AMI-1 (free acid)

AMI-1 free acid is a potent, cell-permeable and reversible inhibitor of protein arginine N-methyltransferases (PRMTs), with IC₅₀s of 8.8 μM and 3.0 μM for human PRMT1 and yeast-Hmt1p, respectively. AMI-1 free acid exerts PRMTs inhibitory effects by blocking peptide-substrate binding^[1]. IC50 & Target: IC50: 8.8 μM (PRMT1), 3.0 μM (yeast-Hmt1p)^[1] In Vitro: AMI-1 free acid can inhibit the in vitro methylation reactions performed by all five recombinantly active PRMTs (PRMT1, -3, -4, and -6 and Hmt1p)^[2].
AMI-1 free acid not only inhibits type I PRMTs (PRMT1, 3, 4 and 6) but also type II PRMT5^[2].
AMI-1 free acid specifically inhibits arginine, but not lysine, methyltransferase activity in vitro and does not compete for the AdoMet binding site^[3].
AMI-1 free acid inhibits methylation of GFP-Npl3 and cellular proteins^[3].
AMI-1 free acid (0.6-2.4 mM; 48-96 hours) inhibits the cell viability of sarcoma in S180 and U2OS cells in a time-dependent and dose-dependent manner in vitro^[4].
AMI-1 free acid (1.2-2.4 mM; 48-72 hours) reduces S180 cell viability through the induction of cell apoptosis^[4].
In Vivo: AMI-1 free acid (0.5 mg; intratumorally; daily; for 7 days) inhibits S180 viability in vivo^[4].
AMI-1 free acid (0.5 mg; intratumorally; daily; for 7 days) downregulates PRMT5 but does not regulate the expression of PRMT7 in a tumor xenograft model^[4].
AMI-1 free acid (0.5 mg; intratumorally; daily; for 7 days) decreases the levels of H4R3me2s and H3R8me2s in a tumor xenograft model^[4].