5-Methoxytryptophol

5-Methoxytryptophol is a 5-methoxyindole alcohol structurally homologous to Melatonin (HY-B0075). It is secreted by the mammalian pineal gland and exhibits an inverse circadian rhythm. 5-Methoxytryptophol regulates bone metabolism by activating the ERK1/2 pathway. It reduces the levels of pro-inflammatory cytokines TNF-α and IL-1β, as well as proteolytic enzymes MMP-1 and MMP-2, in serum and dental pulp tissues, thereby ameliorating acute pulpitis. 5-Methoxytryptophol induces rapid sleep in mice, while high doses cause respiratory depression and death. 5-Methoxytryptophol. 5-Methoxytryptophol can be used in studies related to acute pulpitis, hypnosis, and bone metabolism^[1]. In Vitro:5-Methoxytryptophol (0.001-2.5 mM; 24 h) slightly reduces the metabolic activity of MC3T3-E1 preosteoblasts^[2].
5-Methoxytryptophol (0.001-2.5 mM; 48 h) exhibits cytotoxicity against MC3T3-E1 preosteoblasts at concentrations of 1 mM and 2.5 mM, while doses of 0.001 mM and 0.01 mM exert protective effects^[2].
5-Methoxytryptophol (0.001-2.5 mM; 14 days) reduces the total RNA content of MC3T3-E1 preosteoblasts at the concentration of 2.5 mM^[2].
5-Methoxytryptophol (0.001-1 mM; 14 days) reduces Rankl mRNA expression in MC3T3-E1 preosteoblasts in a dose-dependent manner (with a stronger inhibitory effect at low doses than melatonin), and decreases Opg mRNA expression at concentrations of 0.1 and 1 mM^[2].
5-Methoxytryptophol (0.1 mM; 14 days) significantly promotes osteocalcin secretion by MC3T3-E1 preosteoblasts^[2].
5-Methoxytryptophol (0.1 mM; 14 days) enhances the mineralization of MC3T3-E1 preosteoblasts^[2].
5-Methoxytryptophol (0.1 mM; 5 days) inhibits the formation of multinucleated TRAP-positive osteoclasts in RANKL-stimulated RAW264.7 preosteoclasts^[2].
5-Methoxytryptophol (0.1 mM; 5 days) reduces the mRNA expression of Mmp-9 and CtsK in RANKL-stimulated RAW264.7 preosteoclasts, without altering the mRNA level of Trap^[2].
5-Methoxytryptophol (0.1 mM; 5 days) inhibits the bone resorption activity of RANKL-stimulated RAW264.7 preosteoclasts on dentin slices^[2].
5-Methoxytryptophol (0.1 mM; 2 h) activates the ERK1/2 pathway in MC3T3-E1 osteoprogenitor cells and RAW264.7 preosteoclasts (by upregulating the expression of phosphorylated ERK1/2), and this activation is inhibited by pretreatment with the melatonin receptor antagonist luzindole (HY-101254)^[2].
5-Methoxytryptophol (0.01-10 mM; 50 min) inhibits lipid peroxidation in rat liver microsomal membranes, with an IC₅₀ of 0.7 mM. Concentrations of 0.01-3 mM dose-dependently maintain membrane fluidity against oxidative stress, while the 10 mM concentration, although capable of inhibiting lipid peroxidation, fails to prevent membrane rigidification^[4].
5-Methoxytryptophol (0.01-10 mM; 30 min) reduces the membrane fluidity of rat liver microsomal membranes at concentrations of 0.3-10 mM, and does not alter the level of lipid peroxidation in the absence of oxidative stress^[4]. In Vivo:5-Methoxytryptophol (5 mg/kg; i.p.; single dose) significantly reduces proinflammatory cytokine and matrix metalloproteinase levels in serum and pulp tissue, and improves histopathological outcomes in a rat model of lipopolysaccharide-induced acute pulpitis^[1].
5-Methoxytryptophol (200-700 mg/kg; i.p.; single dose) induces rapid-onset sleep in healthy CD-1 mice, with mean sleep duration ranging from 5.2 min at 300 mg/kg to 43.9 min at 600 mg/kg, and an acute LD₅₀ of about 750 mg/kg^[3].