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 standard substance of Glibenclamide, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Glibenclamide (Glyburide) is an antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.

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.