Pathways

Metabolites of Salicylamide are predicted with biotransformer.

Salicylate-sodium (also named salsonin or clin) is a nonsteroidal anti-inflammatory drug (NSAID). It can be used for relieving pain and reducing fever. Salicylate-sodium 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 salicylate-sodium.

Salicylate-sodium is an NSAID which possesses anti-inflammatory, analgesic and antipyretic activity. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 converts arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Salicylate-sodium inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. Fever is triggered by inflammatory and infectious diseases. Cytokines are produced in the central nervous system (CNS) during an inflammatory response. These cytokines induce COX-2 production that increases the synthesis of prostaglandin, specifically prostaglandin E2 which adjusts hypothalamic temperature control by increasing heat production. Because salicylate-sodium decreases PGE2 in the CNS, it has an antipyretic effect. Antipyretic effects results in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.

Salicylic acid (also named rutranex or salonil) is a nonsteroidal anti-inflammatory drug. Salicylic acid is also an important active metabolite of aspirin (acetylsalicylic acid). It can be used to reduce pain and fever. Salicylic acid 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 Salicylic acid.

Salicylic acid is an acid used to treat acne, psoriasis, calluses, corns, keratosis pilaris, and warts. Salicylate's use in rheumatic diseases is due to it's analgesic and anti-inflammatory activity. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 convert arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase, or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme that is responsible for prostaglandin synthesis during inflammation. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Salicylic acid inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. This drug is administered as a topical cream, ointment, shampoo, patch, lotion, or gel.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.