Loader

Pathways

PathWhiz ID Pathway Meta Data

PW132221

Pw132221 View Pathway
metabolic

Valproate bismuth Drug Metabolism

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

PW146698

Pw146698 View Pathway
drug action

Valproate bismuth Drug Metabolism Action Pathway

Homo sapiens

PW124228

Pw124228 View Pathway
drug action

Valproate w/ Template (New) Drug Action Action Pathway

Homo sapiens

PW124164

Pw124164 View Pathway
drug action

Valproic Acid (Drug Action) - New - DISCARD

Homo sapiens

PW144440

Pw144440 View Pathway
drug action

Valproic acid Drug Metabolism Action Pathway

Homo sapiens

PW124475

Pw124475 View Pathway
drug action

Valproic Acid i.e. Sodium Valproate (New: Drug Action)

Homo sapiens
Sodium valproate, also known as valproic acid, is a fatty acid derivative and anticonvulsant first synthesized in 1881-1882 from an analogue derived from the Valerian herb; however, its mechanism of action is not fully elucidated (yet). Traditionally, researchers and clinicians consider it to be an anticonvulsant due to its effects in the brain: it blocks voltage-gated sodium channels and potentiates gamma-aminobutyric acid (GABA) activity. Over the past centuries, investigations show valproate may also have neuroprotective, anti-manic, and anti-migraine effects. It is a compound of interest in the field of oncology for its anti-proliferative effects and has undergone some clinical trials. Currently, valproate is indicated for use as a monotherapy or adjunct medication in seizure management, for migraine prophylaxis, and for mitigation of acute mania associated with bipolar disorder. Off-label, clinicians may use valproate to manage bipolar disorder or for emergency treatment of status epilepticus. Valproate can be administered orally, in which case it undergoes hepatic first-pass metabolism to enter the bloodstream ___________________ https://go.drugbank.com/drugs/DB00313

PW000611

Pw000611 View Pathway
drug metabolism

Valproic Acid Metabolism Pathway

Homo sapiens
Valproic acid (VPA) is metabolized almost entirely in the liver, via at least there routes: glucuronidation, beta oxidation in the mitochondria, and cytochrome P450 mediated oxidation. The glucuronidation of VPA is mediated by UGT1A3, UGT1A4, UGT1A6, UGT1A8, UGT1A9, UGT1A10, UGT2B7 and UGT2B15. The key CYP-mediated reaction of the VPA metabolic pathway is the generation of 4-ene-VPA by CYP2C9, CYP2A6 and CYP2B6. These three enzymes also catalyze the formation of 4-OH-VPA and 5-OH-VPA. Moreover, CYP2A6 mediates the oxidation of VPA to 3-OH-VPA. Inside the mitochondria, the first step of oxidation is the formation of (VPA-CoA) catalyzed by medium-chain acyl-CoA synthase, followed by the conversion to 2-ene-VPA-CoA through 2-methyl-branched chain acyl-CoA dehydrogenase (ACADSB). 2-ene-VPA-CoA is further converted to 3-hydroxyl-valproyl-VPA (3-OH-VPA-CoA) by an enoyl-CoA hydratase, crotonase (ECSH1) and then 3-OH-VPA-CoA is metabolized to 3-keto-valproyl-CoA (3-oxo-VPA-CoA) through the action of 2-methyl-3-hydroxybutyryl-CoA dehydrogenase. Another route of VPA metabolism in the mitochondria includes the conversion of 4-ene-VPA to 4-ene-VPA-CoA ester catalyzed by ACADSB, followed by a beta-oxidation to form 2,4-diene-VPA-CoA ester. The latter metabolite can furthermore be conjugated to glutathione to form thiol metabolites.

PW127712

Pw127712 View Pathway
drug action

Valrubicin Action Pathway

Homo sapiens
Valrubicin (N-trifluoroacetyladriamycin-14-valerate), also known as Valstar, is a chemotherapy drug from the anthracycline class. It is a semisynthetic analog of doxorubicin. Valrubicin has a more rapid uptake in the tumors than doxorubicin. Moreover, it does not have the preferential negative ion binding in cell membranes thought to be the cause for the cardiac toxicity of doxorubicin. This drug is used to treat BCG-resistant bladder carcinoma and is administered directly in the bladder (intravesical). Valrubicin affects a variety of interrelated biological functions, mostly the one involving the nucleic acid metabolism. It does DNA intercalation, then, it inhibits the incorporation of nucleosides into nucleic acids, causes extensive chromosomal damage, and arrests the cell cycle in the G2 phase. A principal mechanism of its action, mediated by valrubicin metabolites, is interference with the normal DNA breaking-resealing action of DNA topoisomerase II. This drug inhibits the DNA topoisomerase by binding to its 2-alpha part. This action cause DNA strand breaks, partial unwinding/uncoiling of DNA, and inhibition of DNA and RNA synthesis. DNA damage leads to programmed cell death (apoptosis) of the cancer cells, preventing the growth and proliferation of cancer in patients.

PW144511

Pw144511 View Pathway
drug action

Valrubicin Drug Metabolism Action Pathway

Homo sapiens

PW124603

Pw124603 View Pathway
metabolic

Valsartan

Homo sapiens
Valsartan undergoes minimal liver metabolism and is not biotransformed to a high degree, as only approximately 20% of a single dose is recovered as metabolites. The primary metabolite, accounting for about 9% of dose, is valeryl 4-hydroxy valsartan. In vitro metabolism studies involving recombinant CYP 450 enzymes indicated that the CYP 2C9 isoenzyme is responsible for the formation of valeryl-4-hydroxy valsartan. Valsartan does not inhibit CYP 450 isozymes at clinically relevant concentrations. CYP 450 mediated drug interaction between valsartan and coadministered drugs are unlikely because of the low extent of metabolism. (DrugBank)