For research use only. Not for therapeutic Use.
PBT434 methanesulfonate is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 methanesulfonate can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 methanesulfonate inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 methanesulfonate prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 methanesulfonate has the potential for the research of Parkinson’s disease (PD)[1][2].
PBT434 methanesulfonate (0-20 µM; 3 h) significantly inhibits H2O2 production by iron and significantly reduces the rate of Fe-mediated aggregation of α-synuclein[1].
PBT434 methanesulfonate (0-100 µM; 24 h) shows no cytotoxic effects on brain microvascular endothelial cells[2].
PBT434 methanesulfonate (20 µM; 24 h) incrases the expression of total TfR, Cp protein level in hBMVEC[2].
PBT434 methanesulfonate (30 mg/kg; p.o.; daily for 21 days) significantly preserved neuron numbers in the 6-OHDA intoxication model and shows significantly fewer rotations in the L-DOPA model, significantly reducing SNpc neuronal loss in the MPTP model[1].
| Catalog Number | I041820 |
| CAS Number | 2387898-69-1 |
| Synonyms | 5,7-dichloro-2-(ethylaminomethyl)-8-hydroxy-3-methylquinazolin-4-one;methanesulfonic acid |
| Molecular Formula | C13H17Cl2N3O5S |
| Purity | ≥95% |
| InChI | InChI=1S/C12H13Cl2N3O2.CH4O3S/c1-3-15-5-8-16-10-9(12(19)17(8)2)6(13)4-7(14)11(10)18;1-5(2,3)4/h4,15,18H,3,5H2,1-2H3;1H3,(H,2,3,4) |
| InChIKey | UBTJWJNTOFSHON-UHFFFAOYSA-N |
| SMILES | CCNCC1=NC2=C(C(=CC(=C2O)Cl)Cl)C(=O)N1C.CS(=O)(=O)O |
| Reference | [1]. Finkelstein DI, et al. The novel compound PBT434 prevents iron mediated neurodegeneration and alpha-synuclein toxicity in multiple models of Parkinson’s disease. Acta Neuropathol Commun. 2017 Jun 28;5(1):53. [2]. Bailey DK, Clark W, Kosman DJ. The iron chelator, PBT434, modulates transcellular iron trafficking in brain microvascular endothelial cells. PLoS One. 2021 Jul 26;16(7):e0254794. |
