Table 1. Summary of inhibitors used in this study.

Compound	Chemical name	[μM]	Type of inhibition	Specificity	References1
PD0325901	N-[(2R)-2,3-dihydroxypropoxy]-3,4-difluoro-2-[(2-fluoro-4-iodophenyl)amino]-benzamide	1	Non-ATP competitive binding inhibition	MEK12,4	[9, 11, 31–33]
PP2	Pyrazolo-pyrimidine 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine	10	ATP competitive binding inhibition	Src4, p56Lck,4, p59FynT,4, Hck4, EGFR5, RIP25, CK1δ5 and GAK5.3	[34–39]
SB203580	4-(4´-fluorophenyl)-2-(4´-methylsulfinylphenyl)-5-(4´-pyridyl)-imidazole	10	ATP competitive binding inhibition	p38α MAPK4, p38β MAPK4 and CK1δ5.	[31–33, 40–44]
SU6656	2-oxo-3-(4,5,6,7-tetrahydro-1 H-indol-2-ylmethylene)-2,3-dihydro-1H-indole-5-sulfonic acid dimethylamide		ATP competitive binding inhibition	MAPKAP-K1a4, AMPK4, PHK5, p56Lck,4 and DYRK1A4.	[34, 45, 46];

¹ Selected references, prioritized to include those reporting on role of inhibitor in ES cell renewal and differentiation.

² Inhibitor is reported to have activity on MEK1 but not on ERK1, ERK2, p38αMAPK or p38βMAPK [34].

³ PP2 has been shown to have a modest impact on the activity of p38α MAPK, p38β MAPK [34].

⁴ Detected in ES cells.

⁵ Not reported in ES cells.