Antagonist inhibition of GDF11- or MSTN-induced SMAD2/3 signaling
Potency [IC50 and IC90 (nM) ± S.E.M.] and efficacy (percentage of inhibition) of GASP1, GASP2, and follistatin indicate their ability to inhibit the SMAD2/3 signal and block receptor dimerization. Antagonists effect on GDF11 and MSTN-induced SMAD2/3 luciferase activity. All the antagonists effectively inhibited GDF11- and MSTN-induced SMAD2/3 signaling.
| SMAD2/3 | IC50 | IC90 | Inhibition |
|---|---|---|---|
| nM | nM | % | |
| Follistatin_GDF11 | 0.7 ± 0.78 | 14.3 ± 3.79 | 100 |
| Follistatin_MSTN | 0.46 ± 0.028 | 1.63 ± 0.095 | 100 |
| GASP1_GDF11 | 1.16 ± 0.3 | 168 ± 28 | 99 |
| GASP1_MSTN | 1.68 ± 0.072 | 20.5 ± 8.05 | 92 |
| GASP2_GDF11 | 2.66 ± 0.3 | 211.8 ± 70 | 100 |
| GASP2_MSTN | 2.94 ± 0.076 | 24.5 ± 9.85 | 90 |
IC90, 90% inhibitory concentration.