Tenidap sodium

PUFAs are essential nutrients that show distinct deficiency syndromes when not present in adequate amounts in the diet. Virtually all cellular arachidonic acid is esterified in membrane phospholipids where its presence is tightly regulated through

PUFAs are essential nutrients that show distinct deficiency syndromes when not present in adequate amounts in the diet. Virtually all cellular arachidonic acid is esterified in membrane phospholipids where its presence is tightly regulated through

PUFAs are essential nutrients that show distinct deficiency syndromes when not present in adequate amounts in the diet. Virtually all cellular arachidonic acid is esterified in membrane phospholipids where its presence is tightly regulated through

PUFAs are essential nutrients that show distinct deficiency syndromes when not present in adequate amounts in the diet. Virtually all cellular arachidonic acid is esterified in membrane phospholipids where its presence is tightly regulated through

A selective inhibitor of DAGL&beta (IC₅₀ = 42 nM) disrupts the lipid network involved in macrophage inflammatory responses, lowering 2-AG, as well as arachidonic acid and eicosanoids, in mouse peritoneal macrophages.

A selective inhibitor of DAGL&beta (IC₅₀ = 42 nM) disrupts the lipid network involved in macrophage inflammatory responses, lowering 2-AG, as well as arachidonic acid and eicosanoids, in mouse peritoneal macrophages.

A selective inhibitor of DAGL&beta (IC₅₀ = 42 nM) disrupts the lipid network involved in macrophage inflammatory responses, lowering 2-AG, as well as arachidonic acid and eicosanoids, in mouse peritoneal macrophages.

Biochem/physiol Actions NSC61610 is an orally available and potent lanthionine synthetase C-like 2 (LANCL2) ligand that induces IL-10-mediated anti-inflammatory responses that ameliorate disease activity and decrease inflammatory lesions in the

An antagonist of the EP4 receptor (Ki = 1.3 nM) that less potently affects EP3, FP, and TP receptors (Kis = 30, 790, and 2,400 nM, respectively) and is without effect on other prostanoid receptors implicates EP4 signaling in immune and autoimmune

An antagonist of the EP4 receptor (Ki = 1.3 nM) that less potently affects EP3, FP, and TP receptors (Kis = 30, 790, and 2,400 nM, respectively) and is without effect on other prostanoid receptors implicates EP4 signaling in immune and autoimmune

An antagonist of the EP4 receptor (Ki = 1.3 nM) that less potently affects EP3, FP, and TP receptors (Kis = 30, 790, and 2,400 nM, respectively) and is without effect on other prostanoid receptors implicates EP4 signaling in immune and autoimmune

An antagonist of the EP4 receptor (Ki = 1.3 nM) that less potently affects EP3, FP, and TP receptors (Kis = 30, 790, and 2,400 nM, respectively) and is without effect on other prostanoid receptors implicates EP4 signaling in immune and autoimmune