N-Acetyl-L-tryptophan

N-Acetyl-L-tryptophan is an antagonist of the neurokinin-1 receptor (NK-1R), disrupting the binding of substance P (SP) to NK-1R. This action provides neuroprotective effects, improving memory deficits and motor impairments. N-Acetyl-L-tryptophan is also an inhibitor of cytochrome c (Cytochrome c), and it exerts antioxidant and anti-inflammatory effects by inhibiting the expression of IL-1β and the activation of caspase-1. N-Acetyl-L-tryptophan holds promise for research in neurodegenerative and inflammatory diseases^[1][2][3][4]. In Vitro:N-Acetyl-L-tryptophan (0.001–10 nM, 0.1–300 µM, 2 h) exhibits neuroprotective effects in a H₂O₂-induced amyotrophic lateral sclerosis model (cell lines: NSC-34 motoneurons and primary motor neurons.) induced by H₂O₂^[1].
N-Acetyl-L-tryptophan (30 μM, 15 min-6 h) inhibits the secretion of Substance P (HY-P0201) and lL-1β and the activation of caspase-1 in NSC-34 motoneurons^[1].
N-Acetyl-L-tryptophan (10 μM, 2 h) inhibits cell death in a H₂O₂-induced amyotrophic lateral sclerosis model by preventing the release of cytochrome c, Smac, and AIF from the mitochondria^[1].
In Vivo:N-Acetyl-L-tryptophan (10 mg/kg, i.p., single dose) confers hepatoprotection in an ischemia-reperfusion-induced Sprague-Dawley (SD) rat liver injury model by inhibiting excessive mitophagy^[3].
N-Acetyl-L-tryptophan (0.5 mg/kg, s.c., once daily for 21 days) reduces the incidence of L-DOPA (HY-N0304)-induced dyskinesia (LID) in the hemi-parkinsonian rodent model (Sprague-Dawley rats)^[3].
N-Acetyl-L-tryptophan (50 mg/kg, i.p., once daily for 28 days) can improve spatial memory deficits in the AlCl₃-induced Wistar rat dementia model^[4].