Cl-NQTrp signifcantly disrupts the preformed fbrillar aggregates of Tau-derived PHF6 (VQIVYK) peptide and full-length tau protein[1][2].
Cl-NQTrp efciently disassembled pre-formed PHF6 peptide fbrils[1].Cl-NQTrp has the potential to induce conformational changes in PHF6 peptide oligomers[1].
Cl-NQTrp could be a unique potential therapeutic for AD since it targets aggregation of both Aβ and tau[2].Cl-NQTrp significantly alleviates the shorter life span of htau-expressing flies, leading to 58% viability on day 29[2].
References:
[1]. V Guru KrishnaKumar, et al. Mechanistic insights into remodeled Tau-derived PHF6 peptide fibrils by Naphthoquinone-Tryptophan hybrids. Sci Rep. 2018 Jan 8;8(1):71.
[2]. Moran Frenkel-Pinter, et al. Cl-NQTrp Alleviates Tauopathy Symptoms in a Model Organism through the Inhibition of Tau Aggregation-Engendered Toxicity. Neurodegener Dis. 2017;17(2-3):73-82.