Table 1.
GSK-3β inhibitors | IC50a | CAS No. |
---|---|---|
LiCl | 1 mM (O'Brien et al., 2011) | 7447-41-8 |
BIO | 8 nM (Wagner et al., 2016) | 667463-62-9 |
SB-216763 | 12 nM (Wagner et al., 2016) | 280744-09-4 |
SB-415286 | 78 nM (Coghlan et al., 2000) | 264218-23-7 |
CHIR-99021 | 4 nM (Wagner et al., 2016) | 252917-06-9 |
TWS-119 | 30 nM (Wang et al., 2016)] | 601514-19-6 |
AR-A014418 | 142 nM (Wagner et al., 2016) | 487021-52-3 |
LY-2090314 | 10 nM (Atkinson et al., 2015) | 603288-22-8 |
PF-04802367 | 9 nM (Liang et al., 2016) | 1962178-27-3 |
L807mts | 1 μM (Licht-Murava et al., 2016) | N/A |
Tideglusib | Irreversible (Dominguez et al., 2012) | 865854-05-3 |
In general, there is no distinction between inhibition of GSK-3α and GSK-3β, as there is much shared overlap of substrates between the two kinases. It has been suggested that the GSKα and β subunits are redundant in nature (McCubrey et al., 2017; Patel and Woodgett, 2017).