ristocetin

Ristocetin is an antibiotic isolated from Amycolatopsis lurida that is previously used to the treatment of staphylococcal infections. It is no longer used clinically because it caused thrombocytopenia and platelet agglutination.

Ristocetin A, a glycopeptide related to vancomycin, is an antibiotic produced by the microorganism Nocardia lurida[1]. Ristocetin A is currently in clinical use to treat bacterial infections [1]. Ristocetin A is an antibiotic which can be used to treat staphylococcal infections. The side effects of ristocetin A include thrombocytopenia and platelet agglutination. Ristocetin A has been used in two assays: the ristocetin cofactor assay and the ristocetin-induced platelet aggregation assay. These two assays could be used to diagnosis the von Willebrand disease and other bleeding disorders [2, 3]. The structural features of Ristocetin A are similar to vancomycin.

Ristocetin B is a biochemical.

(±)17(18)-EpETE-Ethanolamide, an ω-3 endocannabinoid epoxide, originates from eicosapentaenoic ethanolamide (EPEA) through cytochrome P450 (CYP) epoxygenases action and is decomposed by soluble epoxide hydrolase (sEH) and fatty acid amide hydrolase (FA, AH). Its endogenous synthesis occurs in LPS-stimulated and EPEA-supplemented BV-2 microglia cells, a process inhibited by the CYP inhibitor ketoconazole. This compound mitigates IL-6 and nitrite levels while enhancing IL-10 production following LPS exposure in BV-2 microglia. At a dose of 50 µM, it prevents platelet aggregation caused by arachidonic acid but not that triggered by ADP, collagen, or ristocetin. Additionally, it facilitates the dilation of constricted bovine coronary arteries (ED50= 1.1 µM) and blocks VEGF-driven tubulogenesis in human microvascular endothelial cells (HMVECs).