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Most compounds inhibited the expression of viral antigens HBsAg or HBeAg at low concentration.
The results showed that most compounds inhibited c-Src and iNOS well.
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The most active compounds inhibited HNE activity with IC50 values in the submicromolar range.
The compounds did not inhibit AChE; the most active compounds inhibited BChE and CaE with IC50 values of 0.22 2.3 μM.
Most of the compounds inhibited the CA effectively with IC50 values in the range of 7 152 nM.
Most of the compounds inhibited EGFR kinase wild type (EGFR WT) with IC50 values in the low nanomolar range (<0.495 9.05 nM) and displayed more potent cytotoxic effect in BaF/3 expressing EGFR WT than reference compound gefitinib.
Most of the compounds inhibited wild-type (wt) HIV-1 replication in the lower micromolar concentration range (EC50 = 0.05 35 μM) with high selectivity index (SI) values (ranged from 10 to >4870).
The most of these compounds inhibited the hydrolysis of the specific substrate by factor Xa in a dose-dependent manner.
The most active compound can reduce the lipid accumulation up to 78.4% at 10 μM qPCR and Western blotting results demonstrate that the two most active compounds inhibit both lipodenesis and adipogenesis in 3T3-L1 cells through (1) increasing the phosphorylations of AMPK and ACC, promoting SIRT1 expression.
Most of the tested compounds inhibited the enzyme at this concentration.
With the above exceptions (as well as 2-deoxyglucose, which inhibits glycolysis) we found that most compounds tested inhibit mitochondrial ATP production and thus activate AMPK indirectly by altering cellular AMP ATP ratios.
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