Compound | Teratogenic Potencya (0 to +++++) | IC50(HDAC) ± S.E.b | AcH4-Hyperacetylation (0 to ++) |
---|---|---|---|
μM | |||
I | +++ | 400 ± 50 | ++ |
II | +c | >2000 | 0 |
III | 0 | > 2000 | + |
IV | ++++ | 35 ± 10 | ++ |
V | + | >2000 | 0 |
VI | ++ | >2000 | 0 |
VII | +++ | 870 ± 180 | + |
VIII | 0 | >2000 | 0 |
IX | +++++ | 50 ± 12 | ++ |
X
| ++d | >2000 | 0 |
H4, core histone 4; AcH4, acetylated core histone 4.
↵ a Data from the NMRI-exencephaly-mouse model inferred from Radatz et al. (1998), Bojic et al. (1998), and Volland (2002).
↵ b S.E. representing the goodness of fit of the mathematically fitted function, not the standard error of the mean.
↵ c Not taking into account that valpromide is metabolized to the corresponding valproic acid (Radatz et al., 1998) and, therefore, probably activated and intrinsically not active (also see Results and Discussion).
↵ d Assumed that the solvent enhancer Cremophor EL 25% (v/v) is reducing the teratogenic effect of the compound (also see Results and Discussion).