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PathWhiz ID Pathway Meta Data

PW176624

Pw176624 View Pathway
drug action

Loratadine H1 Antihistamine Smooth Muscle Relaxation Action Pathway

Homo sapiens
Loratadine is a long-acting, second-generation, non-sedating tricyclic antihistamine (piperidine derivative) with selective antagonistic properties to peripheral histamine H1-receptors. Loratadine selectively inhibits H1-receptors primarily located on respiratory smooth muscle cells, vascular endothelial cells, the gastrointestinal tract, and immune cells. Unlike the first-generation antihistamines such as diphenhydramine, loratadine is a competitive histamine antagonist that does not cross the blood-brain barrier. Therefore, it does not affect the neurons of the central nervous system, thereby preventing daytime somnolence or sedation. Loratadine binds to H1-receptors in different cells and causes a decrease in vascular permeability (prevents edema and flushing), decreases smooth muscle tone (bronchodilation), and decreases the activation of the peripheral nociceptive receptors (decreases pain and pruritus). At high concentrations, second-generation antihistamines such as loratadine can inhibit histamine release from mast cells and basophils, thereby reducing ICAM-1 expression in epithelial cells and inhibiting type 1 hypersensitivity reactions (e.g., hay fever, urticaria, pruritus, edema).

PW061144

Pw061144 View Pathway
drug action

Loratadine H1-Antihistamine Action

Homo sapiens
Loratadine is a second-generation 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.

PW126586

Pw126586 View Pathway
drug action

Lorazepam Action Pathway

Homo sapiens
Lorazepam is a short-acting benzodiazepine commonly used for the short-term relief of anxiety symptoms related to anxiety disorders and anxiety associated with depressive symptoms such as anxiety-associated insomnia. It is as well used as an anesthesia premedication in adults to relieve anxiety or to produce sedation/amnesia and for the treatment of status epilepticus. Some off-label indications of lorazepam include rapid tranquilization of an agitated patient, alcohol withdrawal delirium, alcohol withdrawal syndrome, muscle spasms, insomnia, panic disorder, delirium, chemotherapy-associated anticipatory nausea and vomiting, and psychogenic catatonia. Lorazepam allosterically binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane. According to the binding site of lorazepam, we can observe different activities as the binding in the amygdala is known to help mainly in anxiety disorders while the binding in the cerebral cortex helps in seizure disorders.

PW144317

Pw144317 View Pathway
drug action

Lorazepam Drug Metabolism Action Pathway

Homo sapiens

PW145604

Pw145604 View Pathway
drug action

Lorcaserin Drug Metabolism Action Pathway

Homo sapiens

PW146497

Pw146497 View Pathway
drug action

Lorlatinib Drug Metabolism Action Pathway

Homo sapiens

PW176084

Pw176084 View Pathway
metabolic

Lorlatinib Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Lorlatinib are predicted with biotransformer.

PW127715

Pw127715 View Pathway
drug action

Lormetazepam Action Pathway

Homo sapiens
Lormetazepam is a benzodiazepine indicated in the treatment of anxiety and the induction of anesthesia. Lormatazepam is an orally available benzodiazepine used in the UK for the treatment of short-term insomnia. It can be found under the brand names Noctamid, Aldosomnil, Ergocalm, and Metatop. Lormetazepam is a benzodiazepine which reduces central nervous system (CNS) activity. It produces anxiolytic, muscle relaxant, sedative and hypnotic effects. Because it is a short-acting benzodiapine, it does not produce significant sedation after waking. Lormetazepam, as a benzodiazepine, binds to the regulatory site between the α and γ subunits of γ-aminobutryic acid (GABA) A receptors with γ2 and α1, α2, α3, or α5 subunits. This facilitates the opening of the chloride channel allowing chloride ions to flow into the neuron resulting in hyperpolarization. Hyperpolarized neurons require greater simulation to reach their action potential threshold. The general inhibitory effect on neuronal depolarization produces the effects of lormetazepam. Some side effects of using lormetazepam may include aggression, lightheadedness, confusion, and headache.

PW146689

Pw146689 View Pathway
drug action

Lormetazepam Drug Metabolism Action Pathway

Homo sapiens

PW000677

Pw000677 View Pathway
drug action

Lornoxicam Action Pathway

Homo sapiens
Lornoxicam (also named Chlortenoxicam or Xefocam) is a nonsteroidal anti-inflammatory drug. It can be used to treat moderate pain such as pain relieving. It can also treat swelling and fever reducing. Lornoxicam can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Lornoxicam.