glibenclamide

Glibenclamide (Glyburide) is an antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.

Glibenclamide potassium, also known as Glyburide potassium, is a potassium salt form of Glibenclamide. It is available in both anhydrous and hydrate versions, exhibiting greater solubility than the pure Glibenclamide [1].

Glibenclamide (Standard) is the analytical reference standard of Glibenclamide intended for research and quantitative applications, and as an orally active ATP-sensitive potassium channel inhibitor, Glibenclamide directly binds SUR1 subunits of KATP channels, inhibits P-glycoprotein and CFTR, alters mitochondrial membrane ion permeability, induces autophagy, and supports research in diabetes, obesity, and cellular bioenergetics.

Iodoglibenclamide is a bioactive chemical.

NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide), an intermediate capable of synthesizing glibenclamide, exerts an inhibitory effect on the formation of NLRP3 inflammatory vesicles in cardiomyocytes, limiting infarct size after myocardial ischemia/reperfusion in mice and has no effect on metabolism.

Glibornuride, a blocker of ATP-sensitive K+ channels (pKi: 5.75), inhibits high-affinity [3H]-glibenclamide binding with potencies corresponding to its K+ channel activity.

ATB-429 is a mesalazine derivative capable of releasing H2S, demonstrating significant analgesic and anti-inflammatory effects in an irritable bowel syndrome (IBS) model. By releasing hydrogen sulfide (H2S), ATB-429 modulates hypersensitivity induced by colorectal distension in healthy and post-colitis rats. It alleviates abdominal withdrawal responses and inhibits spinal c-Fos mRNA expression, indicating its potential to relieve pain associated with gastrointestinal inflammation. Furthermore, ATB-429 downregulates mRNA expression of colonic cyclooxygenase-2 (COX-2) and IL-1β, an effect not observed with mesalazine alone. The mechanism involves ATP-sensitive K+ (KATP) channels, evidenced by the reversal of ATB-429's effects with glibenclamide. These findings suggest that ATB-429 may offer therapeutic benefits for treating inflammatory pain-related bowel conditions.

AZ-DF 265 is a hypoglycaemic drug which stimulates insulin release. AZ-DF-265 inhibits ATP-sensitive potassium channels and displaces [3H]-glibenclamide from the sulphonylurea receptor.

Glyburide-d3 is the deuterated form of Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor, utilized in the research of diabetes and obesity. It inhibits P-glycoprotein, directly binds to and blocks the SUR1 subunit of KATP, and suppresses the cystic fibrosis transmembrane conductance regulator (CFTR). Additionally, Glibenclamide interferes with mitochondrial bioenergetics by inducing membrane ion permeability and can induce autophagy.

Glyburide-d11 is a deuterated form of Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor used in the study of diabetes and obesity. It inhibits P-glycoprotein and directly binds to block the SUR1 subunit of KATP, also inhibiting cystic fibrosis transmembrane conductance regulator (CFTR). Glibenclamide interferes with mitochondrial bioenergetics by inducing membrane ion permeability and can induce autophagy.