NSC45586 sodium

NSC45586 (0-100 μM; 35 min) sodium activates basal AKT in primary rat cortical neurons and enhances IGF-1-induced AKT activation^[1].
NSC45586 (0-250 μM; 24 h) sodium significantly reduces STS (HY-15141)-induced death of primary rat cortical neurons^[1].
NSC45586 (200 μM; 24 h) sodium increases the number of viable cells in rat primary neuron/astrocyte co-cultures following exposure to STS^[1].
NSC45586 (50 μM; 35 min) sodium significantly inhibits basal AKT and ERK phosphorylation in primary rat astrocytes^[1].
NSC45586 (100 μM; 24 h) sodium reduces the expression of PHLPP1 protein in degenerative human nucleus pulposus (NP) cells, with a more significant effect in male cells^[2].
NSC45586 (0-100 μM; 24 h) sodium exhibits cytocompatibility and significantly promotes the proliferation of degenerated male human nucleus pulposus cells^[2].
NSC45586 (25-100 μM; 24 h) sodium promotes the formation of healthy nucleus pulposus cell phenotypes by upregulating the expression of KRT19, ACAN and SOX9 and downregulating the expression of MMP13 in degenerative human nucleus pulposus cells, and this effect is more pronounced in male cells^[2].
NSC45586 (25-100 μM; 30 min) sodium upregulates the phosphorylation level of AKT and the expression of FOXO1 protein in degenerative human nucleus pulposus cells from male donors in a dose-dependent manner^[2].
NSC45586 (100 μM; 24 h) sodium promotes a healthy nucleus pulposus cell phenotype in degenerative human nucleus pulposus cells from male donors by activating the FOXO1 signaling pathway^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.