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Dorsomorphin dihydrochloride

MCE 国际站：Dorsomorphin dihydrochloride

品牌：MedChemExpress (MCE)

货号：HY-13418

CAS：1219168-18-9

Synonyms：Compound C dihydrochloride; BML-275 dihydrochloride

纯度：0.9973

存储条件：4°C,密封保存，远离潮湿 *溶剂中：-80°C, 1年; -20°C, 6个月（密封保存，远离潮湿）

运输条件：美国大陆的室温；其他地方可能有所不同。

产品活性：Dorsomorphin (Compound C) dihydrochloride 是一种有效，选择性和 ATP 竞争性的 AMPK 抑制剂，Ki 为 109 nM。Dorsomorphin dihydrochloride 通过靶向抑制 I 型受体 ALK2，ALK3 和 ALK6 来抑制 BMP 途径。Dorsomorphin dihydrochloride 还能够逆转 Urolithin A (HY-100599) 导致的自噬 (autophagy) 激活和抗炎作用。

体外：Dorsomorphin (compound C; 0-10 μM; 18 h) dihydrochloride 以剂量依赖性方式抑制人纤维肉瘤 HT1080 细胞中 2DG 诱导的 GRP78 启动子活性，但对衣霉素 (HY-A0098) 诱导的 GRP78 启动子活性几乎没有影响。Dorsomorphin dihydrochloride 还抑制葡萄糖戒断诱导的 GRP78 启动子活性。Dorsomorphin dihydrochloride 对 2DG 诱导的 PERK 激活没有影响，并降低 HT1080 细胞中基础和 2DG 诱导的 AMPK 磷酸化水平[2]。 MCE尚未独立证实这些方法的准确性。仅供参考。

体内：Dorsomorphin (化合物 C; 10 mg/kg; 静脉注射一次) dihydrochloride 处理导致总血清铁浓度增加 60%，降低成年小鼠铁调素表达的基础水平并增加血清铁浓度[3]。 Dorsomorphin (0.2 mg/kg，静脉注射，LPS 注射前 30 分钟) dihydrochloride 降低注射 LPS 的大鼠主动脉中的 ICAM-1 和 VCAM-1 表达[4]。 Dorsomorphin (25 mg/kg；腹腔注射，在雄性 BALB/c 小鼠中) dihydrochloride 在注射脂多糖 (LPS) 之前进行处理，与仅接受 LPS 处理的动物相比，显著降低了致死率[5]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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

销售产品：Suc-Ala-Leu-Pro-Phe-pNA  | 187-1, N-WASP inhibitor  | Caftaric acid  | Clonidine (hydrochloride)  | Lenvatinib-d4  | N-3-Oxo-tetradecanoyl-L-homoserine lactone  | BTX161  | Pelargonidin (chloride)  | 2-Iminothiolane (hydrochloride)  | Adenosine dialdehyde

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参考文献：

[1]. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of action. J Clin Invest. 2001 Oct;108(8):1167-74.[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.[3]. Yu PB, et al. Dorsomorphin inhibits BMP signals required for embryogenesis and iron metabolism. Nat Chem Biol. 2008 Jan;4(1):33-41.[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.[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.[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.