Dorsomorphin (Compound C)
目录号：S7840 别名： BML-275,Compound C
Molecular Weight(MW): 399.49
Dorsomorphin (Compound C)是一种有效的，可逆选择性 AMPK 抑制剂，无细胞试验中 Ki 为 109 nM，对几个结构相关的激酶，包括ZAPK，SYK，PKCθ，PKA，和 JAK3没有显著的抑制作用。 也会抑制 I型 BMP receptor 活性。
(A) Cells were pre-treated with 10 ng/ml TGF-β for 24 h, then 5 mM metformin and/or 1 uM (μM) dorsomorphin were added to the medium for another 24 h. Immunofluorescence staining showed that AMPK inhibition abolished metformin's effect of decreasing TGF-β-induced α-actin expression in HFL-1 cells. The nucleus were stained with 4', 6-diamidino-2-phenylindole in the merged images. Scale bars: 150 μm.
Oncotarget, 2016, 6(41):43605-19.. Dorsomorphin (Compound C) purchased from Selleck.
FGF21 activates myogenic and aerobic myofiber-associated genes expression via AMPK pathway. The activator (acadesine) or inhibitor (dorsomorphin) of AMPK pathway were used to treat the pcDNA3.1-21 or control transfected C2C12 myoblasts. For this experiment, four groups were set up: FGF21-ACA (pcDNA3.1-21‡acadesine), Control-ACA (control‡acadesine), FGF21-DOR (pcDNA3.1-21‡dorsomorphin), and Control-DOR(control‡dorsomorphin). The qRT-PCR was performed to detect the genes expression of FGF21 (A), AMPK (B), Sirt 1, Myoglobin(C), Desmin (D), MEF2c (E), a-actin (F). (G) The C2C12 myoblasts were transiently transfected with pCDNA3.1-21 or pCDNA3.1, Western blot showed FGF21 activated AMPK signal via FGF21-Sirt1-AMPK. For the phosphorylated AMPK (right), the intensity of band was normalized total AMPK, and then normalized by control. (H and I) FGF21, as well as AMPK activator acadesine (ACA), increased phosphorylation of AMPM, and myogenic genes expression, especially MyHC I, which was activated by ACA (FGF21‡ACA) and suppressed by AMPK inhibitor DOR(FGF21‡DOR). The data are presented as mean±SD (*P<0.05, **P<0.01, and P<0.001), n=ˆ3.
J Cell Physiol, 2017, 232(7):1893-1906. Dorsomorphin (Compound C) purchased from Selleck.
ZLN005 increased autophagic activities in cardiomyocytes under HG conditions by SIRT1 pathway. LC3, ATG5, Beclin1, and SIRT1 expression of cardiomyocytes was measured by Western blot analysis. EX527: SIRT1-specific inhibitor. Compound C: AMPK-specific inhibitor Dorsomorphin. The results are expressed as the means±SEM, n=3. The value of LC3 II/LC3 I in ZLN005(−)EX527(−) groups was set as 1. (D): *P<0.05 compared with the ZLN005(−) Compound C(−) groups. ZLN005 (+): 4 μM. Compound C (+): 5 μM.
Exp Cell Res, 2016, 345(1):25-36.. Dorsomorphin (Compound C) purchased from Selleck.
Effect of dorsomorphin on MCP-1 and adiponectin production in TNFα-stimulated 3T3-L1 adipocytes with or without AICAR. 3T3-L1 cells were preincubated with 1–10 µM of dorsomorphin (Compound C) with or without 2 mM of AICAR for 1 h and then treated with 50 ng/ml of TNFα (TD1, TD3, TD10, and TAD1, TAD3, TAD10). After 24 h, the MCP-1 (a) and adiponectin (b) concentration in the culture medium was assayed. Data are means ± SD of five observations. D10: Only dorsomorphin treated cells. a: Control (C) vs T, TD1, TD3 or TD10: p < 0.001, T, TD1, TD3 or TD10 vs TA, TAD1, TAD3, TAD10 or D10: p < 0.001, TA vs C or D10: p < 0.05.b: C or D10 vs T, TD1, TD3 or TD10: p < 0.001, T vs TA or TAD3: p < 0.005, T vs TAD1: p < 0.01, T vs TAD10: p < 0.001, TD1, TD3 or TD10 vs TA, TAD3 or TAD10: p < 0.001, TD1, TD3 or TD10 vs TAD1: p < 0.005.
J Atheroscler Thromb, 2016, 23(12):1345-1354.. Dorsomorphin (Compound C) purchased from Selleck.
a. Western blots were performed after 12 h of RA treatment, followed by 2 h of Dorso or SB431542 (Activator of Smad1/5 phosphorylation) in the absence of RA. Similar results were obtained in two separate experiments.
BMC Biotechnol, 2017, 17(1):17. Dorsomorphin (Compound C) purchased from Selleck.
Effects of BMP-7 and downstream pathways on the protectiveeffect of OGDPC against OGD/R in SH-SY5Y cells. BMP-7 was blockedby Noggin (200 ng/mL), MAPK signal was blocked by U0126 andSB203580 mixture (10 μmol/L each) and Smad signal was blocked byDorsomorphin (1 μmol/L) and Smad 1 RNAi. BMP-7 blockage com-pletely inhibited the protective effect of OGDPC as represented by (a)decreasing cell viability and (b) increasing LDH activity to the level of OGD/R treatment. MAPK and Smad blockage could partly inhibit theprotective effect. Values are presented as mean±standard deviation (SD)(n = 3). **P < 0.01 compared with control group;##P < 0.01 comparedwith OGD/R group;§§P < 0.01 compared with OGDPC group. MAPKi:MAPK inhibitors, U0126 and SB203580 mixture; Dors: Dorsomorphin
Clin Exp Pharmacol Physiol, 2016, 43(1):125-34. . Dorsomorphin (Compound C) purchased from Selleck.
Levels of phosphorylated AMPK, phosphorylated AKT, GK, PEPCK, and G6pase, PI3K in four groups were analyzed by Western blots in the presence of ASCs co-culturing for 12 h. C.C=compound C:Dorsomorphin, PA:palmitate, ASC:mesenchymal stem cells.
Biochem Biophys Res Commun, 2017, 483(1):435-441.. Dorsomorphin (Compound C) purchased from Selleck.
|产品描述||Dorsomorphin (Compound C)是一种有效的，可逆选择性 AMPK 抑制剂，无细胞试验中 Ki 为 109 nM，对几个结构相关的激酶，包括ZAPK，SYK，PKCθ，PKA，和 JAK3没有显著的抑制作用。 也会抑制 I型 BMP receptor 活性。|
在肝细胞中，Dorsomorphin通过AICAR或二甲双胍抑制ACC失活，并减弱AICAR或二甲双胍增加脂肪酸氧化或抑制脂肪生成基因的作用。 HT-29细胞中，Dorsomorphin对AMPK活性的抑制几乎完全抑制自噬蛋白质水解。此外，Dorsomorphin选择性抑制BMP I型受体ALK2，ALK3和ALK6，从而阻断BMP介导的SMAD1/5/8磷酸化，靶点基因转录和成骨分化。
|体内研究||Dorsomorphin (10 mg/kg)降低成年小鼠体内铁调素表达的基础水平，并增加血清铁的浓度。 Dorsomorphin (0.2 mg/kg, i.v.)显著减少LPS处理的大鼠胸主动脉中VCAM-1和ICAM-1的表达。|
|体外||Ethanol||2 mg/mL warmed (5.0 mM)|
|DMSO||1 mg/mL warmed (2.5 mM)|
质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)
*在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。
开始浓度 x 开始体积 = 最终浓度 x 最终体积
稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )
在配置溶液时，请务必参考Selleck产品标签上、MSDS / COA（可在Selleck的产品页面获得）批次特异的分子量使用本工具。.