Metformin HCl

目录号:S1950

Metformin HCl  Chemical Structure

Molecular Weight(MW): 165.62

Metformin HCl 降低肝细胞中高血糖症,主要通过抑制肝糖原的产生(肝脏糖异生作用)发挥作用。

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客户使用Selleck该产品发表文献12篇:

客户使用该产品的2个实验数据:

  • Cropped immunoblot analyses for downstream effector proteins of the MAPK and PI3K/AKT/mTOR signaling pathways for NRASQ61 mutant lung carcinoma and neuroblastoma cell lines. Dual pathway inhibition can be achieved by combining metformin and trametinib, as evidenced by the abolishment of p-ERK and p-S6.

    Oncotarget, 2015, 6(2): 969-78 . Metformin HCl purchased from Selleck.

    Metformin added to atorvastatin therapy has no additional lipid-lowering effect. At the beginning of the experiment, rabbits were fed a high-cholesterol diet. After 2 weeks, rabbits were randomly stratified into the normal sodium (Ctrl group), atorvastatin (AT group), metformin (MT group), or atorvastatin/metformin combination therapy (AT + MT group) for a period of 10 weeks. Lipid levels were measured at −2, 0, 2, 6, 10 weeks after drug administration. Time-dependent changes and their AUC values of serum TC levels (A,B) are presented. Data are mean ± SD, n = 7 for each group. *P < 0.05, compared with Ctrl group. AUC, area under the curve; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TC, total cholesterol.

    Sci Rep, 2017, 7(1):2169. Metformin HCl purchased from Selleck.

产品安全说明书

Carbohydrate Metabolism抑制剂选择性比较

生物活性

产品描述 Metformin HCl 降低肝细胞中高血糖症,主要通过抑制肝糖原的产生(肝脏糖异生作用)发挥作用。
靶点
AMPK [1]
(Hepatocytes)
体外研究

Metformin (500 μM)激活肝细胞中AMPK,导致乙酰辅酶a羧化酶(ACC)活性下降,诱导脂肪酸氧化,抑制脂肪生成酶表达。Metformin (2 mM)激活肌肉中的AMPK,促进葡萄糖摄取。Metformin (500 μM) 或者 AICAR强烈抑制大鼠肝细胞中的SREBP-1 mRNA水平。Metformin改善高血压,不激活胰岛素分泌,促进体重增加或者引发低血糖症。Metformin对循环脂类导致的心血管风险增加具有有益作用。Metformin降低肝脏葡萄糖生成,增加肌肉细胞葡萄糖摄取。[1]Metformin需要肝脏中的LKB1降低血糖浓度。[2]Metformin (2 mM)导致肌肉细胞中α1- 和α2-复合体的活性增加。Metformin (2 mM) 增加肌肉细胞中172位点苏氨酸磷酸化。[3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human HepG2 cells MUHGeY5kfGmxbjDhd5NigQ>? MV:yOEBp MnrnTY5kemWjc3WgbY4h\2y3Y3;z[UBkd26|dX3weIlwdiCrbjDpcpN2dGmwLYLld4l{fGGwdDDoeY1idiCKZYDHNkBk\WyuczDh[pRmeiB{NDDodpMtKEWFNUC9NE4zPyEQvF2u M1;6UFIyQDV4MES4
human MDA-MB-231 cells MnjhSpVv[3Srb36gZZN{[Xl? NWLR[XhEOSC2bzCyNEBuVQ>? MV2yOEBp NITVOGxCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIF3ERU1OSi1{M{GgZ4VtdHNiYYSgNUB1dyB{MDDtUUBi\nSncjCyOEBpenNiYomgUXRVKGG|c3H5Mi=> MnzvNlI1PTl{MEi=
human HepG2 cells NFv5d3BHfW6ldHnvckBie3OjeR?= MkmyNUBuVQ>? NVzjTGxQOjRiaB?= MY\S[YR2[3Srb36gc4Yh\2y3Y3;z[UBkd26|dX3weIlwdiCrbjDpcpN2dGmwLYLld4l{fGGwdDDoeY1idiCKZYDHNkBk\WyuczDheEAyKG2PIHHmeIVzKDJ2IHjyd{BjgSCpbIXjc5NmKG:6aXThd4UhdWW2aH;kJIlvKHC{ZYPlcoNmKG:oIEKyMlIhdU1ib3[g[4x2[2:|ZR?= MV:yN|AzPTJ2NB?=
mouse 3T3L1 cells MVTGeY5kfGmxbjDhd5NigQ>? M1y2XVEhdU1? MlPFTY5lfWO2aX;uJI9nKEGPUFugdIhwe3Cqb4L5cIF1cW:wIHnuJI1wfXOnIEPUN2wyKGOnbHzzJIF1KDFibV2gZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m| MkLDNlUzOTZ|N{m=
human HepG2 cells NWj2[npGTnWwY4Tpc44h[XO|YYm= M3TYTVEhdU1? NH[zTlYzPCCq MnHMRYN1cX[jdHnvckBw\iCDTWDLJIlvKGi3bXHuJGhmeEd{IHPlcIx{KGG|c3Xzd4VlKGG|IILl[JVkfGmxbjDv[kBodHWlb37lc4dmdmW|aYOgZZQhOSCvTTDh[pRmeiB{NDDodpMh[nliZX76fY1ifGmlIHPvcI9zcW2ndILpZ{Bie3OjeR?= MUiyOlQ4OTB7MB?=

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-AMPK / AMPK / p-mTOR / mTOR / p-S6K / S6K; 

PubMed: 24505341     


The combined effects of metformin and heating were studied by heating the cells at 39.5–41°C for 1 h with 5 mM metformin and then incubating at 37°C for 47 h.

TTP / p-STAT3 / STAT3 / c-Myc ; 

PubMed: 26956973     


Metformin treatment increases phospho-AMPK (pAMPK) but decreases c-Myc and phospho-STAT3 (pSTAT3) in MCF7 and MDA-MB-231 cells. MCF7 and MDA-MB-231 cells were treated with 6 mM metformin for the indicated length of time, and the levels of TTP, STAT3, pSTAT3, AMPK, pAMPK, and c-Myc were measured by Western blotting.

pACC / ACC / pS6 / S6; 

PubMed: 26172303     


Western blot of pACC Ser79 (280 kDa), ACC (265 kDa), pS6 Ser240/244 (32 kDa), S6 (32 kDa), and β-actin (42 kDa) in HeyA8 cells treated with 0-5 mM metformin in normoglycemic or hyperglycemic conditions for 24 h.

pSTAT3 (Ser727) / STAT3 / Jak2 / Cdk5 / pNFκB / Bcl-2 / Bcl-XL / c-Myc; 

PubMed: 28114390     


Western blot of STAT3 and its regulatory proteins in Ishikawa cells after treatment with control, 10 mM, or 20 mM metformin for 48h in high-glucose conditions.

24505341 26956973 26172303 28114390
Immunofluorescence
LKB1; 

PubMed: 29601127     


LKB1 location with or without 10 lmol/L metformin treatment in Capan-2 wtLKB1 cell line. Scale bar, 50 μm.

PAR ; 

PubMed: 21422199     


A. MCF7 (left panel) or MDA-MB-231 (right panel) cells were treated with (Met) or without (Con) metformin for 2.5 days and then PAR (red) was detected by immunofluorescence using confocal microscopy. Nuclei (blue) were stained with DAPI.

CD86 / CD206; 

PubMed: 30899369     


Representative images of immunofluorescence analysis of macrophage phenotype in vitro, CD86 (M1 green) or CD206 (M2 red) were analysis. Scale bar 50 μm.

beta-catenin / AMPK; 

PubMed: 30854043     


Cells were treated with metformin for 24 h and subjected to immunofluorescence staining for β-catenin and AMPK. Magnification, ×400.

29601127 21422199 30899369 30854043
Growth inhibition assay
Cell viability ; 

PubMed: 26956973     


MCF7 and MDA-MB-231 cells were treated with the indicated concentrations of metformin for 24 h. Cell viability was assessed by measuring absorbance at 490 nm using an MTS cell proliferation assay. The values obtained with mock-treated cells were set to 100. Values are the mean ± SD (n = 3). *p < 0.05, **p < 0.01, ***p < 0.001.

26956973
体内研究 在SD大鼠中,Metformin (100毫克/毫升,口服)显著降低肝脏中SREBP-1,FAS,和S14 mRNA水平,这与细胞水平的实验结果是一致的。在肥胖小鼠中,Metformin降低肝脏脂类。[1]Metformin (250 毫克/千克,腹腔注射)增加野生型小鼠中肝脏中AMPK的磷酸化作用。Metformin (250毫克/千克,腹腔注射)降低50%高脂饮食的野生型小鼠的血糖,Metformin (250 毫克/千克,腹腔注射)也会降低ob/ob小鼠40%的血糖。[2]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

溶解度 (25°C)

体外 Water 33 mg/mL warmed (199.25 mM)
DMSO Insoluble
Ethanol Insoluble

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 165.62
化学式

C4H11N5.HCl

CAS号 1115-70-4
储存条件 powder
in solvent
别名 N/A

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*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。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

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。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03686657 Not yet recruiting Type 2 Diabetes|High Blood Pressure|Arthritis|Obesity ARKAY Therapeutics|Albany Medical College August 5 2019 Phase 1|Phase 2
NCT03499704 Not yet recruiting Diabetes Mellitus Type 2 Takeda August 31 2019 Phase 4
NCT03499704 Not yet recruiting Diabetes Mellitus Type 2 Takeda August 31 2019 Phase 4
NCT03686657 Not yet recruiting Type 2 Diabetes|High Blood Pressure|Arthritis|Obesity ARKAY Therapeutics|Albany Medical College August 5 2019 Phase 1|Phase 2
NCT03452267 Not yet recruiting Insulin Sensitivity Wayne State University June 2019 Phase 2|Phase 3
NCT03452267 Not yet recruiting Insulin Sensitivity Wayne State University June 2019 Phase 2|Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID