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Showing 48551 - 48560 of 605359 pathways
SMPDB ID Pathway Name and Description Pathway Class Chemical Compounds Proteins

SMP0059702

Pw060645 View Pathway

Phenbenzamine H1-Antihistamine Action

Phenbenzamine is a first-generation ethylenediamine 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.
Drug Action

SMP0057581

Pw058506 View Pathway

Triprolidine H1-Antihistamine Action

Triprolidine is a first-generation alkylamine 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.
Drug Action

SMP0060743

Pw061693 View Pathway

Quifenadine H1-Antihistamine Action

Quifenadine is a second-generation 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.
Drug Action

SMP0062884

Pw063841 View Pathway

Quetiapine H1-Antihistamine Action

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.
Drug Action

SMP0061190

Pw062141 View Pathway

Phenindamine H1-Antihistamine Action

Phenindamine is a first-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.
Drug Action

SMP0000454

Pw000433 View Pathway

Repaglinide Action Pathway

Repaglinide is a non-sulfonylurea insulin secretagogue used in the treatment of type 2 diabetes. As the name of the drug class suggests, repaglinide acts on pancreatic beta-cells to stimulate insulin secretion. Under physiological conditions, insulin secretion from beta-cells is mediated by elevated glucose concentration in the blood. Glucose enters the cell via GLUT2 (SLC2A2) transporters. Once inside the cell, glucose is metabolized to produce ATP. High concentration of ATP will inhibit ATP-dependent potassium channels (ABCC8), which depolarizes the cell. Depolarization causes opening of voltage-gated calcium channels, allowing calcium to enter cell. High intracellular calcium subsequently stimulate vesicle exocytosis and insulin secretion. Repaglinide stimulate insulin secretion in a glucose-sensitive manner by inhibiting ATP-dependent potassium channels. As a result, there tends to be a lesser likelihood of hypoglycemia with repaglinide therapy compared to sulfonylureas.
Drug Action

SMP0000500

Pw000476 View Pathway

5-Oxoprolinase Deficiency

5-Oxoprolinase deficiency, also called OPLAHD, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of glutathione metabolism caused by a defective 5-oxoprolinase. 5-Oxoprolinase catalyzes the conversion of 5-oxoproline into glutamate which is an important neurotransmitter. This disorder is characterized by a large accumulation of 5-oxoproline in the urine. Symptoms of the disorder include enterocolitis, mental retardation, kidney stone formation, and hypoglycemia. 5-Oxoprolinase deficiency has been reported in approximately 8 people.
Disease

SMP0000532

Pw000508 View Pathway

Sulfite Oxidase Deficiency

Sulfite oxidase deficiency (SOD) is a disorder, an autosomal recessive disease. In classic SOD, it is usually identified a few days after the birth of an affected individual, and is recognizable through characteristic dysmorphic features, seizures, and other signs of progressive encephalopathy. Patients also have ocular lenses that are dislocated, and usually die within a few months of being born. In late- onset SOD, the disorder is identified only in the later months, usually 6-18 months, of the child’s life by a delay or regression of neurological progress. This disorder is very rare, but the actual prevalence is not known. It can be diagnosed through a sulfite test strip in urine or by a skin fibroblast culture, which will indicate an absence of sulfite oxidase.
Disease

SMP0000647

Pw000623 View Pathway

Thioguanine Metabolism Pathway (old)

Thioguanine is a purine antimetabolite prodrug closely related to mercaptopurine and similarly inhibits purine metabolism. The thioguanine pathway is shown as a part of the mercaptopurine pathway. Thioguanine exerts cytotoxic effects via incorporation of thiodeoxyguanosine triphosphate into DNA and thioguanosine triphosphate into RNA and inhibition of Ras-related C3 botulinum toxin substrate 1, which induces apoptosis of activated T cells. Once in a cell, thioguanine is converted to thioguanosine monophosphate by hypoxanthine-guanine phosphoribosyltransferase. Thioguanosine monophosphate is then phosphorylated to thioguanosine diphosphate, which is converted via a thiodeoxyguanosine diphosphate intermediate to thiodeoxyguanosine triphosphate. Thiodeoxyguanosine triphosphate is incorporated into DNA causing cytotoxicity. Thioguanosine diphosphate is also converted to thioguanosine triphosphate which is incorporated into RNA. The thioguanosine triphosphate metabolite also inhibits Ras-related C3 botulinum toxin substrate 1, a plasma membrane-associated small GTPase that regulates cellular processes, inducing apoptosis in activated T cells.
Drug Metabolism

SMP0000652

Pw000628 View Pathway

Mycophenolic Acid Metabolism Pathway (old)

Mycophenolic Acid (MPA) is an immunosuppressive agent that acts as a noncompetitive, selective and reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH). It is available as a prodrug, Mycophenolate mofetil (MMF), which is a 2-morpholinoethyl ester with improved bioavailability. After absorption, MMF is hydrolyzed to MPA and N-(2-carboxymethyl)- morpholine, N-(2-hydroxyethyl)-morpholine, and the N-oxide of N-(2-hydroxyethyl)-morpholine by the carboxylesterases CES-1 (in the liver only) and CES-2 (in the liver and intestine). The morpholine metabolites are excreted in the urine. MPA is glucuronidated by UDP glucuronosyl transferases (UGTs) UGT1A7, UGT1A8, UGT1A9 and UGT1A10 to MPA-7-O-glucuronide, which is excreted in the urine. Other metabolites of MPA include MPA-acyl glucoronide, which is formed by UGT2B7, and 6-O-desmethyl-MPA, which is formed by the CYP enzymes CYP3A4, CYP3A5 and CYP2C8. MPA enters hepatocytes by the organic anion transport proteins (OATPs) SLCO1B1 and SLCO1B3. MPA and its metabolites are excreted in the bile via the ABCC2, ABCG2, and ABCB1 proteins.
Drug Metabolism
Showing 48551 - 48560 of 65005 pathways