Pathways

Zoledronate (also named zoledronic acid, Zometa or Reclast) is a type of medication that used to treat numbers of bone diseases because of its affinity for hydroxyapatite. Zoledronate targets farnesyl pyrophosphate (FPP) synthase by inhibiting the function of this enzyme in the mevalonate pathway, which prevent the biosynthesis of Geranyl-PP and farnesyl pyrophosphate. Geranyl-PP and farnesyl pyrophosphate are important for geranylgeranylation and farnesylation of GTPase signalling proteins. Lack of Geranyl-PP and farnesyl pyrophosphate will result in decreased rate of bond resorption and turnover as well as block the osteoclast activity, which lead to an increasing mass gain in bone (i.e. net gain in bone mass).

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.

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.

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.

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.

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.

Metabolites of Zolpidem are predicted with biotransformer.

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.