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Every lot is tried & tested in a relevant biological assay.
Our Bioassay
- Babes, A. et al. (2013) Eur. J. Pharmacol. 704, 15.
Alomone Labs Glibenclamide activates TRPA1 channels expressed in HEK-293 cells.Dose-response curve for the activation of human TRPA1 expressing HEK-293 cells loaded with Calcium 5 dye for changes in intracellular Ca2+ measurements. Calcium signal was apparent with 50 and 100 µM Glibenclamide (#G-150).
- Babes, A. et al. (2013) Eur. J. Pharmacol. 704, 15.
- Caffes, N. et al. (2015) Int. J. Mol. Sci. 16, 4973.
- Kimber-Trojnar, Z. et al. (2008) Pharmacol. Rep. 60, 308.
- Khanna, A. et al. (2014) Neurosurg. Focus 36, 11.
- Simard, J.M. et al. (2014) Neurocrit. Care 20, 319.
Glibenclamide is a member of the sulfonylurea class of drugs, an anti-diabetic that inhibits KATP channels in pancreatic β-cells, leading to increased insulin release. Sulfonylurea drugs work by inhibiting sulfonylurea receptor 1 (SUR1). In addition, this drug acts as aTRPA1 agonist and demonstrates pleiotropic protective effects in acute CNS injury. Glibenclamide activates human TRPA1 in a concentration range that is commonly used to inhibit KATP channels in vitro. It has an EC50 value isof 48 nM at pH 7.45.
Glibenclamide exhibits adverse effects such as abdominal pain, gastrointestinal disturbances and nocturia1,2. It is a weak acid, lipid soluble, with an oral clearance ranging from 11.2 to 230 l/h, with an elimination half-life estimated at about 4 h3.
Promising preclinical results suggest that glibenclamide significantly reduces cerebral edema and lowers the rate of hemorrhagic conversion following ischemic stroke. In non-lethal models, glibenclamide reduces brain swelling and infarct volume and improves neurological function. In lethal models of malignant cerebral edema, glibenclamide reduces edema, brain swelling, and mortality3,4.
Glibenclamide (#G-150) is a highly pure, synthetic, and biologically active compound.
