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PathWhiz ID Pathway Meta Data

PW176666

Pw176666 View Pathway
drug action

Mirtazapine H1-Antihistamine Blood Vessel Constriction Action Pathway

Homo sapiens
Mirtazapine is a first-generation ethanolamine 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. Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage. Mirtazapine 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.

PW176759

Pw176759 View Pathway
drug action

Mirtazapine H1-Antihistamine Immune Response Action Pathway

Homo sapiens
Mirtazapine is a first-generation ethanolamine 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.

PW176272

Pw176272 View Pathway
metabolic

Mirtazapine Predicted Metabolism Pathway

Homo sapiens
Metabolites of Mirtazapine are predicted with biotransformer.

PW128422

Pw128422 View Pathway
drug action

Mirtazapine Serotonin Antagonist Action Pathway

Homo sapiens
The mechanism of action of mirtazapine, atypical antidepressant is not fully understood, but may be explained by its effects on central adrenergic and serotonergic activity. This drug exhibits a fast onset of action, a high level of response, a manageable side-effect profile, and dual noradrenergic and serotonergic effects that are unique from the effects of other antidepressants. It has been shown that both noradrenergic and serotonergic activity increase following mirtazapine administration. The results of these studies demonstrate mirtazapine exerts antagonist activity at presynaptic α2-adrenergic inhibitory autoreceptors and heteroreceptors in the central nervous system. This is thought to lead to enhanced noradrenergic and serotonergic activity Label, which are known to improve the symptoms of depression and form the basis of antidepressant therapy. Mirtazapine is a strong antagonist of serotonin 5-HT2 and 5-HT3 receptors. It has not been found to bind significantly to the serotonin 5-HT1A and 5-HT1B receptors but indirectly increases 5-HT1A transmission. In addition to the above effects, mirtazapine is a peripheral α1-adrenergic antagonist. This action may explain episodes of orthostatic hypotension that have been reported after mirtazapine use. Mirtazapine is a potent histamine (H1) receptor antagonist, which may contribute to its powerful sedating effects. The pain-relieving effects of mirtazapine may be explained by its effects on opioid receptors.

PW131745

Pw131745 View Pathway
metabolic

Mirvetuximab Drug Metabolism

Homo sapiens

PW123904

Pw123904 View Pathway
physiological

Mismatch repair

Homo sapiens

PW126203

Pw126203 View Pathway
drug action

Misoprostol Action Pathway

Homo sapiens
Misoprostol is a prostaglandin E1 analog that reduces the risk of NSAID-induced gastric ulcers. Misoprostol is indicated as a tablet to reduce the risk of NSAID-induced gastric ulcers but not duodenal ulcers in high-risk patients. Misoprostol is also formulated with diclofenac to treat symptoms of osteoarthritis or rheumatoid arthritis in patients with a high risk of developing gastric ulcers. Misoprostol is used off-label for the management of miscarriages, prevention of post-partum hemorrhage, and is also used alone or in combination with mifepristone in other countries for first-trimester abortions Misoprostol stimulates prostaglandin receptors on parietal cells in the stomach to reduce gastric acid secretion. Misoprostol activates prostaglandin EP3 receptors in parietal cells. Activation of this receptor triggers the Gi protein signaling cascade, inhibiting adenylate cyclase. Adenylate cyclase is responsible for converting ATP to cAMP, therefore, inhibition of adenylate cyclase reduces cytosolic cAMP concentration. cAMP is responsible for activating protein kinase A. With lower concentrations of cAMP, less protein kinase A is activated. Protein kinase A activates the proton pump in the luminal membrane of the parietal cell. The role of the proton pump is to secrete acid (H+) into the stomach lumen. With reduced protein kinase A activation, this decreases the activity of the proton pump, fewer H+ ions are pumped into the lumen, reducing the acidity and thus allowing stomach ulcers to heal and reducing the pain caused by the ulcers. Misoprostol may also promote ulcer healing by increasing mucus and bicarbonate secretion and thickening the mucosal bilayer so the mucosa can generate new cells.

PW145029

Pw145029 View Pathway
drug action

Misoprostol Drug Metabolism Action Pathway

Homo sapiens

PW146957

Pw146957 View Pathway
drug action

Mitapivat Drug Metabolism Action Pathway

Homo sapiens

PW176095

Pw176095 View Pathway
metabolic

Mitapivat Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Mitapivat are predicted with biotransformer.