De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/10:0),Metabolic


biolink:Pathway biolink:OntologyClass biolink:BiologicalProcess biolink:Occurrent biolink:BiologicalProcessOrActivity biolink:BiologicalEntity biolink:ThingWithTaxon biolink:NamedThing biolink:PhysicalEssenceOrOccurrent

De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/12:0),Metabolic

A triglyceride (TG, triacylglycerol, TAG, or triacylglyceride) is an ester derived from glycerol and three fatty acids. Triglycerides are the main constituents of body fat in humans and other animals, as well as vegetable fat. They are also present in the blood to enable the bidirectional transference of adipose fat and blood glucose from the liver, and are a major component of human skin oils. (Wikipedia) De novo biosynthesis of triglycerides is also known as the phosphatidic acid pathway, and it is mainly associated with the liver and adipose tissue. All membrane-localized enzymes are coloured dark green in the image. First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate. Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA). The next three steps are localized to the endoplasmic reticulum membrane. The enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone. Next, magnesium-dependent phosphatidate phosphatase catalyzes the conversion of phosphatidic acid into diacylglycerol. Last, the enzyme diacylglycerol O-acyltransferase synthesizes triacylglycerol from diacylglycerol and a fatty acyl-CoA.


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-13:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-15:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-17:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-21:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/a-25:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-12:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-13:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-14:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-15:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-16:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-17:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-18:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-19:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-20:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-21:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-22:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/10:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/8:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/a-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/a-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/a-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/a-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/a-25:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-12:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-13:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-14:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-15:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-16:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-17:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-18:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-19:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-20:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-21:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-22:0),Metabolic


De Novo Triacylglycerol Biosynthesis TG(i-24:0/i-24:0/i-24:0),Metabolic


Cardiolipin (CL) is an important component of the inner mitochondrial membrane where it constitutes about 20% of the total lipid composition. It is essential for the optimal function of numerous enzymes that are involved in mitochondrial energy metabolism. (Wikipedia) Cardiolipin biosynthesis occurs mainly in the mitochondria, but there also exists an alternative synthesis route for CDP-diacylglycerol that takes place in the endoplasmic reticulum. This second route may supplement this pathway. All membrane-localized enzymes are coloured dark green in the image. First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate. Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA). Third, the enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (PA or 1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone. PA is then transferred to the inner mitochondrial membrane to continue cardiolipin synthesis. Fourth, magnesium-dependent phosphatidate cytidylyltransferase catalyzes the conversion of PA into CDP-diacylglycerol. Fifth, CDP-diacylglycerol--glycerol-3-phosphate 3-phosphatidyltransferase synthesizes phosphatidylglycerophosphate (PGP). Sixth, phosphatidylglycerophosphatase and protein-tyrosine phosphatase dephosphorylates PGP to form phosphatidylglycerol (PG). Last, cardiolipin synthase catalyzes the synthesis of cardiolipin by transferring a phosphatidyl group from a second CDP-diacylglycerol to PG. It requires a divalent metal cation cofactor. Newly synthesized cardiolipins undergo remodeling, a process carried out by the enzyme tafazzin. A mutated tafazzin gene disrupts this post-synthetic remodeling and causes Barth syndrome (BTHS), an X-linked human disease (PMID: 16973164). BTHS patients seem to lack acyl specificity and consequently, many potential cardiolipin species can exist (PMID: 16226238).


Lafutidine H2-Antihistamine Action,Drug Action,Lafutidine (also known as INN) is a second generation histamine H2 receptor antagonist that can be used for treating ulcers and reflux. Inhibition of histamine H2 receptor can inhibit histamine-stimulated gastric acid secretion which will lead to reduced gastric volume and acidity.


Chlorphenamine H1-Antihistamine Action,Drug Action

Chlorphenamine (chlorpheniramine) 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.


Pheniramine H1-Antihistamine Action,Drug Action

Pheniramine 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.


Dexchlorpheniramine H1-Antihistamine Action,Drug Action

Dexchlorpheniramine 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.


Brompheniramine H1-Antihistamine Action,Drug Action

Brompheniramine 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.


Dexbrompheniramine H1-Antihistamine Action,Drug Action

Dexbrompheniramine 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.


Triprolidine H1-Antihistamine Action,Drug 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.


Dimetindene H1-Antihistamine Action,Drug Action

Dimetindene 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.


Mepyramine H1-Antihistamine Action,Drug Action

Mepyramine (pyrilamine) 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.


Antazoline H1-Antihistamine Action,Drug Action

Antazoline 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.


Chloropyramine H1-Antihistamine Action,Drug Action

Chloropyramine 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.


Talastine H1-Antihistamine Action,Drug Action

Talastine 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.


Tripelennamine H1-Antihistamine Action,Drug Action

Tripelennamine 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.


Histapyrrodine H1-Antihistamine Action,Drug Action

Histapyrrodine 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.


Methapyrilene H1-Antihistamine Action,Drug Action

Methapyrilene 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. Methapyrilene, formerly marketed in many drug products, was shown to be a potent carcinogen. Manufacturers voluntarily withdrew methapyriline drug products from the market in May and June 1979 (DB04819).


Thonzylamine H1-Antihistamine Action,Drug Action

Thonzylamine 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.


Cardiolipin (CL) is an important component of the inner mitochondrial membrane where it constitutes about 20% of the total lipid composition. It is essential for the optimal function of numerous enzymes that are involved in mitochondrial energy metabolism. (Wikipedia) Cardiolipin biosynthesis occurs mainly in the mitochondria, but there also exists an alternative synthesis route for CDP-diacylglycerol that takes place in the endoplasmic reticulum. This second route may supplement this pathway. All membrane-localized enzymes are coloured dark green in the image. First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate. Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA). Third, the enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (PA or 1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone. PA is then transferred to the inner mitochondrial membrane to continue cardiolipin synthesis. Fourth, magnesium-dependent phosphatidate cytidylyltransferase catalyzes the conversion of PA into CDP-diacylglycerol. Fifth, CDP-diacylglycerol--glycerol-3-phosphate 3-phosphatidyltransferase synthesizes phosphatidylglycerophosphate (PGP). Sixth, phosphatidylglycerophosphatase and protein-tyrosine phosphatase dephosphorylates PGP to form phosphatidylglycerol (PG). Last, cardiolipin synthase catalyzes the synthesis of cardiolipin by transferring a phosphatidyl group from a second CDP-diacylglycerol to PG. It requires a divalent metal cation cofactor. Newly synthesized cardiolipins undergo remodeling, a process carried out by the enzyme tafazzin. A mutated tafazzin gene disrupts this post-synthetic remodeling and causes Barth syndrome (BTHS), an X-linked human disease (PMID: 16973164). BTHS patients seem to lack acyl specificity and consequently, many potential cardiolipin species can exist (PMID: 16226238).


Diphenhydramine H1-Antihistamine Action,Drug Action

Diphenhydramine is a first-generation ethanolamine 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.


Carbinoxamine H1-Antihistamine Action,Drug Action

Carbinoxamine is a first-generation ethanolamine 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.


Doxylamine H1-Antihistamine Action,Drug Action

Doxylamine is a first-generation ethanolamine 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.


Orphenadrine H1-Antihistamine Action,Drug Action

Orphenadrine is a first-generation ethanolamine 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.


Bromodiphenhydramine H1-Antihistamine Action,Drug Action

Bromodiphenhydramine (Bromazine) is a first-generation ethanolamine 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.


Clemastine H1-Antihistamine Action,Drug Action

Clemastine is a first-generation ethanolamine 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.


Chlorphenoxamine H1-Antihistamine Action,Drug Action

Chlorphenoxamine (Phenoxene) is a first-generation ethanolamine 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.


Diphenylpyraline H1-Antihistamine Action,Drug Action

Diphenylpyraline is a first-generation piperidine 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.


Phenyltoloxamine H1-Antihistamine Action,Drug Action

Phenyltoloxamine is a first-generation ethanolamine 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.


Cyclizine H1-Antihistamine Action,Drug Action

Cyclizine is a first-generation piperazine 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.


Chlorcyclizine H1-Antihistamine Action,Drug Action

Chlorcyclizine is a first-generation piperazine 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.


Hydroxyzine H1-Antihistamine Action,Drug Action

Hydroxyzine is a first-generation piperazine 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.


Meclizine H1-Antihistamine Action,Drug Action

Meclizine (Meclozine) is a first-generation piperazine 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.


Buclizine H1-Antihistamine Action,Drug Action

Buclizine is a first-generation piperazine 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.


Oxatomide H1-Antihistamine Action,Drug Action

Oxatomide is a first-generation piperazine 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.


Cetirizine H1-Antihistamine Action,Drug Action

Cetirizine is a second-generation piperazine 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.


Cardiolipin (CL) is an important component of the inner mitochondrial membrane where it constitutes about 20% of the total lipid composition. It is essential for the optimal function of numerous enzymes that are involved in mitochondrial energy metabolism. (Wikipedia) Cardiolipin biosynthesis occurs mainly in the mitochondria, but there also exists an alternative synthesis route for CDP-diacylglycerol that takes place in the endoplasmic reticulum. This second route may supplement this pathway. All membrane-localized enzymes are coloured dark green in the image. First, dihydroxyacetone phosphate (or glycerone phosphate) from glycolysis is used by the cytosolic enzyme glycerol-3-phosphate dehydrogenase [NAD(+)] to synthesize sn-glycerol 3-phosphate. Second, the mitochondrial outer membrane enzyme glycerol-3-phosphate acyltransferase esterifies an acyl-group to the sn-1 position of sn-glycerol 3-phosphate to form 1-acyl-sn-glycerol 3-phosphate (lysophosphatidic acid or LPA). Third, the enzyme 1-acyl-sn-glycerol-3-phosphate acyltransferase converts LPA into phosphatidic acid (PA or 1,2-diacyl-sn-glycerol 3-phosphate) by esterifying an acyl-group to the sn-2 position of the glycerol backbone. PA is then transferred to the inner mitochondrial membrane to continue cardiolipin synthesis. Fourth, magnesium-dependent phosphatidate cytidylyltransferase catalyzes the conversion of PA into CDP-diacylglycerol. Fifth, CDP-diacylglycerol--glycerol-3-phosphate 3-phosphatidyltransferase synthesizes phosphatidylglycerophosphate (PGP). Sixth, phosphatidylglycerophosphatase and protein-tyrosine phosphatase dephosphorylates PGP to form phosphatidylglycerol (PG). Last, cardiolipin synthase catalyzes the synthesis of cardiolipin by transferring a phosphatidyl group from a second CDP-diacylglycerol to PG. It requires a divalent metal cation cofactor. Newly synthesized cardiolipins undergo remodeling, a process carried out by the enzyme tafazzin. A mutated tafazzin gene disrupts this post-synthetic remodeling and causes Barth syndrome (BTHS), an X-linked human disease (PMID: 16973164). BTHS patients seem to lack acyl specificity and consequently, many potential cardiolipin species can exist (PMID: 16226238).


Cinnarizine H1-Antihistamine Action,Drug Action

Cinnarizine is a first-generation piperazine 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.


Levocetirizine H1-Antihistamine Action,Drug Action

Levocetirizine is a second-generation piperazine H1-antihistamine. It has also been labeled as a third-generation antihistamine because it is developed from a second-generation antihistamine (cetirizine). 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.


Promethazine H1-Antihistamine Action,Drug Action

Promethazine is a first-generation phenothiazine 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.


Alimemazine H1-Antihistamine Action,Drug Action

Alimemazine (trimeprazine) is a first-generation phenothiazine 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.


Cyproheptadine H1-Antihistamine Action,Drug Action

Cyproheptadine is a first-generation piperidine 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.


Phenbenzamine H1-Antihistamine Action,Drug 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.


Fenethazine H1-Antihistamine Action,Drug Action

Fenethazine (phenethazinum) is a first-generation phenothiazine 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.


Hydroxyethylpromethazine H1-Antihistamine Action,Drug Action

Hydroxyethylpromethazine is a first-generation phenothiazine 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.


Isothipendyl H1-Antihistamine Action,Drug Action

Isothipendyl is a first-generation phenothiazine 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.


Mequitazine H1-Antihistamine Action,Drug Action

Mequitazine is a first-generation phenothiazine 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.


Methdilazine H1-Antihistamine Action,Drug Action

Methdilazine is a first-generation phenothiazine 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.


Oxomemazine H1-Antihistamine Action,Drug Action

Oxomemazine is a first-generation phenothiazine 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.


Azatadine H1-Antihistamine Action,Drug Action

Azatadine is a first-generation piperidine 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.


Ketotifen H1-Antihistamine Action,Drug Action

Ketotifen is a first-generation piperidine 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.


Doxepin H1-Antihistamine Action,Drug Action

Doxepin 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.