Dorsomorphin (dihydrochloride)

1219168-18-9

C24H27Cl2N5O

DMSO : 5.2 mg/mL (11.01 mM; Need ultrasonic); H2O : >= 50 mg/mL (105.84 mM)

Autophagy; Epigenetics; PI3K/Akt/mTOR; TGF-beta/Smad

Dorsomorphin dihydrochloride (BML-275 dihydrochloride; Compound C dihydrochloride) is a potent, selective and ATP-competitive AMPK inhibitor, with a K_i of 109 nM^[1]. Dorsomorphin dihydrochloride inhibits BMP pathway by targeting the type I receptors ALK2, ALK3, and ALK6^[2]. IC50 & Target: Ki: 109+/-16 nM (AMPK)^[1] In Vitro: Dorsomorphin (compound C) (0-10 uM, 18 h) suppresses 2DG-induced GRP78 promoter activity in human fibrosarcoma HT1080 cells in a dose-dependent manner but has little effect on tunicamycin-induced GRP78 promoter activity. Dorsomorphin (compound C) C also suppresses GRP78 promoter activity induced by glucose withdrawal. Dorsomorphin (compound C) has no effect on 2DG-induced PERK activation and reduces the both basal and 2DG-induced AMPK phosphorylation levels in HT1080 cells^[2]. In Vivo: Dorsomorphin (compound C: 10 mg/kg, intravenously once) treatment leads to a 60% increase in total serum iron concentrations, reduces basal levels of hepcidin expression and increasing serum iron concentrations in adult mice^[3].
Dorsomorphin (compound C: 0.2 mg/kg, i.v., 30 min before LPS injection) reduces ICAM-1 and VCAM-1 expression in LPS-injected rat aorta^[4].
Dorsomorphin (compound C; 25 mg/kg; i.p. injection, in male BALB/c mice) treatment before lipopolysaccharide (LPS) injection significantly reduces lethality in contrast to animals treated with LPS challenge only^[5].