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PathWhiz ID Pathway Meta Data

PW132535

Pw132535 View Pathway
metabolic

Pyrvinium Drug Metabolism

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

PW145817

Pw145817 View Pathway
drug action

Pyrvinium Drug Metabolism Action Pathway

Homo sapiens

PW132266

Pw132266 View Pathway
metabolic

Quaternium-15 Drug Metabolism

Homo sapiens
Quaternium-15 is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Quaternium-15 passes through the liver and is then excreted from the body mainly through the kidney.

PW146794

Pw146794 View Pathway
drug action

Quaternium-15 Drug Metabolism Action Pathway

Homo sapiens

PW127720

Pw127720 View Pathway
drug action

Quazepam Action Pathway

Homo sapiens
Quazepam is a long-acting benzodiazepine used to manage insomnia. It appears to be unique amongst other benzodiazepine derivatives in its relatively high affinity for sleep-promoting α1 subunit-containing GABAA receptors and low affinity for other receptors. It can be found under the brand name Doral. Quazepam is indicated for the treatment of insomnia characterized by difficulty falling asleep, frequent nocturnal awakenings, and/or early morning awakenings. Like other benzodiazepines, quazepam likely exerts its effects by potentiating the effect of gamma-aminobutyric acid (GABA) on GABA(A) receptors, the main inhibitory neurotransmitter receptors in the mammalian brain. GABA(A) receptors are a component of GABA-gated ionotropic chloride channels that produce inhibitory postsynaptic potentials - following activation by GABA, the channel undergoes a conformational change that allows the passage of chloride ions through the channel. The inhibitory potentials produced by GABA neurotransmission play an integral role in the suppression and control of epileptiform nerve firing such as that seen in epilepsy, which makes the GABA system a desirable target in the treatment of epilepsy. Benzodiazepines are positive allosteric modulators of GABA(A) function. They bind to the interface between alpha (α) and gamma (γ) subunits on the receptor, commonly referred to as the benzodiazepine binding site, and modulate the receptor such that its inhibitory response to GABA binding is dramatically increased. Quazepam is administered as an oral tablet. Possible side effects of using quazepam may include drowsiness, lowered alertness, confusion, and loss of coordination.

PW145458

Pw145458 View Pathway
drug action

Quazepam Drug Metabolism Action Pathway

Homo sapiens

PW128432

Pw128432 View Pathway
drug action

Quetiapine Dopamine Antagonist Action Pathway

Homo sapiens
Quetiapine is used in the symptomatic treatment of schizophrenia. In addition, it may be used for the management of acute manic or mixed episodes in patients with bipolar I disorder, as a monotherapy or combined with other drugs. It may be used to manage depressive episodes in bipolar disorder. In addition to the above indications, quetiapine is used in combination with antidepressant drugs for the treatment of major depression. Although the mechanism of action of quetiapine is not fully understood, several proposed mechanisms exist. In schizophrenia, its actions could occur from the antagonism of dopamine type 2 (D2) and serotonin 2A (5HT2A) receptors. In bipolar depression and major depression, quetiapine's actions may be attributed to the binding of this drug or its metabolite to the norepinephrine transporter. Additional effects of quetiapine, including somnolence, orthostatic hypotension, and anticholinergic effects, may result from the antagonism of H1 receptors, adrenergic α1 receptors, and muscarinic M1 receptors, respectively.

PW145310

Pw145310 View Pathway
drug action

Quetiapine Drug Metabolism Action Pathway

Homo sapiens

PW176614

Pw176614 View Pathway
drug action

Quetiapine H1 Antihistamine Smooth Muscle Relaxation Action Pathway

Homo sapiens
Quetiapine 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. Quetiapine 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.

PW063841

Pw063841 View Pathway
drug action

Quetiapine H1-Antihistamine Action

Homo sapiens
Quetiapine is a tricyclic 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.