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Pathways

PathWhiz ID Pathway Meta Data

PW145468

Pw145468 View Pathway
drug action

Lopinavir Drug Metabolism Action Pathway

Homo sapiens

PW144572

Pw144572 View Pathway
drug action

Loracarbef Drug Metabolism Action Pathway

Homo sapiens

PW176083

Pw176083 View Pathway
metabolic

Loracarbef Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Loracarbef are predicted with biotransformer.

PW144579

Pw144579 View Pathway
drug action

Loratadine Drug Metabolism Action Pathway

Homo sapiens

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