Metformin hydrochloride

SKU: orb1310334

Description

Metformin hydrochloride

Research Area

Cell Biology, Epigenetics & Chromatin, Signal Transduction

Key Properties

• CAS Number: 1115-70-4
• MW: 165.63
• Purity: 99.97%
• Formula: C₄H₁₂ClN₅
• SMILES: Cl.CN(C)C(=N)NC(N)=N
• Target: Autophagy,Mitophagy,AMPK
• Solubility: H2O:193.21 mM;DMSO:50 mg/mL (301.88 mM)

Bioactivity

• Target IC50:
  MDA-MB-231 cells:149 mM|HepG2 cells:98 mM|MYCN-2 cells:> 100 mM|SK-N-Be2c cells:> 100 mM
• In Vivo:
  METHODS: To model Metformin-induced diarrhea, Metformin hydrochloride (125-500 mg/kg) was administered orally to healthy and diabetic obese db/db C57BL/6J mice twice daily for thirteen days. Results: Metformin at 1000 mg/kg/day significantly increased fecal water content. Although no diarrhea symptoms were observed in healthy C57BL/6J mice the same dose of Metformin induced severe diarrhea in diabetic obese db/db mice. METHODS: To investigat the Protective effect of Metformin in radiation injury, Metformin hydrochloride (200 mg/kg once daily for three days) was administered orally to BAL-/- mice, which were then exposed to 6-8 Gy of gamma radiation. Results: When administered prior to exposure to radiation, Metformin prolonge the survival of mice exposed to 8 Gy-TBI and increase the survival of mice exposed to 6 Gy-TBI. Pretreatment with Metformin attenuated radiation damage.
• In Vitro:
  METHODS: Ovarian cancer cells A2780 and SKOV3 were treated with Metformin hydrochloride (0.001-50 mM) for 24-48 h. Cell viability was assayed usin the MTS RESULTS: Micromolar concentration of Metformin did not statistically reduc the viability o the A2780 or SKOV3 cell lines. At 48 h, millimolar concentration resulted in cell death. METHODS: Human colorectal cancer cells HCT29 were treated with Metformin hydrochloride (0.6 mM) for 90 h. Cell motility was detected usin the wound healing assay and chamber invasion assay. Results: Metformin inhibite the migration and invasion of HCT29 cells, and Metformin decrease the motility of tumor cells.
• Cell Research:
  Hepatocytes were isolated from Male Sprague Dawley (SD) rats by collagenase digestion. Fo the AMPK assay, cells were seeded in six-well plates at 1.5 × 10^6 cells/well in DMEM containing 100 U mL penicillin, 100 μg mL streptomycin, 10% FBS, 100 nM insulin, 100 nM dexamethasone, and 5 μg mL transferrin for 4 hours. Cells were then cultured in serum-free DMEM for 16 hours followed by treatment for 1 hour or 7 hours with control medium, 5-aminoimidazole carboxamide riboside (AICAR), or metformin at concentration indicated. For a 39-hour treatment, cells for both control and metformin (10 or 20 μM) groups were cultured in DMEM plus 5% FBS and 100 nM insulin, an the fresh control and metformin-containing medium were replaced every 12 hours (last medium change was 3 hours before harvest). After treatment the cells were directly lysed in digitonin-containing and phosphatase inhibitor–containing buffer A, followed by precipitation with ammonium sulfate at 35% saturation. AMPK activity was determined by measurement of phosphorylation of a synthetic peptide substratee, SAMS (HMRSAMSGLHLVKRR). For ACC assay the 35% ammonium sulfate precipitate from digitonin-lysed hepatocytes (4 μg each) was used for determination of ACC activity via 14CO2 fixation in the presence of 20 mM citrate as done previously. For fatty acid oxidation the oxidation of 14C-oleate to acid-soluble products was performed as done previously, but in medium M199 in the absence of albumin.
• Animal Research:
  Oral gavage was used to administer 1 mL of metformin (100 mg/ml) or water alone to Male SD rats (300–350 g, n = 7–8). Rats were treated once or twice a day for 5 days. Rats were starved for 20 hours and then re-fed for 2 hours befor the final dose; 4 hours afte the final dose the animals were anesthetized and livers rapidly removed by freeze clamping followed by blood withdrawal. RNA was prepared fro the freeze-clamped liver by RNA isolation reagent. Nuclear extracts were prepared from a pool of seven rat livers. Glucose levels were determined usin the s andard glucose oxidase assay kit; β-hydroxybutyrate concentration were assayed by measurin the reduction of NAD to NADH with a s andard assay kit. FFA levels were measured wit the assay kit. MCF10A-ER-Src cells (5 × 10^6) were injected int the right flank of 18 f Male nu/nu mice, All of which developed tumors in 10 d with a size of ～100 mm^3 the mice were andomly distributed into Six groups (three mice/group) that were untreated or treated by intratumoral injections every 5 d (four cycles) with 1 mg/kg or 4 mg/kg doxorubicin, 200 μg mL metformin (diluted in the drinking water), o the combination. In a Other experiment, LNCaP and DU145 prostate cancer cells (5 × 10^6) were injected int the right flank of 12 f Male nu/nu mice, All of which developed tumors in 10 d with a size of ～75 mM^3 the mice were andomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 4 mg/kg doxorubicin and/or 200 μg mL metformin. In a Other experiment, A375 and MDA-MB-435 melanoma cells (7 × 10^6) were injected int the right flank of 12 f Male nu/nu mice, All of which developed tumors in 10 d with a size of ～50 mm3 the mice were andomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 10 mg/kg cisplatin and/or 200 μg mL metformin.Finally, SNU-449 liver cancer cells (10^7) were injected int the right flank of 12 f Male nu/nu mice, All of which developed tumors in 10 d with a size of ～50 mm^3 the mice were andomly distributed into four groups that were untreated or treated by intratumoral injections every 5 d (four cycles) with 10 mg/kg cisplatin and/or 200 μg mL metformin. Tumor volume (mean ± SD) was measured at various times afte the initial injection.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Disclaimer: For research use only

Alternative Names

diabetes, chain, 1,1-Dimethylbiguanide Hydrochloride, 1,1-Dimethylbiguanide hydrochloride, 1,1-Dimethylbiguanide, 1, 1-Dimethylbiguanide Hydrochloride, 1, 1-Dimethylbiguanide hydrochloride, AMPK, AMP-activated protein kinase, Autophagy, barrier, blood-brain, insulin, Metformin, Metformin HCl, Metformin hydrochloride, Metformin Hydrochloride, Mitophagy, Mitochondrial Autophagy, mitochondrial, Inhibitor, inhibit, liver, type, respiratory, sensitivity

Compound Identifiers

PubChem CID

137704554