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. 2021 Jul 2;29(1):74–83.e4. doi: 10.1016/j.chembiol.2021.06.008

Figure 2.

Figure 2

Detection of competitors of the RBD/ACE2 interaction using the TR-FRET-based assay

(A) Competition of RBD-d2 binding (5 nM) to Lumi4-Tb-SNAP-ACE2 in HEK293 cells by non-labeled RBD or LCB1v3 miniprotein; data are expressed as mean ± SEM of five independent experiments, each performed in triplicate.

(B) Competition of RBD-d2 binding (5 nM) to Lumi4-Tb-SNAP-ACE2 in HEK293 cells by anti-RBD Llamabody VHH (representative curve, n = 3 independent experiments, each performed in triplicate).

(C) Determination of Z′ by collecting TR-FRET signals for RBD-d2 (5 nM) binding to Lumi4-Tb-labeled SNAP-ACE2 expressing HEK293 cells in the absence or presence of RBD (300 nM) from 50 different wells.

(D–H) Competition of RBD-d2 (5 nM) binding to Lumi4-Tb-SNAP-ACE2 by cangrelor (n = 3), elaidic acid (n = 4), fenbendazole (n = 3), enalapril maleate (n = 5), or corilagin (n = 6). “RBD-d2 Binding” corresponds to the TR-FRET ratio and is expressed as percent of control (vehicle-treated group). Data are expressed as mean ± SEM of indicated independent experiments, each performed in triplicate; ∗∗∗∗p < 0.001 by one-way ANOVA.

See also Figure S2.