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Pathways

PathWhiz ID Pathway Meta Data

PW176481

Pw176481 View Pathway
metabolic

Besifloxacin Predicted Metabolism Pathway

Homo sapiens
Metabolites of Besifloxacin are predicted with biotransformer.

PW145780

Pw145780 View Pathway
drug action

Besifloxacin Drug Metabolism Action Pathway

Homo sapiens

PW128486

Pw128486 View Pathway
drug action

Besifloxacin Action Pathway

Haemophilus influenzae
Besifloxacin is a fluoroquinolone antibiotic agent used to treat bacterial conjunctivitis. Besifloxacin inhibits DNA gyrase (topoisomerase II) and topoisomerase IV. These proteins prevent supercoiling in bacterial DNA. The inhibition of DNA gyrase (topoisomerase II) and topoisomerase IV causes supercoiling of the bacterial DNA. This prevents DNA replication.

PW175980

Pw175980 View Pathway
metabolic

Berotralstat Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Berotralstat are predicted with biotransformer.

PW146950

Pw146950 View Pathway
drug action

Berotralstat Drug Metabolism Action Pathway

Homo sapiens

PW176322

Pw176322 View Pathway
metabolic

Berberine Predicted Metabolism Pathway

Homo sapiens
Metabolites of sildenafil are predicted with biotransformer.

PW145548

Pw145548 View Pathway
drug action

Berberine Drug Metabolism Action Pathway

Homo sapiens

PW145330

Pw145330 View Pathway
drug action

Bepridil Drug Metabolism Action Pathway

Homo sapiens

PW176790

Pw176790 View Pathway
drug action

Bepotastine H1-Antihistamine Immune Response Action Pathway

Homo sapiens
Bepotastine is an ophthalmic H1 antagonist used to treat itchiness associated with allergic conjunctivitis. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

PW176698

Pw176698 View Pathway
drug action

Bepotastine H1-Antihistamine Blood Vessel Constriction Action Pathway

Homo sapiens
Bepotastine is an ophthalmic H1 antagonist used to treat itchiness associated with allergic conjunctivitis. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage. Bepotastine inhibits the H1 histamine receptor on blood vessel endothelial cells. This normally activates the Gq signalling cascade which activates phospholipase C which catalyzes the production of Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). Because of the inhibition, IP3 doesn't activate the release of calcium from the sarcoplasmic reticulum, and DAG doesn't activate the release of calcium into the cytosol of the endothelial cell. This causes a low concentration of calcium in the cytosol, and it, therefore, cannot bind to calmodulin. Calcium bound calmodulin is required for the activation of the calmodulin-binding domain of nitric oxide synthase. The inhibition of nitric oxide synthesis prevents the activation of myosin light chain phosphatase. This causes an accumulation of myosin light chain-phosphate which causes the muscle to contract and the blood vessel to constrict, decreasing the swelling and fluid leakage from the blood vessels caused by allergens.