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Results for "

Glyburide-d<sub>3</sub>

" in MedChemExpress (MCE) Product Catalog:

By Targets:	P-glycoprotein (1) Autophagy (1) CFTR (1) Mitochondrial Metabolism (1) Potassium Channel (1)
By Research Areas:	Metabolic Disease (1)

Targets Recommended: P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-15206S1

Glyburide-d3 Glyburide-d<sub>3sub>	Potassium Channel Mitochondrial Metabolism Autophagy CFTR P-glycoprotein	Metabolic Disease
Glyburide-d₃ is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].

Cat. No.	Product Name	Chemical Structure

HY-15206S1

Glyburide-d3
Glyburide-d₃ is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].

Glyburide-d3

Glyburide-d₃ is the deuterium labeled Glibenclamide. Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].

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Glyburide-d<sub>3</sub>

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