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PathWhiz ID Pathway Meta Data

PW127416

Pw127416 View Pathway
drug action

Chloramphenicol Action Pathway - New

Homo sapiens
Chloramphenicol, trade names Pentamycetin and Chloromycetin, is a broad spectrum antibiotic originally derived from Streptomyces venezuelae . It inhibits protein synthesis by binding the 50S ribosomal subunit to prevent bacterial growth. Bacterial resistance has occurred through decreased uptake or permeability, ribosomal mutation and inactivation by acetylation. Adverse side effects such as aplastic anemia, bone-marrow suppression or Gray syndrome in neonates and infants have resulted in limited use. However, due to ampicillin-resistant bacterial meningitis, there has been a renewed interest in the drug.

PW144571

Pw144571 View Pathway
drug action

Chloramphenicol Drug Metabolism Action Pathway

Homo sapiens

PW146874

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drug action

Chloramphenicol palmitate Drug Metabolism Action Pathway

Homo sapiens

PW176000

Pw176000 View Pathway
metabolic

Chloramphenicol Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Chloramphenicol are predicted with biotransformer.

PW127417

Pw127417 View Pathway
drug action

Chloramphenicol succinate Action Pathway

Homo sapiens
CS is a prodrug of chloramphenicol

PW145828

Pw145828 View Pathway
drug action

Chloramphenicol succinate Drug Metabolism Action Pathway

Homo sapiens

PW176001

Pw176001 View Pathway
metabolic

Chloramphenicol succinate Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Chloramphenicol succinate are predicted with biotransformer.

PW145897

Pw145897 View Pathway
drug action

Chlorcyclizine Drug Metabolism Action Pathway

Homo sapiens

PW176617

Pw176617 View Pathway
drug action

Chlorcyclizine H1 Antihistamine Smooth Muscle Relaxation Action Pathway

Homo sapiens
Chlorcyclizine is an H1 antihistamine. 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. 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. Chlorcyclizine also inhibits the H1 histamine receptor on bronchiole smooth muscle myocytes. 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 myosin light chain kinase. This prevents the phosphorylation of myosin light chain 3, causing an accumulation of myosin light chain 3. This causes muscle relaxation, opening up the bronchioles in the lungs, making breathing easier.

PW059865

Pw059865 View Pathway
drug action

Chlorcyclizine H1-Antihistamine Action

Homo sapiens
Chlorcyclizine is a first-generation piperazine H1-antihistamine. 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.