Vildagliptin: Difference between revisions
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<applet load="" size="480" color="" frame="true" spin="on" Scene ="Vildagliptin/Vilda/ | <applet load="" size="480" color="" frame="true" spin="on" Scene ="Vildagliptin/Vilda/3" align="right" caption="Vildagliptin, better known as Galvus"/> | ||
===Better Known as: Galvus=== | ===Better Known as: Galvus=== | ||
* Marketed by: Novartis | * Marketed by: Novartis | ||
* Major Indication: | * Major Indication: [[Hyperglycemia & Type II Diabetes]] | ||
* Drug Class: | * Drug Class: Dipeptidyl Peptidase-4 (DPP-4) Inhibitor | ||
* Date of | * Date of EMA Approval: 2008 | ||
* 2009 Sales: | * 2009 Sales: N/A | ||
* Importance: | * Importance: Part of a new generation of DPP-4 Inhibitors. Was not approved by the FDA due to concerns over kidney impairment associated with the drug. It was however approved by the European Medicines Agency for use within the EU. Increasing evidence exists that all DPP-4 inhibitors can to certain malignant cancers.<ref>PMID:15735018</ref> | ||
* See [[Pharmaceutical Drugs]] for more information about other drugs and diseases. | * See [[Pharmaceutical Drugs]] for more information about other drugs and diseases. | ||
===Mechanism of Action=== | ===Mechanism of Action=== | ||
Dipeptidyl Peptidase-4 (DPP-4) is an antigenic membrane serine exopeptidase that cleaves proline dipeptides form the N-terminal end of protein substrates. DPP-4 plays a major role in [[Carbohydrate Metabolism|glucose metabolism]] as it is responsible for the degradation of incretins, most notably Glucagon-like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIp). Incretins are a group of gastrointestinal hormones that stimulate insulin biosynthesis and inhibit glucagon secretion after consuming high glucose meals. Since [[Diabetes]] is typically caused by a deficiency in [[insulin]] secretion or by increased hepatic glucose production, preventing incretin degradation is a viable treatment for diabetics. Vildagliptin is a competitive inhibitor of DPP-4. By inhibiting DPP-4 and subsequently preventing the enzymatic degradation of GLP-1 and GIP, these incretins are able to potentiate the secretion of insulin and suppress the release of glucagon by the pancreas, resulting in controlled blood-glucose levels.<ref>PMID:17073841</ref> Although no crystal structure of Vildagliptin bound DPP-4 has been solved, it is believed to bind in a similar fashion to [[Sitagliptin]] and [[Saxagliptin]] | Dipeptidyl Peptidase-4 (DPP-4) is an antigenic membrane serine exopeptidase that cleaves proline dipeptides form the N-terminal end of protein substrates. DPP-4 plays a major role in [[Carbohydrate Metabolism|glucose metabolism]] as it is responsible for the degradation of incretins, most notably Glucagon-like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIp). Incretins are a group of gastrointestinal hormones that stimulate insulin biosynthesis and inhibit glucagon secretion after consuming high glucose meals. Since [[Diabetes]] is typically caused by a deficiency in [[insulin]] secretion or by increased hepatic glucose production, preventing incretin degradation is a viable treatment for diabetics. Vildagliptin is a competitive inhibitor of DPP-4. By inhibiting DPP-4 and subsequently preventing the enzymatic degradation of GLP-1 and GIP, these incretins are able to potentiate the secretion of insulin and suppress the release of glucagon by the pancreas, resulting in controlled blood-glucose levels.<ref>PMID:17073841</ref> Although no crystal structure of Vildagliptin bound DPP-4 has been solved, it is believed to bind in a similar fashion to [[Sitagliptin]] and [[Saxagliptin]]. | ||
===Pharmacokinetics=== | ===Pharmacokinetics=== | ||