Cl-NQTrp signifcantly disrupts the preformed fbrillar aggregates of Tau-derived PHF6 (VQIVYK) peptide and full-length tau protein. In Vitro Cl-NQTrp efciently disassembled pre-formed PHF6 peptide fbrils. Cl-NQTrp has the potential to induce conformational changes in PHF6 peptide oligomers. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Cl-NQTrp could be a unique potential therapeutic for AD since it targets aggregation of both Aβ and tau. Cl-NQTrp significantly alleviates the shorter life span of htau-expressing flies, leading to 58% viability on day 29. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Virgin females, carrying either the eye GMR -Gal4 driver or the pan-neuronal driver elav c155 -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. 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). Form:Solid