Pathways

Metabolites of Bromocriptine are predicted with biotransformer.

Bromocriptine is an ergot alkaloid derivative in the dopamine D2 agonist class of drugs. Prolactin release-inhibiting hormone (PRIH) is the catecholamine neurotransmitter dopamine. Bromocriptine is an FDA-approved medication indicated for the use of disorders causing hyperprolactinemia, which most often is due to the most common of the pituitary adenomas – prolactinoma. Bromocriptine is a dopamine receptor agonist with selective agonist activity on D2 dopamine receptors while simultaneously acting as a partial antagonist for D1 dopamine receptors. Dopamine agonism has variable effects depending on the target tissue. In Parkinson disease, bromocriptine binds directly to striatal dopamine D2 receptors, stimulating locomotion and attenuating the bradykinetic symptoms caused by the degeneration of dopaminergic nigrostriatal neurons. This same D2 agonistic effect on the D2 receptors of anterior pituitary lactotrophic cells blocks prolactin exocytosis and gene expression, reducing the harmful effects of hyperprolactinemia in the case of a pituitary prolactinoma. In acromegaly, bromocriptine’s dopaminergic effect can cause paradoxical blocking of GH release through tuberoinfundibular pathways, decreasing circulating blood concentrations of GH. he dopamine D2 receptor is a 7-transmembrane G-protein coupled receptor associated with Gi proteins. In lactotrophs, stimulation of dopamine D2 receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca2+ from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through voltage-gated calcium channels, rather than via inhibition of adenylyl cyclase. Additionally, receptor activation blocks phosphorylation of p42/p44 MAPK and decreases MAPK/ERK kinase phosphorylation. Inhibition of MAPK appears to be mediated by c-Raf and B-Raf-dependent inhibition of MAPK/ERK kinase. Dopamine-stimulated growth hormone release from the pituitary gland is mediated by a decrease in intracellular calcium influx through voltage-gated calcium channels rather than via adenylyl cyclase inhibition. Stimulation of dopamine D2 receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders.

Metabolites of Bromhexine are predicted with biotransformer.

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.

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.

Metabolites of Bromazepam are predicted with biotransformer.