Arachidonic acid is metabolized in the vascular endothelium to epoxytrienoic acids (EETs or EpETrEs) by cytochrome P450 enzymes. The EETs are released in response to acetylcholine, bradykinin, arachidonic acid, or cyclic stretch. (±)14(15)-EET-SI is the methyl sulfonamide analog of 14(15)-EET. This substitution results in a metabolically more stable compound because it is not sensitive to β-oxidation or membrane esterification. (±)14(15)-EET-SI is equipotent to 14(15)-EET in vascular agonist activity as measured by relaxation of precontracted bovine coronary arteries. In addition, 14(15)-EET and the methyl sulfonamide analog both stimulate tyrosine phosphorylation and induce mitogenesis in renal epithelial cells.
PD153035 is a ATP-competitive EGFR inhibitor with an IC50 and Ki of 25 and 6 pM. PD153035 effectively blocks the enhancement of mitogenesis, induction of early gene expression, and oncogenic transformation that occur in response to EGF receptor stimulation. With human fibroblasts and epidermoid carcinoma cells, PD153035 at nanomolar concentrations rapidly inhibits EGFR autophosphorylation. With breast and ovarian cancer cells, PD153035 not only blocks cell growth via inhibition of EGFR, but also upregulates the expression of the tumor suppressor retinoic acid receptor-beta 2 (RAR-beta2).
Phosphatidylinositols, comprising about 10% of total cellular phospholipids, are glycerophospholipids featuring a glycerol backbone, two non-polar fatty acid tails (primarily C16:0 and C18:0), and a polar inositol head group. Synthesized from cytidine diphosphate diacylglycerol (CPD-DAG) and myoinositol via phosphoinositol synthase, these compounds play pivotal roles in cellular processes, including calcium regulation, vesicle trafficking, mitogenesis, cell survival, and actin rearrangement. Phosphorylation of their inositol rings produces phosphoinositides, crucial for these cellular functions. [Matreya, LLC. Catalog No. 1048]
Mammalian bombesin-like peptide neurotransmitter that is an agonist for the gastrin-releasing peptide receptor (GRPR). GRP has been reported to activate GABAergic interneurons in the amygdala leading to increased GABA release and fear suppression in mice