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99% Metformin HCL Powder C4H12ClN5 Oral Hypoglycemic Agents

99% Metformin HCL Powder C4H12ClN5 Oral Hypoglycemic Agents

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    Metformin HCL Powder


    C4H12ClN5 Oral Hypoglycemic Agents


    99% Metformin HCL Powder

  • Molecular Formula
  • Product Name
    Metformin HCL
  • Grade
    Pharmaceutical Grade
  • The Boiling Point
    224.1ºC At 760 MmHg
  • Brand Name
    Kan Ying
  • Main Effect
  • Main Ingredient
    Metformin Hydrochloride
  • Storage
    Cool Dry Place
  • Place of Origin
  • Brand Name
    Kan Ying
  • Minimum Order Quantity
  • Price
    To discuss
  • Packaging Details
  • Delivery Time
  • Payment Terms
    L/C, D/A, D/P, T/T, Western Union, MoneyGram,Dollars
  • Supply Ability

99% Metformin HCL Powder C4H12ClN5 Oral Hypoglycemic Agents

diabetes hypoglycemic Oral Hypoglycemic Agents Metformin HCL The high content


* Product title:Metformin Hydrochloride


* Product parameter table:


Product name Metformin HCL appearance White crystalline or crystalline powder
Use of the product hypoglycemic content 99%
Molecular formula C4H12ClN5 Shelf Life 2 Years
CAS 1115-70-4 Storage Cool Dry Place



* Product Description:


Metformin hydrochloride, the main ingredient is metformin hydrochloride, this product can reduce the fasting and postprandial hyperglycemia of Ⅱ type diabetes patients, HBALC can decrease by 1%-2%, is one of the commonly used hypoglycemic drugs. Congestive heart failure, liver and renal insufficiency, diabetes mellitus complicated with ketoacidosis and acute infection are contraindicated. Use with caution in pregnant women.


* Use of the product:


Metformin hydrochloride is a first-line hypoglycemic drug, which is the first choice for patients with type 2 diabetes. Diabetic patients often choose other kinds of hypoglycemic drugs on the basis of metformin to achieve the purpose of controlling blood sugar. Metformin hydrochloride can inhibit glycosides' output and improve blood glucose uptake by surrounding muscles.


* Bioactivity of metformin hydrochloride:

Metformin (Hydrochloride) is an FDA-approved first-line drug for the treatment of type 2 diabetes. Metformin reduces liver glucose production primarily through mild and transient inhibition of mitochondrial respiratory chain complex 1.
Related categories
Signaling pathway >; > Epigenetics > > AMPK
Signaling pathway >; > PI3K/Akt/mTOR signaling pathway > > AMPK
Signaling pathway >; > Autophagy & gt; > autophagy
Signaling pathway >; > Autophagy & gt; > autophagy
Research Fields > > cancer



In vitro, metformin inhibited ESC proliferation in a concentration - dependent manner. The IC50 of A-ESC was 2.45mM and that of N-ESC was 7.87mM. Metformin significantly activates AMPK signaling in secretory A-ESC cells compared with proliferative cells [3]. Metformin (0-500μM) reduced glycogen synthesis in a dose-dependent manner with IC50 values of 196.5μM in cultured rat hepatocytes [4]. Metformin showed cell viability and cytotoxic effects on PC-3 cells with IC50 of 5 mM [5].
In vivo studies using metformin alone (100 mg/kg, orally) and metformin with the isoproterenol group (25,50,100 mg/kg) reduced myocyte necrosis by histomathological analysis [1]. Metformin (>; 900mg/kg/day, oral) resulted in near-death/death and signs of clinical toxicity in CRL: CD (SD) rats [2].
In cell assay, ESC was inoculated in 96-well plates at a concentration of 1×10 3 cells/well. After attachment, the cells were treated with different doses of metformin/compound C for 0 min, 15 min, 1 h and 24 h. MTT assay was performed as described earlier. In brief, MTT (5mg/mL) was added to the 96-well plate at 10μL/ well, and the plate was incubated for 4 h. The MTT reaction was terminated by removing the medium containing MTT, and 100μLDMSO was added to each well and incubated on an oscillator for 10 min at room temperature to ensure full crystal dissolution. The absorbance was measured at 595nm. Cell proliferation (percentage of control) was calculated as follows: absorbance (experimental group)/absorbance (control group). Cell proliferation inhibition (percent of control) was calculated as follows: 100% cell proliferation (percent of control). Each experiment was carried out in duplicate and repeated six times to assess consistency.
The animals were randomly divided into 6 groups with 6 rats in each group. Rats in group 1 (control) received subcutaneous injection of normal saline (0.5mL) and were left untreated throughout the experiment. Rats in group 2 were given metformin orally (100mg/kg; Twice daily) for 2 days and subcutaneously injected with saline at 24 hour intervals for 2 consecutive days. Rats in group 3 (MI control) were given saline orally (twice a day) for 2 days, followed by subcutaneous injection of isoproterenol (100mg/kg) daily for 2 consecutive days, with an interval of 24 hours. Rats in groups 4 to 6 were treated with 25,50 and 100mg/kg of metformin. Metformin was dissolved in saline and force-fed at a volume of 0.25-0.5mL twice daily at 12-hour intervals, beginning immediately before isoproterenol injection.
[1]. Soraya H, et al. Acute treatment with metformin improves cardiac function following isoproterenol induced myocardial infarction in rats. Pharmacol Rep. 2012; 64 (6) : 1476-84.

[2]. Quaile MP, et al. Toxicity and toxicokinetics of metformin in rats. Toxicol Appl Pharmacol. 2010 Mar 15; 243 (3) : 340-7.

[3]. Xue J, et al. Metformin inhibits growth of eutopic stromal cells from adenomyotic endometrium via AMPK activation and subsequent inhibition of AKT phosphorylation: a possible role in the treatment of adenomyosis. Reproduction. 2013 Aug 21; 146 (4) : 397-406.

[4]. Otto M, et al. Metformin inhibits glycogen synthesis and gluconeogenesis in cultured rat hepatocytes. Diabetes Obes Metab. 2003 May; (3) : 189-94.

[5]. Avci CB, et al. Therapeutic potential of an anti-diabetic drug, metformin: alteration of miRNA expression in prostate cancer cells. Asian Pac J Cancer Prev. 2013; 14 (2) : 765-8.

[6]. Nie L, et al. The Landscape of Histone Modifications in a High-Fat Diet-Induced Obese (DIO) Mouse Model. Mol Cell Proteomics. 2017 Jul; 16 (7) : 1324-1334.

[7]. Zhang D, et al. Metformin ameliorates BSCB disruption by inhibiting neutrophil infiltration and MMP-9 expression but not direct TJ proteins expression regulation. J Cell Mol Med. 2017 Jul 12.


* Pictures of the product:

99% Metformin HCL Powder C4H12ClN5 Oral Hypoglycemic Agents 099% Metformin HCL Powder C4H12ClN5 Oral Hypoglycemic Agents 1