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Pathways

PathWhiz ID Pathway Meta Data

PW127917

Pw127917 View Pathway
drug action

Zoledronate Action Pathway

Homo sapiens
Zoledronate also known as zoledronic acid is a third-generation bisphosphonate used to treat malignancy with hypercalcemia, myeloma and bone metastasis from tumors. Zoledronate is taken up into the bone and binds to hydroxyapatite, during bone resorption zoledronate is released and taken up into the osteoclast by endocytosis. Within the cytosol of the osteoclast, it inhibits geranylgeranyl pyrophosphate synthase and farnesyl pyrophosphate synthase. Without these enzymes components needed for the prenylation of proteins are stopped, and this leads to apoptosis of the osteoclast.

PW132274

Pw132274 View Pathway
metabolic

Zoledronate D,L-Lysine Monohydrate Drug Metabolism

Homo sapiens
Zoledronate D,L-Lysine Monohydrate is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Zoledronate D,L-Lysine Monohydrate passes through the liver and is then excreted from the body mainly through the kidney.

PW147111

Pw147111 View Pathway
metabolic

Zoledronate Drug Metabolism Pathway

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

PW144442

Pw144442 View Pathway
drug action

Zolmitriptan Drug Metabolism Action Pathway

Homo sapiens

PW128613

Pw128613 View Pathway
drug action

Zolmitriptan Mechanism of Action Action Pathway

Homo sapiens
Zolmitriptan, like other triptans, is a serotonin (5-hydroxytryptamine; 5-HT) receptor agonist, with enhanced specificity for the 5-HT1B and 5-HT1D receptor subtypes. It is through the downstream effects of 5-HT1B/1D activation that triptans are proposed to provide acute relief of migraines. It has a weak affinity for 5-HT 1A receptor. Zolmitriptan is a vasoconstrictor, leading to possible adverse cardiovascular effects such as myocardial ischemia/infarction, arrhythmias, cerebral and subarachnoid hemorrhage, stroke, gastrointestinal ischemia, and peripheral vasospastic reactions.

PW126605

Pw126605 View Pathway
drug action

Zolpidem Action Pathway (New)

Homo sapiens
Zolpidem is a sedative hypnotic used for the short-term treatment of insomnia to improve sleep latency. Zolpidem binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane. Zolpidem binding to the GABAA receptor chloride channel macromolecular complex is thought to lead to the sedative, anticonvulsant, anxiolytic, and myorelaxant drug effects of the drug.

PW144550

Pw144550 View Pathway
drug action

Zolpidem Drug Metabolism Action Pathway

Homo sapiens

PW176470

Pw176470 View Pathway
metabolic

Zolpidem Predicted Metabolism Pathway

Homo sapiens
Metabolites of Zolpidem are predicted with biotransformer.

PW128267

Pw128267 View Pathway
drug action

Zonisamide Action Pathway

Homo sapiens
Zonisamide is a sulfonamide anticonvulsant used to treat partial seizures. It can be found under the brand names Zonegran and Zonisade and is administered as an oral capsule. Zonisamide is a sulfonamide anticonvulsant used as an adjunctive therapy in adults with partial-onset seizures. Zonisamide may act by blocking repetitive firing of voltage-gated sodium channels, leading to a reduction of T-type calcium channel currents. By stopping the spread of seizure discharges, zonisamide prevents the extensor component of tonic convulsion, restricts the spread of focal seizures and prevents the propagation of seizures from the cortex to subcortical structures. The mechanism of action by which zonisamide controls seizures has not been fully established. However, its antiepileptic properties may be due to its effects on sodium and calcium channels. Zonisamide blocks sodium channels and reduces voltage-dependent, transient inward currents, stabilizing neuronal membranes and suppressing neuronal hypersynchronization. It affects T-type calcium currents, but has no effect on L-type calcium currents. Zonisamide suppresses synaptically-driven electrical activity by altering the synthesis, release, and degradation of neurotransmitters, such as glutamate. The use of zonisamide may lead to potentially fatal reactions. Severe reactions such as Stevens-Johnson syndrome, toxic epidermal necrolysis, fulminant hepatic necrosis, agranulocytosis, and aplastic anemia have been reported in patients treated with sulfonamides such as zonisamide. Zonisamide may also lead to the development of serious hematological events, drug reaction with eosinophilia and systemic symptoms (DRESS) and multi-organ hypersensitivity, acute myopia and secondary angle closure glaucoma, as well as suicidal behaviour and ideation.

PW145010

Pw145010 View Pathway
drug action

Zonisamide Drug Metabolism Action Pathway

Homo sapiens