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Metformin | CAS No: 657-24-9 | GMP-certified suppliers
A medication that supports glycemic control in type 2 diabetes across adult and pediatric populations, including use in various fixed‑dose combination therapies.
Therapeutic categories
Primary indications
- Metformin immediate-release formulations**
- Metformin is indicated as an adjunct to diet and exercise to improve glycemic control in adults and pediatric patients ≥10 years old with type 2 diabetes mellitus
- Metformin extended-release tablet (XR)**
Product Snapshot
- Metformin is an oral small‑molecule API supplied mainly in immediate‑release and extended‑release tablet formulations, including use in fixed‑dose combinations
- It is used across mono and combination products to support glycemic control in type 2 diabetes mellitus
- The API is approved and commercially established in major regulated markets including the US, EU, and Canada
Clinical Overview
The pharmacologic effect of metformin centers on reducing hepatic glucose production, decreasing intestinal glucose absorption, and improving peripheral insulin sensitivity. These actions lower blood glucose without stimulating pancreatic insulin secretion and therefore do not typically cause hypoglycemia. Clinically, metformin reduces fasting plasma glucose and HbA1c. In a 29‑week study, fasting plasma glucose decreased by an average of 59 mg/dL and HbA1c by approximately 1.4 percent versus placebo.
Metformin’s mechanism involves cellular uptake through OCT1, intracellular accumulation driven by membrane potentials, and inhibition of mitochondrial complex I. This inhibition alters cellular energy status, increasing AMP:ATP and ADP:ATP ratios and activating AMPK. Downstream effects include suppression of gluconeogenesis via inhibition of fructose‑1,6‑bisphosphatase and adenylate cyclase, reduced cAMP formation, and modulation of lipid metabolism through acetyl‑CoA carboxylase phosphorylation. Additional evidence highlights intestinal actions such as increased anaerobic glucose metabolism, enhanced GLP‑1 activity, and altered gut glucose utilization.
Metformin is not metabolized and is eliminated unchanged via renal excretion. It is a substrate for OCT1, OCT2, and MATE transporters, making renal function a critical determinant of exposure. Reduced kidney function increases the risk of lactic acidosis, a rare but serious toxicity. Gastrointestinal intolerance is the most common adverse effect.
Notable global brand contexts include Glucophage formulations and multiple combination products. For API procurement, suppliers should provide validated control of impurities, particle size distribution suitable for the intended formulation, and evidence of compliance with pharmacopoeial and regulatory standards.
Identification & chemistry
| Generic name | Metformin |
|---|---|
| Molecule type | Small molecule |
| CAS | 657-24-9 |
| UNII | 9100L32L2N |
| DrugBank ID | DB00331 |
Pharmacology
| Summary | Metformin lowers blood glucose primarily by suppressing hepatic gluconeogenesis, enhancing peripheral insulin sensitivity, and reducing intestinal glucose absorption. Its activity is linked to inhibition of mitochondrial complex I, leading to altered cellular energy states that activate AMPK and other downstream regulators of glucose and lipid metabolism. Additional gut‑mediated effects, including changes in glucose utilization and incretin signaling, also contribute to its antihyperglycemic action. |
|---|---|
| Mechanism of action | Metformin's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (also called gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization.It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism.The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control. After ingestion, the organic cation transporter-1 (OCT1) is responsible for the uptake of metformin into hepatocytes (liver cells). As this drug is positively charged, it accumulates in cells and in the mitochondria because of the membrane potentials across the plasma membrane as well as the mitochondrial inner membrane. Metformin inhibits mitochondrial complex I, preventing the production of mitochondrial ATP leading to increased cytoplasmic ADP:ATP and AMP:ATP ratios.These changes activate AMP-activated protein kinase (AMPK), an enzyme that plays an important role in the regulation of glucose metabolism.Aside from this mechanism, AMPK can be activated by a lysosomal mechanism involving other activators. Following this process, increases in AMP:ATP ratio also inhibit _fructose-1,6-bisphosphatase_ enzyme, resulting in the inhibition of gluconeogenesis, while also inhibiting _adenylate cyclase_ and decreasing the production of cyclic adenosine monophosphate (cAMP),a derivative of ATP used for cell signaling . Activated AMPK phosphorylates two isoforms of acetyl-CoA carboxylase enzyme, thereby inhibiting fat synthesis and leading to fat oxidation, reducing hepatic lipid stores and increasing liver sensitivity to insulin. In the intestines, metformin increases anaerobic glucose metabolism in enterocytes (intestinal cells), leading to reduced net glucose uptake and increased delivery of lactate to the liver. Recent studies have also implicated the gut as a primary site of action of metformin and suggest that the liver may not be as important for metformin action in patients with type 2 diabetes. Some of the ways metformin may play a role on the intestines is by promoting the metabolism of glucose by increasing glucagon-like peptide I (GLP-1) as well as increasing gut utilization of glucose. In addition to the above pathway, the mechanism of action of metformin may be explained by other ways, and its exact mechanism of action has been under extensive study in recent years. |
| Pharmacodynamics | **General effects** Insulin is an important hormone that regulates blood glucose levels.Type II diabetes is characterized by a decrease in sensitivity to insulin, resulting in elevations in blood glucose when the pancreas can no longer compensate. In patients diagnosed with type 2 diabetes, insulin is unable to exert adequate effects on tissues and cells (i.e. insulin resistance)and insulin deficiency may also be present. Metformin reduces hepatic production of glucose, decreases the intestinal absorption of glucose, and enhances insulin sensitivity by increasing both peripheral glucose uptake and utilization. In contrast with drugs of the sulfonylurea class, which lead to hyperinsulinemia, the secretion of insulin is unchanged with metformin use. **Effect on fasting plasma glucose (FPG) and Glycosylated hemoglobin (HbA1c)** HbA1c is an important periodic measure of glycemic control used to monitor diabetic patients. Fasting plasma glucose is also a useful and important measure of glycemic control. In a 29-week clinical trial of subjects diagnosed with type II diabetes, metformin decreased the fasting plasma glucose levels by an average of 59 mg/dL from baseline, compared to an average increase of 6.3 mg/dL from baseline in subjects taking a placebo.Glycosylated hemoglobin (HbA1c) was decreased by about 1.4% in subjects receiving metformin, and increased by 0.4% in subjects receiving placebo only. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Electron transfer flavoprotein-ubiquinone oxidoreductase, mitochondrial | Humans | inhibitor |
| 5'-AMP-activated protein kinase subunit beta-1 | Humans | inducer, activator |
| Glycerol-3-phosphate dehydrogenase [NAD(+)], cytoplasmic | Humans | inhibitor |
ADME / PK
| Absorption | **Regular tablet absorption** The absolute bioavailability of a metformin 500 mg tablet administered in the fasting state is about 50%-60%. Single-dose clinical studies using oral doses of metformin 500 to 1500 mg and 850 to 2550 mg show that there is a lack of dose proportionality with an increase in metformin dose, attributed to decreased absorption rather than changes in elimination. At usual clinical doses and dosing schedules of metformin, steady-state plasma concentrations of metformin are achieved within 24-48 hours and are normally measured at <1 μg/mL. **Extended-release tablet absorption** After a single oral dose of metformin extended-release, Cmax is reached with a median value of 7 hours and a range of between 4 and 8 hours. Peak plasma levels are measured to be about 20% lower compared to the same dose of regular metformin, however, the extent of absorption of both forms (as measured by area under the curve - AUC), are similar. **Effect of food** Food reduces the absorption of metformin, as demonstrated by about a 40% lower mean peak plasma concentration (Cmax), a 25% lower area under the plasma concentration versus time curve (AUC), and a 35-minute increase in time to peak plasma concentration (Tmax) after ingestion of an 850 mg tablet of metformin taken with food, compared to the same dose administered during fasting. Though the extent of metformin absorption (measured by the area under the curve - AUC) from the metformin extended-release tablet is increased by about 50% when given with food, no effect of food on Cmax and Tmax of metformin is observed. High and low-fat meals exert similar effects on the pharmacokinetics of extended-release metformin. |
|---|---|
| Half-life | The plasma elimination half-life of metformin is 6.2 hours in the plasma.The elimination half-life in the blood is approximately 17.6 hours, suggesting that the erythrocyte mass may be a compartment of distribution. |
| Protein binding | Metformin is negligibly bound to plasma proteins. |
| Metabolism | Intravenous studies using a single dose of metformin in normal subjects show that metformin is excreted as unchanged drug in the urine and does not undergo hepatic metabolism (no metabolites have been identified in humans) or biliary excretion. |
| Route of elimination | This drug is substantially excreted by the kidney. Renal clearance of metformin is about 3.5 times higher than creatinine clearance, which shows that renal tubular secretion is the major route of metformin elimination. After oral administration, about 90% of absorbed metformin is eliminated by the kidneys within the first 24 hours post-ingestion. |
| Volume of distribution | The apparent volume of distribution (V/F) of metformin after one oral dose of metformin 850 mg averaged at 654 ± 358 L. |
| Clearance | Renal clearance is about 3.5 times greater than creatinine clearance, which indicates that tubular secretion is the major route of metformin elimination. Following oral administration, approximately 90% of the absorbed drug is eliminated via the renal route within the first 24 hours. |
Formulation & handling
- Oral small‑molecule biguanide suitable for conventional and extended‑release tablets; high dose load impacts tablet size and excipient selection.
- Highly hydrophilic (low LogP, moderate water solubility), enabling solution and suspension formulations but requiring attention to taste‑masking and osmolarity in liquids.
- Gastrointestinal irritation is food‑sensitive, so formulations often target controlled release or buffering to improve gastric tolerability.
Regulatory status
| Lifecycle | The product’s intellectual property has largely expired in Canada and parts of the United States, with remaining U.S. protection ending in 2027. Given availability across Canada, the US, and the EU, the market appears mature with increasing potential for generic competition as final U.S. patents expire. |
|---|
| Markets | Canada, US, EU |
|---|
Supply Chain
| Supply chain summary | Metformin’s supply landscape is dominated by numerous generic manufacturers, with the original branded presence historically linked to a small number of originator companies that first introduced metformin‑containing products. The drug is widely available in the US, EU, and Canada, supported by an extensive network of manufacturers and packagers. Core compound patents have long expired, and remaining patents relate mainly to specific formulations, indicating an established and mature generic market. |
|---|
Safety
| Toxicity | **Metformin (hydrochloride) toxicity data**: Oral LD50 (rat): 1 g/kg; Intraperitoneal LD50 (rat): 500 mg/kg; Subcutaneous LD50 (rat): 300 mg/kg; Oral LD50 (mouse): 1450 mg/kg; Intraperitoneal LD50 (mouse): 420 mg/kg; Subcutaneous LD50 (mouse): 225 mg/kg. **A note on lactic acidosis** Metformin decreases liver uptake of lactate, thereby increasing lactate blood levels which may increase the risk of lactic acidosis.There have been reported postmarketing cases of metformin-associated lactic acidosis, including some fatal cases. Such cases had a subtle onset and were accompanied by nonspecific symptoms including malaise, myalgias, abdominal pain, respiratory distress, or increased somnolence. In certain cases, hypotension and resistant bradyarrhythmias have occurred with severe lactic acidosis.Metformin-associated lactic acidosis was characterized by elevated blood lactate concentrations (>5 mmol/L), anion gap acidosis (without evidence of ketonuria or ketonemia), as well as an increased lactate:pyruvate ratio; metformin plasma levels were generally >5 mcg/mL. Risk factors for metformin-associated lactic acidosis include renal impairment, concomitant use of certain drugs (e.g. carbonic anhydrase inhibitors such as topiramate), age 65 years old or greater, having a radiological study with contrast, surgery and other procedures, hypoxic states (e.g., acute congestive heart failure), excessive alcohol intake, and hepatic impairment. **A note on renal function** In patients with decreased renal function, the plasma and blood half-life of metformin is prolonged and the renal clearance is decreased. Metformin should be avoided in those with severely compromised renal function (creatinine clearance < 30 ml/min), acute/decompensated heart failure, severe liver disease and for 48 hours after the use of iodinated contrast dyes due to the risk of lactic acidosis.Lower doses should be used in the elderly and those with decreased renal function. Metformin decreases fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Metformin may also have a positive effect on lipid levels. **A note on hypoglycemia** When used alone, metformin does not cause hypoglycemia, however, it may potentiate the hypoglycemic effects of sulfonylureas and insulin when they are used together. **Use in pregnancy** Available data from post-marketing studies have not indicated a clear association of metformin with major birth defects, miscarriage, or adverse maternal or fetal outcomes when metformin was ingested during pregnancy. Despite this, the abovementioned studies cannot definitively establish the absence of any metformin-associated risk due to methodological limitations, including small sample size and inconsistent study groups. **Use in nursing** A limited number of published studies indicate that metformin is present in human milk. There is insufficient information to confirm the effects of metformin on the nursing infant and no available data on the effects of metformin on the production of milk. The developmental and health benefits of breastfeeding should be considered as well as the mother’s clinical need for metformin and any possible adverse effects on the nursing child. |
|---|
- Acute toxicity is moderate, with reported LD50 values ranging from ~225 mg/kg (mouse, SC) to ~1 g/kg (rat, oral), indicating higher hazard potential with parenteral exposure
- Accumulation can elevate lactate levels
- Severe metformin‑associated lactic acidosis has been documented and is characterized by high lactate (›5 mmol/L), anion‑gap acidosis, and elevated metformin plasma concentrations
Metformin is a type of Biguanides
Biguanides are a subcategory of pharmaceutical Active Pharmaceutical Ingredients (APIs) that play a significant role in the treatment of various medical conditions. These organic compounds exhibit antihyperglycemic properties, making them particularly important in the management of diabetes mellitus type 2.
The primary biguanide compound utilized in pharmaceutical formulations is metformin. Metformin works by decreasing glucose production in the liver and improving insulin sensitivity in peripheral tissues. These mechanisms contribute to lower blood glucose levels and better glycemic control.
One of the key advantages of biguanides, particularly metformin, is their favorable safety profile. They are generally well-tolerated, with minimal risk of causing hypoglycemia compared to other antidiabetic medications. Biguanides also offer additional benefits such as cardiovascular protection and potential weight loss.
In addition to their role in diabetes management, biguanides are being investigated for their potential therapeutic applications in polycystic ovary syndrome (PCOS) and cancer treatment. Studies have shown promising results in reducing androgen levels and improving menstrual irregularities in PCOS patients. Furthermore, emerging research suggests that biguanides may have antineoplastic effects by targeting cancer cell metabolism and inhibiting tumor growth.
Overall, biguanides, with metformin being the most commonly prescribed, have become a cornerstone in the management of diabetes and are being explored for their potential in other medical conditions. Their favorable safety profile, efficacy in glycemic control, and additional health benefits make them an important class of pharmaceutical APIs in the modern healthcare landscape.
Metformin (Biguanides), classified under Anti-diabetics
Anti-diabetics, belonging to the pharmaceutical API (Active Pharmaceutical Ingredient) category, are a group of compounds designed to manage and treat diabetes mellitus, a chronic metabolic disorder characterized by high blood sugar levels. These medications play a vital role in controlling diabetes and preventing complications associated with the disease.
Anti-diabetics encompass a wide range of drug classes, including biguanides, sulfonylureas, thiazolidinediones, dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium-glucose cotransporter-2 (SGLT2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists. Each class works through different mechanisms to regulate blood sugar levels and improve insulin sensitivity.
Biguanides, such as metformin, reduce glucose production by the liver and enhance insulin sensitivity in peripheral tissues. Sulfonylureas, like glipizide, stimulate insulin secretion from pancreatic beta cells. Thiazolidinediones, including pioglitazone, improve insulin sensitivity in muscle and adipose tissues. DPP-4 inhibitors, such as sitagliptin, increase insulin release and inhibit glucagon secretion. SGLT2 inhibitors, like dapagliflozin, decrease renal glucose reabsorption, leading to increased urinary glucose excretion. GLP-1 receptor agonists, such as exenatide, enhance insulin secretion, suppress glucagon release, slow gastric emptying, and promote satiety.
These anti-diabetic APIs serve as the foundational ingredients for the formulation of various oral tablets, capsules, and injectable medications used in the treatment of diabetes. By targeting different aspects of glucose regulation, they help patients achieve and maintain optimal blood sugar levels, thus reducing the risk of diabetic complications, such as cardiovascular disease, neuropathy, and nephropathy.
It is crucial for healthcare professionals to prescribe and administer these anti-diabetic medications appropriately, considering factors like the patient's medical history, co-existing conditions, and potential drug interactions. Regular monitoring of blood glucose levels and close medical supervision are necessary to ensure effective diabetes management.
In conclusion, anti-diabetics form a critical category of pharmaceutical APIs used for the treatment of diabetes. These compounds, encompassing various drug classes, work through distinct mechanisms to regulate blood sugar levels and improve insulin sensitivity. By facilitating glucose control, anti-diabetic APIs help mitigate the risk of complications associated with diabetes mellitus, ultimately promoting better health outcomes for patients.
Metformin API manufacturers & distributors
Compare qualified Metformin API suppliers worldwide. We currently have 33 companies offering Metformin API, with manufacturing taking place in 7 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Aarambh Life Science | Producer | India | India | CoA, GMP | 19 products |
| Aastrid International | Producer | India | India | CEP, CoA | 1 products |
| Abhilash Chemicals | Producer | India | India | CEP, CoA, FDA, KDMF, WC | 1 products |
| Angels Pharma | Producer | India | India | CoA, WC | 2 products |
| Auro Laboratories | Producer | India | India | CEP, CoA, GMP, KDMF, USDMF, WC | 6 products |
| Aurora Industry Co., Ltd | Distributor | China | China | BSE/TSE, CEP, CoA, EDMF/ASMF, GMP, MSDS, USDMF | 250 products |
| AXXO GmbH | Distributor | Germany | World | CEP, CoA, GMP, GDP, MSDS, USDMF | 243 products |
| Blue Circle Organics | Producer | India | India | CEP, CoA, FDA | 2 products |
| Chr. Olesen Group | Distributor | Denmark | China | CEP, CoA, GMP, MSDS | 252 products |
| Danashmand | Producer | India | India | CoA, WC | 3 products |
| Duchefa Farma B.V. | Distributor | Netherlands | India | CoA, GMP, ISO9001, MSDS | 170 products |
| Exemed Pharma | Producer | India | India | CEP, CoA, FDA, GMP, KDMF, USDMF, WC | 1 products |
| G.C. Chemie Pharmie Ltd | Producer | India | India | CoA | 21 products |
| Gennex Laboratories | Producer | India | India | CoA | 1 products |
| Harman Finochem | Producer | India | India | CEP, CoA, FDA, GMP, JDMF, KDMF, USDMF, WC | 34 products |
| Ipca Labs. | Producer | India | India | CEP, CoA, FDA, GMP, KDMF, USDMF, WC | 69 products |
| Laurus Labs | Producer | India | India | CoA, GMP, USDMF, WC | 50 products |
| LGM Pharma | Distributor | United States | World | BSE/TSE, CEP, CoA, GMP, MSDS, USDMF | 441 products |
| Lupin | Producer | India | India | CoA, USDMF | 155 products |
| Rochem International, Inc... | Distributor | United States | United States | BSE/TSE, CEP, CoA, GMP, ISO9001, MSDS, USDMF | 144 products |
| Shandong Fangxing Technol... | Producer | China | China | CoA | 5 products |
| Shouguang Fukang | Producer | China | Unknown | CEP, CoA, FDA, JDMF, KDMF, USDMF, WC | 13 products |
| Sinoway industrial Co.,Lt... | Distributor | China | China | CEP, CoA, GMP, ISO9001, MSDS, USDMF | 762 products |
| Sun Pharma | Producer | India | India | CEP, CoA, KDMF, USDMF, WC | 219 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
| THINQ Pharma | Producer | India | India | CEP, CoA, FDA | 6 products |
| Tresinde Biotech | Producer | India | India | CoA, GMP | 50 products |
| Unnati Pharmaceuticals Pv... | Distributor | India | India | CoA | 70 products |
| USV | Producer | India | India | CEP, CoA, FDA, GMP, KDMF, USDMF, WC | 35 products |
| Veeprho Group | Producer | Czech Republic | Czech Republic | CoA | 138 products |
| Vistin Pharma | Producer | Norway | Norway | CEP, CoA, FDA, GMP, JDMF, KDMF, USDMF | 2 products |
| Wanbury | Producer | India | India | CEP, CoA, FDA, GMP, JDMF, KDMF, USDMF, WC | 15 products |
| Yantai Dongcheng Bio. | Producer | China | China | CoA, WC | 10 products |
When sending a request, specify which Metformin API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Metformin API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Metformin API
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Technical
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Regulatory
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