N-Salicyloyltryptamine

• CAT Number: I042926
• CAS Number: 31384-98-2
• Molecular Formula: C17H16N2O2
• Molecular Weight: 280.32
• Purity: ≥95%
• Synonyms: 2-hydroxy-N-[2-(1H-indol-3-yl)ethyl]benzamide
• InChI: InChI=1S/C17H16N2O2/c20-16-8-4-2-6-14(16)17(21)18-10-9-12-11-19-15-7-3-1-5-13(12)15/h1-8,11,19-20H,9-10H2,(H,18,21)
• InChIKey: XBPYTDZHCNJRBY-UHFFFAOYSA-N
• SMILES: C1=CC=C2C(=C1)C(=CN2)CCNC(=O)C3=CC=CC=C3O

N-Salicyloyltryptamine acts on voltage-dependent Na+, Ca2+, and K+ ion channels inhibitor. N-Salicyloyltryptamine inhibits K+ currents with an IC50 value of 34.6 μM (Ito). N-Salicyloyltryptamine also exhibits anticonvulsant, anti-inflammatory, analgesic, and vasorelaxation effect[1]-[5].
N-Salicyloyltryptamine (1 ng/mL-1 μg/mL; 24 h) presents no cytotoxicity and causes no oxidative stress in RAW 264.7 cells at low concentration, but (50 and 100 μg/mL) inhibits cell viability with an IC50 value of 22.75 μg/mL[1].
N-Salicyloyltryptamine (1 μg/mL; 24 h) reverses some redox and inflammatory parameters induced by LPS without interfering in cell viability[1].
N-Salicyloyltryptamine (1 μg/mL; 24 h) inhibits LPS-induced TNF-α and IL-1β release, as well as CD40 and TNF-α protein up-regulation[1].
N-Salicyloyltryptamine (1 μg/mL; 24 h) inhibits phosphorylation of ERK 1/2 and IκBα and p65 nuclear translocation (NF-kB activation)[1].
N-Salicyloyltryptamine (17 μM) inhibits K+ current by 59.27% (Ito) and 73.18% (IKD), inhibits L-type Ca2+ currents by 54.9%, and shows few inhibition with high concentration (170 μM) on TTX-sensitive Na+ current by 22.1% in GH3 cells[2].
N-Salicyloyltryptamine (0.01 nM-100 µM) produces vasorelaxation through activation of the NO/sGC/cGMP pathway and reduction of calcium influx[3].
N-Salicyloyltryptamine (100 mg/kg; i.p.; 60 min before stimulation challenge) significantly inhibits pentylenetetrazol (PTZ)-induced seizures and partially eliminates the extensor reflex of maximal electric-induced seizures test[4].
N-Salicyloyltryptamine (100 mg/kg, 200 mg/kg; i.p.; single dose) shows antinociceptive and nerve excitability effects[5].

Reference

[1]. Gasparotto J, et al Effect of N-salicyloyltryptamine (STP), a novel tryptamine analogue, on parameters of cell viability, oxidative stress, and immunomodulation in RAW 264.7 macrophages. Cell Biol Toxicol. 2013 Jun;29(3):175-87.
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[2]. Araújo DA, et al. N-salicyloyltryptamine, a new anticonvulsant drug, acts on voltage-dependent Na+, Ca2+, and K+ ion channels. Br J Pharmacol. 2003 Dec;140(7):1331-9.
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[3]. Veras RC, et al. N-Salicyloyltryptamine, an N-Benzoyltryptamine Analogue, Induces Vasorelaxation through Activation of the NO/sGC Pathway and Reduction of Calcium Influx. Molecules. 2018 Jan 28;23(2):253.
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[4]. Oliveira FA, et al. Anticonvulsant properties of N-salicyloyltryptamine in mice. Pharmacol Biochem Behav. 2001 Feb;68(2):199-202.
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[5]. Quintans LJ Jr, et al. Bioassay-guided evaluation of antinociceptive effect of N-salicyloyltryptamine: a behavioral and electrophysiological approach. J Biomed Biotechnol. 2010;2010:230745.
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