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PathWhiz ID Pathway Meta Data

PW128037

Pw128037 View Pathway
drug action

Rivaroxaban Action Pathway

Homo sapiens
Rivaroxaban is an anticoagulant that inhibits coagulation factor X, typically used to treat deep vein thrombosis (DVT) and pulmonary embolism (PE). Rivaroxaban is indicated for patients at high risk of DVT, PE and any other recurrent thrombotic events. Rivaroxaban is also indicated, in combination with aspirin, for reducing the risk of major cardiovascular events in patients with chronic coronary artery disease or peripheral artery disease. Rivaroxaban competitively inhibits free and clot-bound factor X. Coagulation factor X makes up a part of the prothrombinase complex that is responsible for the conversion of prothrombin to thrombin. Thrombin is a serine protease that is required to activate fibrinogen to fibrin, which creates the loose meshwork that eventually forms into a blood clot. Patients should avoid herbs and supplements with anticoagulant activity such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba. In addition, St. John's Wort should also be avoided as it will decrease blood concentration levels of rivaroxaban.

PW132486

Pw132486 View Pathway
metabolic

Rivaroxaban Drug Metabolism

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

PW145688

Pw145688 View Pathway
drug action

Rivaroxaban Drug Metabolism Action Pathway

Homo sapiens

PW128009

Pw128009 View Pathway
drug action

Rivastigmine Action Pathway

Homo sapiens
Rivastigmine is a cholinesterase inhibitor used in the treatment of symptoms of dementia in Alzheimer's and Parkinson's. The drug reversible binds to and inhibits acetylcholinesterase and cholinesterase which stops the breakdown of acetylcholine which increases the concentration in the synaptic cleft. It is metabolized by the enzymes it inhibits and forms the metabolite NAP226-90.

PW128292

Pw128292 View Pathway
drug action

Rivastigmine Action Pathway (new)

Homo sapiens
Rivastigmine is a cholinesterase inhibitor used in the treatment of symptoms of dementia in Alzheimer's and Parkinson's. The drug reversible binds to and inhibits acetylcholinesterase and cholinesterase which stops the breakdown of acetylcholine which increases the concentration in the synaptic cleft. It is metabolized by the enzymes it inhibits and forms the metabolite NAP226-90.

PW145087

Pw145087 View Pathway
drug action

Rivastigmine Drug Metabolism Action Pathway

Homo sapiens

PW176230

Pw176230 View Pathway
metabolic

Rivastigmine Predicted Metabolism Pathway

Homo sapiens
Metabolites of Rivastigmine are predicted with biotransformer.

PW145052

Pw145052 View Pathway
drug action

Rizatriptan Drug Metabolism Action Pathway

Homo sapiens

PW128616

Pw128616 View Pathway
drug action

Rizatriptan Mechanism of Action Action Pathway

Homo sapiens
Rizatriptan is a triptan used to treat migraines with or without aura. Rizatriptan is a second-generation triptan and a selective 5-HT1B and 5-HT1D receptor agonist. Rizatriptan is not indicated for the prophylactic therapy of migraine nor the treatment of cluster headache. Rizatriptan has a weak affinity for other 5-HT1 receptor subtypes (5-HT1A, 5-HT1E, 5-HT1F) and the 5-HT7 receptor but has no significant activity at 5-HT2, 5-HT3, alpha- and beta-adrenergic, dopaminergic, histaminergic, muscarinic or benzodiazepine receptors. Rizatriptan is a selective agonist at the 5-HT1B and 5-HT1D receptors on intracranial blood vessels and sensory nerves of the trigeminal system. It binds to these receptors with high affinity. The exact mechanism of action of rizatriptan has not been fully elucidated; however, several documented pharmacological actions of rizatriptan may contribute to its antimigraine effects. Rizatriptan causes vasoconstriction of intracranial extracerebral blood vessels, which is thought to occur primarily via 5-HT1B receptors. Rizatriptan also inhibits nociceptive neurotransmission in trigeminal pain pathways. It attenuates the release of vasoactive neuropeptides by the trigeminal nerve, which is thought to occur via neurogenic and central 5-HT1D receptors. Rizatriptan inhibited neurogenic dural vasodilation and plasma protein extravasation in animal studies.

PW123685

Pw123685 View Pathway
metabolic

RL Test

Pseudomonas aeruginosa
Rhamnolipids (RL) consist of a fatty acyl moiety composed of a 3-(3-hydroxyalkanoyloxy)alkaloid acid (HAA) and a sugar moiety composed of one or two rhamnose sugars. Rhamnolipids function as surfactants and virulence factors and are involved in biofilm formation and cell motility. The rhamnose sugar component is produced via the dTDP-L-rhamnose biosynthetic pathway which forms dTDP-L-rhamnose from glucose 6-phosphate (G6P) in five steps. First, glucose 6-phosphate is converted into glucose 1-phosphate (G1P) via the enzyme phosphoglucomutase (AlgC). Second, glucose 1-phosphate is converted into dTDP-D-glucose via the enzyme glucose-1-phosphate thymidylyltransferase (RmlA). Third, dTDP-D-glucose is converted into dTDP-4-dehydro-6-deoxy-D-glucose via the enzyme dTDP-glucose 4,6-dehydratase (RmlB). Fourth, dTDP-4-dehydro-6-deoxy-D-glucose is converted into dTDP-4-dehydro-L-rhamnose via the enzyme dTDP-4-dehydrorhamnose 3,5-epimerase (RmlC). Fifth, dTDP-4-dehydro-L-rhamnose is converted into dTDP-L-rhamnose via the enzyme dTDP-4-dehydrorhamnose reductase (RmlD). The HAA component is synthesized from 3-hydroxyacyl-[acyl-carrier protein] diverted from fatty acid biosynthesis via the enzyme 3-(3-hydroxydecanoyloxy)decanoate synthase (RhIA). The final step in rhamnolipid biosynthesis is the formation of the glycosidic link between the rhamnose sugar component and the HAA component. This is accomplished by two rhamnosyltransferases (RhlB and RhlC) which catalyze sequential glycosyl transfer reactions to first form mono-rhamnolipids (via RhIB) and then di-rhamnolipids (via RhIC). RHlA, RHlB, and RHlC are associated with the inner membrane.