GLPBio

Glimepiride

Catalog No.: GC10104Purity:>98.00%Synonyms: HOE 490
COASDSData Sheet
Glimepiride is a second-generation sulfonylurea that stimulates pancreatic β cells to release insulin. Glimepiride is used for the treatment of type 2 diabetes mellitu as monotherapy as well as in combination with metformin or insulin.

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Glimepiride
Cas No.: 93479-97-1
10mM (in 1mL DMSO)In Stock
$39.00
1
500mgIn Stock
$35.00
1
1gIn Stock
$59.00
1
5gIn Stock
$200.00
1
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Description

Glimepiride is a second-generation sulfonylurea that stimulates pancreatic β cells to release insulin. Glimepiride is used for the treatment of type 2 diabetes mellitu as monotherapy as well as in combination with metformin or insulin[1].

In vitro, Glimepiride (0, 0.3, 0.6, 1.2, 2.5 and 5μM; 1h) stimulated the release of CD14 from RAW 264 cells[2]. Glimepiride (10μM; 1, 4 and 7 days) induced the proliferation and differentiation of rat osteoblasts in a high glucose microenvironment[3]. Glimepiride (10µM; 30min) induces NO production by HCAECs[4].

In vivo, Glimepiride (1, 2 or 4mg/kg; 4 days; p.o.) prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced dopamine neurons degeneration through attenuation of glia activation and oxidative stress in mice[5]. Glimepiride (4mg/kg; 3 weeks; i.p.) ameliorates renal toxicity induced by cadmium in mice[6].

References:
[1] Basit A, Riaz M, Fawwad A. Glimepiride: evidence-based facts, trends, and observations (GIFTS). [corrected]. Vasc Health Risk Manag. 2012;8:463-72.
[2] Ingham V, Williams A, Bate C. Glimepiride reduces CD14 expression and cytokine secretion from macrophages. J Neuroinflammation. 2014 Jun 21;11:115.
[3] Ma P, Gu B, Xiong W, Tan B, Geng W, Li J, Liu H. Glimepiride promotes osteogenic differentiation in rat osteoblasts via the PI3K/Akt/eNOS pathway in a high glucose microenvironment. PLoS One. 2014 Nov 12;9(11):e112243.
[4] Ueba H, Kuroki M, Hashimoto S, Umemoto T, Yasu T, Ishikawa SE, Saito M, Kawakami M. Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway. Atherosclerosis. 2005 Nov;183(1):35-9.
[5] Oduola-Akande MD, Ishola IO, Olubodun-Obadun TG, Akande AJ, Adeyemi OO. Glimepiride Prevents 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Induced Dopamine Neurons Degeneration Through Attenuation of Glia Activation and Oxidative Stress in Mice. Neurotox Res. 2023 Jun;41(3):212-223.
[6] ElMahdy MK, Zaki MO, Al-Karmalawy AA, Abdo W, Alnasser SM, Antar SA. Glimepiride ameliorates renal toxicity induced by cadmium in mice: Modulation of Jun N terminal kinase (JNK)/nuclear factor kappa B (NF-κB) and phosphatidylinositol 3-kinases (PI3K)/protein kinase (AKT) pathways. Life Sci. 2022 Dec 15;311(Pt B):121184.

Protocol

Cell experiment [1]:

Cell lines

HCAECs

Preparation Method

HCAECs were incubated with 10µM Glimepiride, HGF (positive control) or vehicle in Krebs’ buffer (118mM NaCl, 4.7mM KCl, 2.5mM CaCl₂, 1.2mM MgSO₄, 1.2mM KH₂PO₄, 11mM glucose, 25mM NaHCO₃, 20mM HEPES, pH 7.4) pre-warmed to 37°C; after 30min the supernatant was collected from the dishes and kept at 4°C. The released nitric oxide (NO) was quantified within 24h of each collection using a NOx-analyzing HPLC system.

Reaction Conditions

10µM; 30min

Applications

Glimepiride induces NO production by HCAECs.

Animal experiment [2]:

Animal models

20 to 25g mice

Preparation Method

During the experimental period, animals had ad libitum access to food and water; they were divided into four groups: Group 1 received saline as the normal control, Group 2 received intraperitoneal CdCl₂ (6.5mg/kg) for seven consecutive days as the CdCl₂ control, Group 3 received Glimepiride (4mg/kg; i.p.), and Group 4 was co-treated with CdCl₂ plus Glimepiride, with Glimepiride continued for 3 weeks. Twenty-four hours after the last dose, mice were anaesthetized with thiopental sodium (50mg/kg) and euthanized; blood collected via cardiac puncture into dry Eppendorf tubes was allowed to clot for 30min and then centrifuged at 2000g for 15min, and the serum was stored at -20°C for biochemical assays; both kidneys were excised—one fixed in 10% paraformaldehyde for histopathology and the other snap-frozen at -80°C for ELISA.

Dosage form

4mg/kg; 3 weeks; i.p.

Applications

Glimepiride ameliorates renal toxicity induced by cadmium in mice.

References:
[1] Ueba H, Kuroki M, Hashimoto S, Umemoto T, Yasu T, Ishikawa SE, Saito M, Kawakami M. Glimepiride induces nitric oxide production in human coronary artery endothelial cells via a PI3-kinase-Akt dependent pathway. Atherosclerosis. 2005 Nov;183(1):35-9.
[2] ElMahdy MK, Zaki MO, Al-Karmalawy AA, Abdo W, Alnasser SM, Antar SA. Glimepiride ameliorates renal toxicity induced by cadmium in mice: Modulation of Jun N terminal kinase (JNK)/nuclear factor kappa B (NF-κB) and phosphatidylinositol 3-kinases (PI3K)/protein kinase (AKT) pathways. Life Sci. 2022 Dec 15;311(Pt B):121184.

Product Documents

Purity:>98.00%Appearance:A solid
COASDSData Sheet

Chemical Properties

CAS No.
93479-97-1
Synonyms
HOE 490
Chemical Name
4-ethyl-3-methyl-N-[2-[4-[(4-methylcyclohexyl)carbamoylsulfamoyl]phenyl]ethyl]-5-oxo-2H-pyrrole-1-carboxamide
SMILES
CCC1=C(CN(C1=O)C(=O)NCCC2=CC=C(C=C2)S(=O)(=O)NC(=O)NC3CCC(CC3)C)C
Molecular Formula
C24H34N4O3S
Molecular Weight
490.62
Solubility
≥ 21.45 mg/mL in DMSO
Storage
Store at -20°C,dry,protect from light
General tips
Select a suitable solvent according to the product solubility data. Once prepared, aliquot the stock solution to avoid repeated freeze-thaw cycles.
Use stock solutions within 6 months when stored at -80°C or within 1 month when stored at -20°C.
To improve solubility, warm the tube to 37°C and sonicate it for an appropriate period.
Shipping Condition
Evaluation samples are shipped with blue ice. Other available sizes are shipped at room temperature or with blue ice upon request.

CalculatorsMolarity / Dilution / Molecular Weight / Unit Conversion / In Vivo Formulation / Solubility

g/mol

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