Cl-NQTrp

Cl-NQTrp signifcantly disrupts the preformed fbrillar aggregates of Tau-derived PHF6 (VQIVYK) peptide and full-length tau protein[1][2].

Research Areas >> Neurological Disease

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]. Animal Model: Virgin females, carrying either the eye GMR -Gal4 driver or the pan-neuronal driver elavc155 -Gal4 on chromosome X, were collected and crossed with males carrying UAS-h tau on the 2nd chromosome or with wild-type Oregon-R (OR) males as a control[2]. Dosage: 0.75 mg/mL. Administration: Dripped every other day. Result: Inhibited PHF6 aggregation and ameliorates eye neurodegeneration Drosophila overexpressing the human tau protein (htau).

[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.