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Dorsomorphin dihydrochloride

MCE China：Dorsomorphin dihydrochloride

Brand：MedChemExpress (MCE)

Cat. No.HY-13418

CAS：1219168-18-9

Synonyms：Compound C dihydrochloride; BML-275 dihydrochloride

Purity：99.73%

Storage：4°C, sealed storage, away from moisture *In solvent : -80°C, 1 year; -20°C, 6 months (sealed storage, away from moisture)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Dorsomorphin (Compound C) dihydrochloride is a potent, selective and ATP-competitive AMPK inhibitor, with a Ki of 109 nM. Dorsomorphin dihydrochloride inhibits BMP pathway by targeting the type I receptors ALK2, ALK3, and ALK6. Dorsomorphin dihydrochloride can reverse autophagy activation and anti-inflammatory effect of Urolithin A (HY-100599).

In Vitro：Dorsomorphin (compound C; 0-10 μM; 18 h) dihydrochloride suppresses 2DG-induced GRP78 promoter activity in human fibrosarcoma HT1080 cells in a dose-dependent manner but has little effect on Tunicamycin (HY-A0098)-induced GRP78 promoter activity. Dorsomorphin dihydrochloride also suppresses GRP78 promoter activity induced by glucose withdrawal. Dorsomorphin dihydrochloride 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) dihydrochloride treatment leads to a 60% increase in total serum iron concentrations, reduces basal levels of hepcidin expression and increases serum iron concentrations in adult mice[3]. Dorsomorphin (0.2 mg/kg, i.v., 30 min before LPS injection) dihydrochloride reduces ICAM-1 and VCAM-1 expression in LPS-injected rat aorta[4]. Dorsomorphin (25 mg/kg; i.p. injection, in male BALB/c mice) dihydrochloride treatment before lipopolysaccharide (LPS) injection significantly reduces lethality in contrast to animals treated with LPS challenge only[5].

IC50 & Target：AMPK 109 nM (Ki) ACVR1 BMPR1A ALK6 Autophagy

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References：

[1]. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of action. J Clin Invest. 2001 Oct;108(8):1167-74.  [Content Brief]

[2]. Saito S, et al. Compound C prevents the unfolded protein response during glucose deprivation through a mechanism independent of AMPK and BMP signaling. PLoS One. 2012;7(9):e45845.  [Content Brief]

[3]. Yu PB, et al. Dorsomorphin inhibits BMP signals required for embryogenesis and iron metabolism. Nat Chem Biol. 2008 Jan;4(1):33-41.  [Content Brief]

[4]. Kim YM, et al. Compound C independent of AMPK inhibits ICAM-1 and VCAM-1 expression in inflammatory stimulants-activated endothelial cells in vitro and in vivo. Atherosclerosis. 2011 Nov;219(1):57-64.  [Content Brief]

[5]. Guo Y, et al. AMPK inhibition blocks ROS-NFκB signaling and attenuates endotoxemia-induced liver injury. PLoS One. 2014 Jan 24;9(1):e86881.  [Content Brief]

[6]. Zhang Y, et al. Urolithin A suppresses glucolipotoxicity-induced ER stress and TXNIP/NLRP3/IL-1β inflammation signal in pancreatic β cells by regulating AMPK and autophagy. Phytomedicine. 2021 Dec;93:153741.  [Content Brief]