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PathWhiz ID Pathway Meta Data

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

Pw144685 View Pathway
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.

PW176672

Pw176672 View Pathway
drug action

Cinnarizine H1-Antihistamine Blood Vessel Constriction 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.

PW176764

Pw176764 View Pathway
drug action

Cinnarizine H1-Antihistamine Immune Response 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.

PW132475

Pw132475 View Pathway
metabolic

Cinoxacin Drug Metabolism

Homo sapiens
Cinoxacin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Cinoxacin passes through the liver and is then excreted from the body mainly through the kidney.

PW144933

Pw144933 View Pathway
drug action

Cinoxacin Drug Metabolism Action Pathway

Homo sapiens