C-DIM12 induced expression of Nurr1-regulated genes. C-DIM12 increased expression of transfected human Nurr1, induced Nurr1 protein expression in primary dopaminergic neurons and enhanced neuronal survival from exposure to 6-OHDA.

C-DIM12 induces Nurr1 and DA gene expression in cell lines and primary neurons[3]. C-DIM12 suppresses astrocyte inflammatory signaling in vitro. C-DIM12 inhibits lipopolysaccharide (LPS)–induced expression of NF-κB-regulated genes in BV-2 microglia including nitric oxide synthase (NOS2), interleukin-6 (IL-6), and chemokine (C-C motif) ligand 2 (CCL2), and the effects were attenuated by Nurr1-RNA interference. Additionally, C-DIM12 decreased NF-κB activation in NF-κB–GFP (green fluorescent protein) reporter cells and enhanced nuclear translocation of Nurr1 primary microglia. C-DIM12 decreases lipopolysaccharide-induced p65 binding to the NOS2 promoter and concurrently enhanced binding of Nurr1 to the p65-binding site. C-DIM12 also stabilized binding of the Corepressor for Repressor Element 1 Silencing Transcription Factor (CoREST) and the Nuclear Receptor Corepressor 2 (NCOR2)[2].

C-DIM12 has the neuroprotective activity in MPTPp-treated mice[2].

NF-κB–GFP HEK cells are exposed to 30 ng/ml of TNFα in the presence of 100 μM C-DIM12 for up to 24 hours. C-DIM12 is efficient at blocking NF-κB–GFP expression in the NF-κB–GFP HEK cells after TNFα treatment, displaying a statistically significant reduction in total GFP fluorescence per cell.(Only for Reference)