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PathWhiz ID Pathway Meta Data

PW124427

Pw124427 View Pathway
metabolic

Vitamin K Metabolism 1610307792

Homo sapiens
Vitamin K describes a group of lipophilic, hydrophobic vitamins that exist naturally in two forms (and synthetically in three others): vitamin K1, which is found in plants, and vitamin K2, which is synthesized by bacteria. Vitamin K is an important dietary component because it is necessary as a cofacter in the activation of vitamin K dependent proteins. Metabolism of vitamin K occurs mainly in the liver. In the first step, vitamin K is reduced to its quinone form by a quinone reductase such as NAD(P)H dehydrogenase. Reduced vitamin K is the form required to convert vitamin K dependent protein precursors to their active states. It acts as a cofactor to the integral membrane enzyme vitamin K-dependent gamma-carboxylase (along with water and carbon dioxide as co-substrates), which carboxylates glutamyl residues to gamma-carboxy-glutamic acid residues on certain proteins, activating them. Each converted glutamyl residue produces a molecule of vitamin K epoxide, and certain proteins may have more than one residue requiring carboxylation. To complete the cycle, the vitamin K epoxide is returned to vitamin K via the vitamin K epoxide reductase enzyme, also an integral membrane protein. The vitamin K dependent proteins include a number of important coagulation factors, such as prothrombin. Thus, warfarin and other coumarin drugs act as anticoagulants by blocking vitamin K epoxide reductase.

PW124428

Pw124428 View Pathway
metabolic

Vitamin K Metabolism 1610307897

Homo sapiens
Vitamin K describes a group of lipophilic, hydrophobic vitamins that exist naturally in two forms (and synthetically in three others): vitamin K1, which is found in plants, and vitamin K2, which is synthesized by bacteria. Vitamin K is an important dietary component because it is necessary as a cofacter in the activation of vitamin K dependent proteins. Metabolism of vitamin K occurs mainly in the liver. In the first step, vitamin K is reduced to its quinone form by a quinone reductase such as NAD(P)H dehydrogenase. Reduced vitamin K is the form required to convert vitamin K dependent protein precursors to their active states. It acts as a cofactor to the integral membrane enzyme vitamin K-dependent gamma-carboxylase (along with water and carbon dioxide as co-substrates), which carboxylates glutamyl residues to gamma-carboxy-glutamic acid residues on certain proteins, activating them. Each converted glutamyl residue produces a molecule of vitamin K epoxide, and certain proteins may have more than one residue requiring carboxylation. To complete the cycle, the vitamin K epoxide is returned to vitamin K via the vitamin K epoxide reductase enzyme, also an integral membrane protein. The vitamin K dependent proteins include a number of important coagulation factors, such as prothrombin. Thus, warfarin and other coumarin drugs act as anticoagulants by blocking vitamin K epoxide reductase.

PW146428

Pw146428 View Pathway
drug action

Voclosporin Drug Metabolism Action Pathway

Homo sapiens

PW123615

Pw123615 View Pathway
metabolic

volatiles

Arabidopsis thaliana

PW130757

Pw130757 View Pathway
metabolic

Von Willebrand factor human Drug Metabolism

Homo sapiens

PW132564

Pw132564 View Pathway
metabolic

Vonoprazan Drug Metabolism

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

PW128158

Pw128158 View Pathway
drug action

Vorapaxar Action Pathway

Homo sapiens
Vorapaxar also known as Zontivity, is an inhibitor for platelet aggregation used to treat patients with a history of myocardial infarction or peripheral arterial disease to reduce the chance of thrombotic cardiovascular events. Vorapaxar inhibits protease-activated receptor 1 (PAR-1), which is a G protein-coupled receptor that is expressed on the platelet. Inhibition of PAR-1 prevents platelet aggregation and activation. Vorapaxar is administered orally and rapidly absorbs and travels through the bloodstream. It is metabolized to major metabolites M20 and M19 by CYP3A4 and CYP2J2. This is then eliminated primarily through feces and urine. Due to the anticoagulant and antiplatelet nature, herbs and supplements with similar activity should be avoided such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba. St.John's Wort should also be avoided as it induces CYP3A metabolism and will reduce the concentration of Vorapaxar. Caution should be exercised with grapefruit products, as coadministration with strong inhibitors should be avoided.

PW145927

Pw145927 View Pathway
drug action

Vorapaxar Drug Metabolism Action Pathway

Homo sapiens

PW126994

Pw126994 View Pathway
drug action

Voriconazole Action Pathway

Homo sapiens
Voriconazole is a triazole antifungal agent used to treat invasive fungal infections, generally seen in patients who are immunocompromised. It has an increased affinity to 14-alpha sterol demethylase, and therefore makes it useful against fluconazole-resistant fungal infections. It is taken orally and used to treat esophageal candidiasis, cadidemia, invasive pulmonary aspergillosis, and serious fungal infections caused by Scedosporium apiospermum and Fusarium spp. Voriconazole is effective against all Candida species (including those resistant to other antifungal drugs), Cryptococcus neoformans, Trichosporon beigelii, and Saccharomyces cerevisiae. Voriconazole inhibits and antagonizes the production of ergosterol by inhibiting Lanosterol 14-alpha demethylase. It has a higher affinity for Lanosterol 14-alpha demethylase than other antifungal agents. Lanosterol 14-alpha demethylase is the enzyme that catalyzes the synthesis of 4,4'-dimethyl cholesta-8,14,24-triene-3-beta-ol from lanosterol. With this enzyme inhibited ergosterol synthesis cannot occur which causes a significant low concentration of ergosterol in the fungal cell. Ergosterol is essential in maintaining membrane integrity in fungi. Without ergosterol, the fungus cell cannot synthesize membranes thereby increasing fluidity and preventing growth of new cells. With fungal growth limited, it allows the immune system to destroy the fungal cells.

PW144699

Pw144699 View Pathway
drug action

Voriconazole Drug Metabolism Action Pathway

Homo sapiens