Reticuline shows anti-inflammatory effects through JAK2/STAT3 and NF-κB signaling pathways. Reticuline inhibits mRNA expressions of TNF-α, and IL-6 and reduces the phosphorylation levels of JAK2 and STAT3 Reticuline exhibits cardiovascular effects . In Vitro Reticuline (3 μM, 30 μM, 300 μM, 900 μM and 1.5 mM) inhibits in a concentration-dependent manner the contractions induced by Phenylephrine (1 μM), KCl (80 mM) and KCl (30 mM), (IC 50 =40±10, 240±40 and 300±40 μM, respectively) in isolated rat aortic rings with intact endothelium. Reticuline (3 μM, 30 μM, 300 μM, 900 μM and 1.5 mM) antagonizes CaCl 2 -induced contractions, and also inhibits the intracellular calcium dependent transient contractions induced by Norepinephrine (1μM), but not those induced by Caffeine (20 mM). MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Reticuline (5, 10 and 20 mg/kg, i. v., randomly) injections produced an intense hypotension in normotensive rats. The hypotensive effect of Reticuline is probably due to a peripheral vasodilation in consequence of: 1) muscarinic stimulation and NOS activation in the vascular endothelium, 2) voltage-dependent Ca 2+ channel blockade and/or 3) inhibition of Ca 2+ release from norepinephrine-sensitive intracellular stores. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid IC50& Target:JAK2 STAT3 NF-κB Human Endogenous Metabolite