogenic substrate in reaction buffer (1 M NaCl, 1 mM EDTA, 0.1 M sodium acetate [pH 5.5], 0.1% polyethylene glycol 8000) in the presence or absence of Atazanavir. Cleavage of the substrate is quantified by measuring an increase in fluorescent emission at 490 nM after excitation at 340 nM using a Cytofluor 4000. Reactions are carried out using 1.36 μM, 1.66 μM, 2.1 μM, 3.0 μM, 5.0 μM, or 15 μM substrate in the presence of five concentrations of Atazanavir (1.25 nM to 25 nM). Substrate cleavage is monitored at 5-min intervals for 30 min. Cleavage rates are then determined for each sample at early time points in the reaction, and Ki values are determined from the slopes of the resulting Michaelis-Menten plots.
-  Robinson BS, et al. Antimicrob Agents Chemother, 2000, 44(8), 2093-2099.
-  Zhang D, et al. Drug Metab Dispos, 2005, 33(11), 1729-1739.
-  Pyrko P, et al. Cancer Res, 2007, 67(22), 10920-10928.
|In vitro||DMSO||104 mg/mL (129.52 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
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