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PathWhiz ID Pathway Meta Data

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.

PW146040

Pw146040 View Pathway
drug action

Tolfenamic acid Drug Metabolism Action Pathway

Homo sapiens

PW176443

Pw176443 View Pathway
metabolic

Tolfenamic acid Predicted Metabolism Pathway

Homo sapiens
Metabolites of Tolfenamic acid are predicted with biotransformer.

PW122218

Pw122218 View Pathway
protein

Toll-Like Receptor Pathway 1

Rattus norvegicus
Toll-like receptors (TLRs) are part of the innate immune system. These receptors recognize pathogen-associated molecular patterns from different microbes. TLR2 recognizes a variety of PAMPs including lipoproteins, peptidoglycans, lipotechoic acids, and mannan. TLR3 recognizes viral double-stranded RNA, small interfering RNAsa, and self-RNAs. TLR4 recognizes lipopolysaccharides. TLR7 recognizes single-stranded RNA. TLR9 recognizes bacterial and viral DNA with unmethylated CpG-DNA motifs. TLRs are synthesized in the endoplasmic reticulum, moved to the Golgi, and then recruited to the cell surface or intracellular compartments. TLRs recruit adaptor molecules such as MYD88, TRIF, TIRAP, or TRAM leading to the activation of transcription factors NF-kappa-B causing innate immune responses. MYD88 is recruited by all TLRs. Adaptor TIRAP recruits MYD88 to cell surface TLRs, including TLR2 and TLR4. TLR signaling molecule IRAK1 activation activates TRAF6 causing the activation of IKK complex then NF-kappa-B and kinases. Activated TRAF6 promotes polyubiquination of TRAF6 and TAK1, TAB1, TAB2 complex. TAK1 activates pathways causing activation of IKK complex and NF-kappa-B and MAPK pathways. The IKK complex phosphorylates and activates IKK-beta. IKK complex also phosphorylates I-kappa-B-alpha allowing dissociation and translocation of NF-kappa-B to the nucleus resulting in proinflammatory gene expression. Activated TAK1 complex also activates p38 and JNK, regulating the activation of AP-1 transcription factors to regulate inflammatory responses. Many transmembrane molecules, such as glycophosphatidylinositol-anchored protein CD14, also regulate TLR signaling pathways.