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Pathways

PathWhiz ID Pathway Meta Data

PW176518

Pw176518 View Pathway
metabolic

Torasemide Predicted Metabolism Pathway

Homo sapiens
Metabolites of Torasemide are predicted with biotransformer.

PW144657

Pw144657 View Pathway
drug action

Toremifene Drug Metabolism Action Pathway

Homo sapiens

PW000338

Pw000338 View Pathway
drug action

Torsemide Action Pathway

Homo sapiens
Torsemide, also known as torasemide is a pharmacologically-active small molecule that belongs to the drug class of loop diuretics. It is commonly used to manage hypertension and edema in cases of congestive heart failure as it acts as a diuretic by blocking sodium transporters NKCC2 on the thick ascending limb of the Loop of Henle in the renal tissues. Specifically it acts on solute carrier family 12 member 1. This prevents the reuptake of sodium into the Loop of Henle which consequentially reduces the uptake of water and serves to both increase water loss and reduce blood pressure. Torsemide appears to reduce blood pressure beyond its action in reducing salt uptake in the Loop of Henle; it also seems to be involved in reducing vasoconstriction by blocking the action of angiotensin II.

PW122253

Pw122253 View Pathway
metabolic

TPN B biosynthesis

Bacteria
Terpenoids, also known as isoprenoids, are a large class of natural products consisting of isoprene (C5) units. There are two biosynthetic pathways, the mevalonate pathway and the non-mevalonate pathway or the MEP/DOXP pathway, for the terpenoid building blocks: isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP). The action of prenyltransferases then generates higher-order building blocks: geranyl diphosphate (GPP), farsenyl diphosphate (FPP), and geranylgeranyl diphosphate (GGPP), which are the precursors of monoterpenoids (C10), sesquiterpenoids (C15), and diterpenoids (C20), respectively. Condensation of these building blocks gives rise to the precursors of sterols (C30) and carotenoids (C40). The MEP/DOXP pathway is absent in higher animals and fungi, but in green plants, the MEP/DOXP and mevalonate pathways co-exist in separate cellular compartments. The MEP/DOXP pathway, operating in the plastids, is responsible for the formation of essential oil monoterpenes and linalyl acetate, some sesquiterpenes, diterpenes, and carotenoids and phytol. However, the mevalonate pathway is absent in this organism.

PW112895

Pw112895 View Pathway
signaling

TPO Signaling Pathway

Homo sapiens
Thrombopoietin (TPO) is the cytokine that is chiefly responsible for megakaryocyte production but increasingly attention has turned to its role in maintaining hematopoietic stem cells (HSCs). HSCs are required to initiate the production of all mature hematopoietic cells, but this differentiation needs to be balanced against self-renewal and quiescence to maintain the stem cell pool throughout life. TPO has been shown to support HSC quiescence during adult hematopoiesis, with the loss of TPO signaling associated with bone marrow failure and thrombocytopenia. The binding of TPO to its receptor, c-Mpl, promotes the phosphorylation of cytoplasmic signaling proteins and activation of a number of cascades that control cellular proliferation, megakaryocyte development, and survival. Suppressors of cytokine signaling (SOCS), phosphatases, and other proteins, such as focal adhesion kinase and members of the Src family kinases can suppress TPO signaling.

PW128216

Pw128216 View Pathway
drug action

Trabectedin Action Pathway

Homo sapiens
Trabectedin is an antineoplastic from the alkylating agent drug class. It is derived from a marine-derived antitumor molecule discovered in the Caribbean tunicate Ecteinascidia turbinata. This drug is indicated in the treatment of advanced soft tissue sarcoma (liposarcoma or leiomyosarcoma) in Europe, Russia, and South Korea. It is also approved as an orphan drug by the FDA for the treatment of soft tissue sarcomas and ovarian cancer. Trabectedin binds covalently to the DNA minor groove. This molecule binds and alkylates guanine bases to the N2 position with its two rings in its structure, causing the equivalent of a functional interstrand crosslink. The third ring protrudes from the DNA strand which lets it interact with nearby nuclear proteins. It affects various transcription factors involved in cell proliferation via the transcription-coupled nucleotide excision repair system (NER). With this mechanism of action, trabectedin blocks the cell cycle at the G2 phase, resulting in the apoptosis of the cancerous cell, This drug is administered as an intravenous injection.

PW145629

Pw145629 View Pathway
drug action

Trabectedin Drug Metabolism Action Pathway

Homo sapiens

PW000648

Pw000648 View Pathway
drug action

Tramadol Action Action Pathway

Homo sapiens
Tramadol is an analgesic drug consisting of two enantiomer forms (+)-Tramadol and (-)-Tramadol. Both contribute to pain relief by inhibiting pain transmission in the spinal cord via different mechanisms. (+)-Tramadol is a selective agonist of the mu receptor (OP3) inhibiting serotonin reuptake, while (-)-Tramadol inhibits norepinephrine reuptake in the central nervous system. Although tramadol is structurally related to codeine and morphine, it’s affinity for the mu receptor compared to other opioids is significantly less. Therefore tramadol is used when treatment with strong opioids is not necessary since it’s pharmacodynamic and pharmacokinetic properties suggest the low likelihood of patients becoming dependent.

PW144324

Pw144324 View Pathway
drug action

Tramadol Drug Metabolism Action Pathway

Homo sapiens

PW000613

Pw000613 View Pathway
drug metabolism

Tramadol Metabolism Pathway

Homo sapiens
Tramadol (also named Ultram) is a class of opioid pain medication that used for treating pain. Metabolism of tramadol mainly happened in liver cell. The N-demethylation of tramadol is catalyzed by the cytochrome CYP3A4 and CYP2B6 to form N-Desmethyltramadol, which further metabolized to N,N-Didesmethyltramadol through CYP3A4 and CYP2B6 and to N,O-Didesmethyltramadol through CYP2D6. The O-demethylation of tramadol is catalyzed by the cytochrome CYP2D6 to form O-Desmethyltramadol, which further metabolized to O-Desmethyltramadol glucuronide through UDP-glucuronosyltransferase 2B7 and UDP-glucuronosyltransferase 1-8. O-Desmethyltramadol can also be metabolized to N,O-Didesmethyltramadol through CYP2D6.