D3822
Dipeptidyl Peptidase IV Inhibitor I
Synonym(s):
Diprotin A
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About This Item
Empirical Formula (Hill Notation):
C17H31N3O4
Molecular Weight:
341.45
UNSPSC Code:
12352202
NACRES:
NA.77
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General description
Dipeptidyl peptidase IV (DPP IV) is a member of the prolyl-specific proteases family. It is a dimeric type II integral membrane glycoprotein that is broadly expressed in the epithelial and nonepithelial tissues. It is majorly expressed in the kidney and the colon.
Application
Dipeptidyl peptidase IV inhibitor I has been used in acute in vivo studies to assess rapid plasma glucagon-like peptide (GLP-1) responses to specified secretory agents in mice.
Biochem/physiol Actions
Dipeptidyl peptidase IV (DPP IV) functions as a modulator of glucagon-like peptide (GLP-1), insulin-stimulating hormones, and glucose-dependent insulinotropic polypeptide (GIP). It is an essential therapeutic target for type 2 diabetes (T2DM). DPP-4 inhibitors are crucial for maintaining glucose homeostasis by prolonging the activity of GLP-1 and GIP. They also enhance glycemic control for a longer period when compared to early oral hypoglycemics. DPP-4 also acts as a binding protein and a ligand of extracellular factors.
Sequence
Ile-Pro-Ile
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Dipeptidyl peptidase 4 (DPP4) inhibitors, commonly known as gliptins, have been an integral part of the treatment of type 2 diabetes mellitus (T2DM) for several years. Despite their remarkable efficacy in lowering glucose levels and their compatibility with other hypoglycemic
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Dipeptidyl peptidase IV (DPP IV) is a key regulator of insulin-stimulating hormones, glucagon-like peptide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), thus it is a promising target for the treatment of Type 2 Diabetes mellitus (T2DM). Inhibition of plasma DPP IV
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Diabetes mellitus is an emerging predator and affecting around 422 million adults worldwide. Higher levels of circulating insulin and increased pressure on the pancreas to produce insulin have been inferred as possible etiology for diabetes leading to a higher risk
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