| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
Cell lines | Six breast cancer cell lines, including MCF7, BT20, T47D, MDA-MB-453, and MDA-MB-231 |
Preparation Method | Human breast cancer cells were plated into 35 mm dishes. After one day cells were treated with metformin at the indicated concentrations or the same volume of sterilized water,incubated with metformin for 1, 2 or 3 days. |
Reaction Conditions | 8 mM for 1, 2 or 3 days |
Applications | Five of six breast cancer cell lines, including MCF7, BT20, T47D, MDA-MB-453, and MDA-MB-474, underwent growth arrest after metformin treatment. |
Animal models | female FVB/N HER-2/neu mice |
Preparation Method | Mice of the first group were given metformin with drinking water (100 mg/kg) for five consecutive days every month for 12 months, whereas the mice of the second group were given tap water without metformin and served as a control. |
Dosage form | 100 mg/kg, oral |
Applications | One control mouse (3%) survived the age of 10 months whereas 9 mice (28%) survived this age in metformin-treated group |
| 产品描述 | Metformin (1,1-Dimethylbiguanide) primarily mediate activation of AMPK, a serine/threonine protein kinase involved in regulating cellular energy metabolism, leading to a reduction in mTOR signaling and protein synthesis in cancer cells. Metformin activates AMPK by inhibiting complex I of the mitochondrial respiratory chain[1]. Metformin treatment reduced 4T1 cell viability with IC50: 16 mM, 24 h; 8 mM, 48 h; 4 mM, 72 h[2]. Metformin inhibited a variety of breast cancer cells growth regardless of oestrogen receptor (ER), PR, HER2 or p53 status[3]. Metformin induced unique responses in the triple-negative (ER, PR and HER2 negative) breast cancer cell line MDA-MB-231, leading to an S phase cell cycle arrest and then increase apoptosis[4]. Metformin may also be effective against ER-positive breast cancers by inhibiting aromatase expression in tumour stroma[5]. Orally administered metformin (at plasma levels (2.7-10.3 mM)) also reduced tobacco carcinogeninduced lung tumourigenesis (NNK) in mice (tumour burden reduced by 53%)[6]. Metformin treatment significantly delayed the appearance of mammary adenocarcinomas, reduced the size of tumours and prolonged the lifespan of MMTV-Her2/Neu mice[7]. Metformin is indicated for treatment of hyperglycemia in type 2 diabetes and improves glycemic control without inducing hypoglycemia or weight gain[8]. Metformin can cross though the blood-brain barrier and induces cell autophagy[9]. References: |
m.cnreagent.com