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PathWhiz ID Pathway Meta Data

PW127726

Pw127726 View Pathway
drug action

Tolazamide Action Pathway

Homo sapiens
Tolazamide is an hypoglycemic agent from the sulfonylurea class used in the treatment of non insulin dependent diabetes mellitus type II. Tolazamide lowers blood glucose by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. This drug binds to ATP-sensitive potassium-channel receptors on the pancreatic cell surface (known as the sulfonylurea receptor 1 (SUR1) subunit (Kir6.2)), reducing potassium conductance and causing depolarization of the membrane. This depolarization stimulates the calcium ion influx through voltage-sensitive calcium channels thus raising intracellular concentrations of calcium ions. The higher concentration of intracellular calcium ions induces the secretion (exocytosis) of insulin into the blood. Tolazamide is administered as an oral tablet.

PW144944

Pw144944 View Pathway
drug action

Tolazamide Drug Metabolism Action Pathway

Homo sapiens

PW176149

Pw176149 View Pathway
metabolic

Tolazamide Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Tolazamide are predicted with biotransformer.

PW132365

Pw132365 View Pathway
metabolic

Tolazoline Drug Metabolism

Homo sapiens
Tolazoline is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Tolazoline passes through the liver and is then excreted from the body mainly through the kidney.

PW144904

Pw144904 View Pathway
drug action

Tolazoline Drug Metabolism Action Pathway

Homo sapiens

PW127737

Pw127737 View Pathway
drug action

Tolbutamide Action Pathway

Homo sapiens
Tolbutamide is an oral antihyperglycemic agent from the sulfonylurea drug class. This drug is used to treat hyperglycemia in patients with type 2 diabetes mellitus (non-insulin-dependent diabetes mellitus (NIDDM)). It is structurally similar to acetohexamide, chlorpropamide, and tolazamide. Sulfonylureas lower blood glucose in patients with NIDDM by directly stimulating the acute release of insulin from beta cells of pancreatic islet tissue. Sulfonylureas inhibit the ATP-potassium channels by linking with the subunit called the ATP-binding cassette sub-family C member 8 on the beta cell membrane and potassium efflux. This binding results in the depolarization of the cell. In consequence, it causes an influx of calcium ions thus releasing the insulin-containing granules by exocytosis. This drug is also an inhibitor of the ATP-sensitive inward rectifier potassium channel 1 presents in the kidney. Its pharmacological action is still unknown. Tolbutamide is administered as an oral tablet.

PW145213

Pw145213 View Pathway
drug action

Tolbutamide Drug Metabolism Action Pathway

Homo sapiens

PW144450

Pw144450 View Pathway
drug action

Tolcapone Drug Metabolism Action Pathway

Homo sapiens

PW176238

Pw176238 View Pathway
metabolic

Tolcapone Predicted Metabolism Pathway

Homo sapiens
Metabolites of Tolcapone are predicted with biotransformer.

PW128149

Pw128149 View Pathway
drug action

Tolfenamic acid Action Pathway

Homo sapiens
Tolfenamic acid is a nonsteroidal anti-inflammatory agent (NSAID) used to treat pain associated with the acute attack of migraine in adults. This drug binds as an antagonist to both prostaglandin G/H synthase 1 and prostaglandin G/H synthase 2 in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 convert arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase, or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. The inhibition of both COX-1 and COX-2 by tolfenamic acid reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. This drug is administered as an oral tablet.