N-Salicyloyltryptamine(STP) is a tryptamine analogue with anticonvulsant, anti-inflammatory, analgesic, and vasorelaxation effect. N-Salicyloyltryptamine acts as the voltage-dependent Na +, Ca 2+, and K + ion channels inhibitor which inhibits K + currents with an IC 50 value of 34.6 μM ( /to) [1] - [5].

N-Salicyloyltryptamine, at concentrations ranging from 1 ng/mL to 1 μg/mL over 24 hours, exhibits no cytotoxic effects or oxidative stress in RAW 264.7 cells at lower concentrations. However, at higher concentrations (50 and 100 μg/mL), it significantly reduces cell viability, demonstrating an IC 50 value of 22.75 μg/mL. At a concentration of 1 μg/mL for 24 hours, this compound counteracts certain redox and inflammatory markers induced by LPS without affecting cell viability. Furthermore, it effectively inhibits the release of LPS-induced TNF-α and IL-1β, as well as the up-regulation of CD40 and TNF-α proteins. It also blocks the phosphorylation of ERK 1/2 and IκBα, alongside preventing the nuclear translocation of p65, thus hindering NF-kB activation. At 17 μM, N-Salicyloyltryptamine significantly suppresses K+ currents by 59.27% (Ito) and 73.18% (IKD), L-type Ca2+ currents by 54.9%, and exerts a moderate inhibition of TTX-sensitive Na+ currents by 22.1% at a high concentration (170 μM) in GH3 cells. This compound induces vasorelaxation from 0.01 nM to 100 μM through the activation of the NO/sGC/cGMP pathway and reducing calcium influx. Assays on RAW 264.7 cells show at 1 μg/mL concentration, N-Salicyloyltryptamine maintains cell viability while reducing CD40, TNF-α, and RAGE immunocontent, and inhibiting the phosphorylation of ERK1/2 and IκBα, along with p65 nuclear translocation.

N-Salicyloyltryptamine administered intraperitoneally (i.p.) at 100 mg/kg, 60 minutes before stimulation challenge, markedly diminishes pentylenetetrazol (PTZ)-induced seizures and mitigates the extensor reflex in maximal electric-induced seizure tests [4]. Furthermore, at dosages of 100 mg/kg and 200 mg/kg, it exhibits antinociceptive effects and reduces nerve excitability [5]. In studies involving male Swiss mice weighing 25-35 g, a single dose of N-Salicyloyltryptamine at 50 mg/kg significantly lowered both the occurrence of clonic PTZ seizures and mortality rates. The same compound, at 100 mg/kg and 200 mg/kg dosages, decreased the incidence of tonic hindlimb extension (THE) triggered by maximal electroshock (MES) [4]. Additionally, a single intraperitoneal injection of N-Salicyloyltryptamine at 100 mg/kg and 200 mg/kg notably lessened the licking response induced by acetic acid in the paw, illustrating its analgesic potential [5].