Glimepiride 1mg tablets
Requires a prescription from a doctor or prescriber
First introduced in 1995, glimepiride is a member of the second-generation sulfonylurea (SU) drug class used for the management of type 2 diabetes mellitus (T2DM) to improve glycemic control.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Glimepiride
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Glimepiride
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
31 branded products available
MHRA licensed products
View all licensed products for Glimepiride on the MHRA register
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
Glimepiride 1mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
2 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Glimepiride
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
5 to 8 hours
Mechanism
ATP-sensitive potassium channels on pancreatic beta cells that are gated by intracellular ATP and ADP.
Food interactions
2 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 hour
[A177703]…
Half-life
5 to 8 hours
[A177709]
Protein binding
99.5%
[L10319]
Volume of distribution
8.8 L
[L10319]
Metabolism
3-6 hours
Elimination
60%
Clearance
8 mg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Glimepiride works by stimulating the secretion of insulin granules from pancreatic islet beta cells by blocking ATP-sensitive potassium channels (KATP channels) and causing depolarization of the beta cells. Compared to [glipizide], another second SU drug, glimepiride has a longer duration of action. It is sometimes classified as a third-generation SU because it has larger substitutions than other second-generation SUs.[A177703] Compared to other SUs, glimepiride was associated with a lower risk of developing hypoglycemia and weight gain in clinical trials [A177709] as well as fewer cardiovascular effects than other SUs due to minimal effects on ischemic preconditioning of cardiac myocytes.[A177703] It is effective in reducing fasting plasma glucose, postprandial glucose, and glycosylated hemoglobin levels and is considered to be a useful, cost-effective treatment option for managing type 2 diabetes mellitus.[A177703] Glimepiride was approved by the Food and Drug Administration (FDA) in the United States in 1995 for the treatment of T2DM. It is commonly marketed under the brand name Amaryl as oral tablets and is typically administered once daily.
It may also be indicated for use in combination with metformin or insulin to lower blood glucose in patients with type 2 diabetes whose high blood sugar levels cannot be controlled by diet and exercise in conjunction with an oral hypoglycemic (a drug used to lower blood sugar levels) agent alone.
[L10322]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1077 interactions
Continued observation and additional carbohydrate intake may be necessary since hypoglycemia may recur after apparent clinical recovery.
[L10319]
In a study of rats given doses of up to 5000 parts per million (ppm) in complete feed for 30 months, there were no signs of carcinogenesis. Meanwhile, the administration of glimepiride at a dose much higher than the maximum human recommended dose for 24 months in mice resulted in an increase in benign pancreatic adenoma formation in a dose-related manner, which was thought to be the result of chronic pancreatic stimulation.
[L10319]
Glimepiride was non-mutagenic in in vitro and in vivo mutagenicity studies. In male and female rat studies, glimepiride was shown to have no effects on fertility.
[L10319]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A177703]
Following administration of a single oral dose of glimepiride in healthy subjects and with multiple oral doses with type 2 diabetes, the peak plasma concentrations (Cmax) were reached after 2 to 3 hours post-dose.
[L10319]
Accumulation does not occur after multiple doses.
[A177703]
When glimepiride was given with meals, the time to reach Cmax was increased by 12% while the mean and AUC (area under the curve) were decreased by 8 to 9%, respectively.
[L10322]
In a pharmacokinetic study of Japanese patients with T2DM, Cmax value in once-daily dose was higher than those in twice-daily doses.
[A177724]
The absolute bioavailability of glimepiride is reported to be complete following oral administration.
[A177721]
[A177709]
[L10319]
[L10319]
M1 retained approximately one third of the pharmacologic activity of its parent in an animal model, with a half-life of 3-6 hours.
[A177715]
However, whether the glucose-lowering effect of M1 is clinically significant is not clear.
[L10319]
Approximately 40% of the total radioactivity was recovered in feces where M1 and M2 accounted for about 70% of the radioactivity and a ratio of M1 to M2 being 1:3. No parent drug was recovered from urine or feces.
[L10319]
[L10322]
Following intravenous dosing in healthy subjects, the total body clearance was 47.8 mL/min.
[L10319]
Proteins and enzymes this drug interacts with in the body
PMID:29286281 PMID:34815345
Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium.
Can be blocked by extracellular barium (By similarity). In pancreatic cells, it forms KATP channels with ABCC8/SUR1 .
PMID:29286281 PMID:34815345
Can form cardiac and smooth muscle-type KATP channels with ABCC9
This channel is activated by internal ATP and can be blocked by external barium. In the kidney, probably plays a major role in potassium homeostasis
PMID:9831708
Can form a sulfonylurea-sensitive but ATP-insensitive potassium channel with KCNJ8 (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
ATC A10BD04
ATC A10BB12
ATC A10BD06
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Glimepiride
Additional database identifiers
Drugs Product Database (DPD)
12597
ChemSpider
16740595
BindingDB
50237590
ZINC
ZINC000100070954
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6257
GenAtlas
KCNJ11
GeneCards
KCNJ11
GenBank Gene Database
D50582
GenBank Protein Database
1088445
UniProt Accession
KCJ11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6255
GenAtlas
KCNJ1
GeneCards
KCNJ1
GenBank Gene Database
U12541
GenBank Protein Database
529313
Guide to Pharmacology
429
UniProt Accession
KCNJ1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:59
GenAtlas
ABCC8
GeneCards
ABCC8
GenBank Gene Database
L78243
GenBank Protein Database
1374919
Guide to Pharmacology
2594
UniProt Accession
ABCC8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:60
GenAtlas
ABCC9
GeneCards
ABCC9
GenBank Gene Database
AF061323
GenBank Protein Database
3127176
Guide to Pharmacology
2746
UniProt Accession
ABCC9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:42
GenAtlas
ABCB11
GeneCards
ABCB11
GenBank Gene Database
AF091582
GenBank Protein Database
3873243
Guide to Pharmacology
778
UniProt Accession
ABCBB_HUMAN
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
2 active patents, 6 expired
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: