N-Salicyloyltryptamine 是一种电压依赖性离子通道抑制剂，包括 Na+、Ca2+、K+通道。N-Salicyloyltryptamine 抑制 K+电流的IC50为 34.6 μM (Ito)。N-Salicyloyltryptamine 还具有抗惊厥、抗炎、镇痛，和血管舒张的作用。
| 生物活性 | N-Salicyloyltryptamine acts on voltage-dependent Na+, Ca2+, and K+ion channels inhibitor. N-Salicyloyltryptamine inhibits K+currents with anIC50value of 34.6 μM (Ito). N-Salicyloyltryptamine also exhibits anticonvulsant, anti-inflammatory, analgesic, and vasorelaxation effect[1]-[5]. |
| IC50& Target | L-type calcium channel | potassium channel 34.6 μM (IC50) |
|
体外研究
(In Vitro) | 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 IC50value 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].
Cell Viability Assay[1] | Cell Line: | RAW 264.7 cell | | Concentration: | 0.001, 0.05, 1, 50, 100 μg/mL | | Incubation Time: | 24 hours | | Result: | Resulted no effect on RAW 264.7 cell viability at 1 μg/mL; however, concentrations of 50 and 100 μg/mL significantly decreased both MTT reduction and SRB incorporation. |
RT-PCR[1] | Cell Line: | RAW 264.7 cell | | Concentration: | 1 μg/mL | | Incubation Time: | 24 hours | | Result: | Reduced CD40, TNF-α, and RAGE immunocontent.
Inhibited ERK1/2 and IκBα phosphorylation and nuclear translocation of p65. |
|
体内研究
(In Vivo) | 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].
| Animal Model: | Male Swiss mice (25-35 g)[4] | | Dosage: | 50, 100, 200 mg/kg | | Administration: | Intraperitoneal injection; single dose; 60 min before stimulation challenge | | Result: | Reduced the incidence of clonic pentylenetetrazol (PTZ) seizures and mortality at 50 mg/kg, and decreased the incidence of tonic hindlimb extension (THE) produced by MES at 100, 200 mg/kg. |
| Animal Model: | Male Swiss mice (25-35 g)[5] | | Dosage: | 100 mg/kg; 200 mg/kg | | Administration: | Intraperitoneal injection; single dose | | Result: | Reduced the acetic acid-induced licking response of the injected paw. |
|
| 分子量 | |
| Formula | |
| CAS 号 | |
| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | Please store the product under the recommended conditions in the Certificate of Analysis. |
m.cnreagent.com