Dorsomorphin

866405-64-3

C24H25N5O

DMSO : 2 mg/mL (5.01 mM; Need ultrasonic); Ethanol : 3.33 mg/mL (8.34 mM; Need ultrasonic)

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

Dorsomorphin (BML-275; Compound C) is a potent and selective AMPK inhibitor, that is competitive with ATP, with K_i=109 nM in the absence of AMP^[1]. Dorsomorphin 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].