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Pathways

PathWhiz ID Pathway Meta Data

PW176325

Pw176325 View Pathway
metabolic

Brivaracetam Predicted Metabolism Pathway

Homo sapiens
Metabolites of sildenafil are predicted with biotransformer.

PW127461

Pw127461 View Pathway
drug action

Brivudine Action Pathway

Homo sapiens
Brivudine is a drug used to treat herpes zoster. Although not approved in the U.S. or Canada, it is approved in several European countries. Brivudine exerts its antiviral activity by a selective inhibition at the pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular DNA polymerases. Foscarnet inhibits the activity of DNA polymerase by competing with its substrate dGTP. Less viral proteins produced, fewer viruses can form.

PW145533

Pw145533 View Pathway
drug action

Brivudine Drug Metabolism Action Pathway

Homo sapiens

PW128528

Pw128528 View Pathway
drug action

Brolucizumab Action Pathway

Homo sapiens
Brolucizumab, also known as RTH258 or ESBA1008, is a monoclonal antibody used for the treatment of neovascular age-related macular degeneration. It functions as a vascular endothelial growth factor (VEGF) inhibitor, specifically targeting major VEGF-A isoforms (VEGF110, VEGF121, and VEGF165). By inhibiting these isoforms, brolucizumab reduces the proliferation of endothelial cells, vascularization of tissue, and permeability of blood vessels, which are processes associated with neovascular AMD. It has a relatively long duration of action, typically administered on a monthly basis. Patients should be informed about potential risks, including endophthalmitis, retinal detachment, and arterial thromboembolic events, associated with this medication.

PW126603

Pw126603 View Pathway
drug action

Bromazepam Action Pathway

Homo sapiens
Bromazepam is a short-acting benzodiazepine with intermediate onset commonly used to treat panic disorders and severe anxiety. Bromazepam is a lipophilic, long-acting benzodiazepine and with sedative, hypnotic, anxiolytic and skeletal muscle relaxant properties. It does not possess any antidepressant qualities. Bromazepam, like other benzodiazepines, presents a risk of abuse, misuse, and dependence. According to many psychiatric experts, Bromazepam has a greater abuse potential than other benzodiazepines because of fast resorption and rapid onset of action. Bromazepam allosterically 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, ultimately leading to a sedative-like effect.

PW145443

Pw145443 View Pathway
drug action

Bromazepam Drug Metabolism Action Pathway

Homo sapiens

PW175983

Pw175983 View Pathway
metabolic

Bromazepam Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Bromazepam are predicted with biotransformer.

PW000259

Pw000259 View Pathway
drug action

Bromfenac Action Pathway

Homo sapiens
Bromfenac (also named Prolensa, Bromday or Xibrom) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used to reduce ocular inflammation and pain after cataract surgery. Bromfenac is also a type of ophthalmic anti-inflammatory medicines. Bromfenac can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of bromfenac.

PW145061

Pw145061 View Pathway
drug action

Bromfenac Drug Metabolism Action Pathway

Homo sapiens

PW127971

Pw127971 View Pathway
drug action

Bromfenac NSAID Action Pathway

Homo sapiens
Bromfenac is a nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. Non-ophthalmic formulations of bromfenac were withdrawn in the US in 1998 due to cases of severe liver toxicity. The mechanism of its action is due to the ability of bromfenac to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2 with selectivity for COX-2 over COX-1. Prostaglandins are mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produce disruption of the blood-aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure.