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PW124719

Pw124719 View Pathway
metabolic

Cimetidine metabolism

Homo sapiens
Cimetidine, an H2 receptor antagonist drug mainly used to treat peptic ulcers and heartburns, is absorbed through the cells that line the small intestine into portal circulation. After it enters the liver hepatocyte from portal circulation, Cimetidine is metabolized by flavin containing monooxygenases and other P450 enzymes into cimetidine sulfoxide and hydroxymethyl cimetidine. These metabolites then enter systemic circulation. Research is still being conducted to find the specific types of enzymes that are involved in the metabolism of the drug into these metabolites.

PW125940

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metabolic

Cimetidine metabolism 1619814130

Homo sapiens

PW000593

Pw000593 View Pathway
drug metabolism

Cimetidine Metabolism Pathway

Homo sapiens
Cimetidine, sold as Tagamet, is a compound related to histamine. It is a H2 antagonist drug, also called H2RAs or H2 blockers, and was the first of this class to be discovered. H2 antagonist drugs compete with histamine to bind to the histamine H2-receptors found on the basolateral membrane of gastric parietal cells. This blocks histamine effects, resulting in reduced gastric acid secretion and a reduction in gastric volume and acidity. Cimetidine also helps to block pepsin and gastrin output, and due to the inhibition of gastric acid secretion, it is typically used to treat heartburn and ulcers. Cimetidine also blocks the activity of cytochrome P-450 enzymes CYP1A2, 2C9, 2C19, 2D6, 2E1 and 3A4, which may affect the metabolism of other drugs.

PW145110

Pw145110 View Pathway
drug action

Cinacalcet Drug Metabolism Action Pathway

Homo sapiens

PW146780

Pw146780 View Pathway
drug action

Cinnamaldehyde Drug Metabolism Action Pathway

Homo sapiens

PW146782

Pw146782 View Pathway
drug action

Cinnamyl alcohol Drug Metabolism Action Pathway

Homo sapiens

PW128271

Pw128271 View Pathway
drug action

Cinnarizine Calcium Channel Vasodilation Action Pathway

Homo sapiens
Cinnarizine is a drug used for the management of labyrinthine disorder symptoms, including vertigo, tinnitus, nystagmus, nausea, and vomiting. Cinnarizine could be also viewed as a nootropic drug because of its vasorelaxating abilities (due to calcium channel blockage), which happen mostly in brain. Combination use of cinnarizine with other nootropics, such as piracetam resulted in enhanced effect of boosting brain oxygen supply. Cinnarizine is an antihistamine and a calcium channel blocker. Cinnarizine inhibits contractions of vascular smooth muscle cells by blocking L-type and T-type voltage gated calcium channels. By blocking the entrance of extracellular calcium into the cell, it prevents smooth muscle contraction. This produces vasodilation which decreases blood pressure. Side effects experienced while taking cinnarizine range from the mild to the quite severe. Possible side effects include drowsiness, sweating, dry mouth, headache, skin problems, lethargy, gastrointestinal irritation, hypersensitivity reactions, as well as movement problems/muscle rigidity, and tremor.

PW144685

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drug action

Cinnarizine Drug Metabolism Action Pathway

Homo sapiens

PW176579

Pw176579 View Pathway
drug action

Cinnarizine H1 Antihistamine Smooth Muscle Relaxation Action Pathway

Homo sapiens
Cinnarizine is an anti-histaminic drug. 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. Cinnarizine 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.

PW060049

Pw060049 View Pathway
drug action

Cinnarizine H1-Antihistamine Action

Homo sapiens
Cinnarizine 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.