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PathWhiz ID Pathway Meta Data

PW059857

Pw059857 View Pathway
drug action

Cyclizine H1-Antihistamine Action

Homo sapiens
Cyclizine 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.

PW176683

Pw176683 View Pathway
drug action

Cyclizine H1-Antihistamine Blood Vessel Constriction Action Pathway

Homo sapiens
Cyclizine is an H1 antihistamine and antiemetic drug used for the prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness, and vertigo. 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. Cyclizine 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.

PW176775

Pw176775 View Pathway
drug action

Cyclizine H1-Antihistamine Immune Response Action Pathway

Homo sapiens
Cyclizine is an H1 antihistamine and antiemetic drug used for the prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness, and vertigo. 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.

PW145025

Pw145025 View Pathway
drug action

Cyclobenzaprine Drug Metabolism Action Pathway

Homo sapiens

PW176505

Pw176505 View Pathway
metabolic

Cyclobenzaprine Predicted Metabolism Pathway

Homo sapiens
Metabolites of Cyclobenzaprine are predicted with biotransformer.

PW128450

Pw128450 View Pathway
drug action

Cyclobenzaprine Serotonin antagonist Action Pathway

Homo sapiens
Cyclobenzaprine is a centrally acting skeletal muscle relaxant structurally related to tricyclic antidepressants. Cyclobenzaprine relieves skeletal muscle spasms of local origin without interfering with muscle function. In preclinical research, cyclobenzaprine reduced skeletal muscle hyperactivity. Research indicates that it primarily acts within the central nervous system in the brain stem. Cyclobenzaprine does not work directly on skeletal muscle or the neuromuscular junction, although an overlapping action on the spinal cord may contribute to its overall skeletal muscle relaxant activity. Evidence implies that the resultant impact of cyclobenzaprine is a decline of tonic somatic motor activity, affecting both gamma(γ) and alpha(α) motor systems. Recent research suggests that cyclobenzaprine is a (5-HT2) receptor antagonist, and this additional action is responsible for its antispasmodic effect. Cyclobenzaprine effectively improves muscle spasms, reduces local pain and tenderness, and increases the range of motion in acute, painful musculoskeletal conditions. Cyclobenzaprine is an antispasmodic drug effective in treating muscle spasms. However, cyclobenzaprine is not an antispasticity drug. Therefore, cyclobenzaprine is ineffective in treating spasticity associated with cerebral or spinal cord pathology or children with cerebral palsy.

PW132439

Pw132439 View Pathway
metabolic

Cycloguanil Drug Metabolism

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

PW146890

Pw146890 View Pathway
drug action

Cycloguanil Drug Metabolism Action Pathway

Homo sapiens

PW132465

Pw132465 View Pathway
metabolic

Cyclopenthiazide Drug Metabolism

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

PW146658

Pw146658 View Pathway
drug action

Cyclopenthiazide Drug Metabolism Action Pathway

Homo sapiens