1. Neuronal Signaling
  2. α-synuclein
  3. PBT434

PBT434 is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 has the potential for the research of Parkinson’s disease (PD).

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PBT434 Chemical Structure

PBT434 Chemical Structure

CAS No. : 1232841-78-9

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Description

PBT434 is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 has the potential for the research of Parkinson’s disease (PD)[1].

In Vitro

PBT434 (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 (0-100 µM; 24 h) shows no cytotoxic effects on brain microvascular endothelial cells[2].
PBT434 (20 µM; 24 h) incrases the expression of total TfR, Cp protein level in hBMVEC[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay[2]

Cell Line: hBMVEC
Concentration: 1, 10, 20, 50, 100 µM
Incubation Time: 24 h
Result: Showed no cytotoxic effects on brain microvascular endothelial cells.

Western Blot Analysis[2]

Cell Line: hBMVEC
Concentration: 20 μM
Incubation Time: 24 h
Result: Increased the expression of total TfR, Cp protein level.
In Vivo

PBT434 (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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 12 weeks, 25 g, Male C57BL/6 J mice (6-OHDA intoxication model)[1]
Dosage: 30 mg/kg
Administration: P.o.; daily for 21 days (commencing 3 days following induction of lesion)
Result: Prevented neuronal loss following 6-OHDA, preserving up to 75% of the SNpc neurons remaining (both Nissl and tyrosine hydroxylase (TH) positive neurons) after the initial phase of cell death.
Animal Model: 12 weeks, 25 g, Male C57BL/6 J mice (6-OHDA intoxication model)[1]
Dosage: 1, 3, 10, 30, 80 mg/kg
Administration: P.o.; daily for 21 days (commenced 24 h after induction of lesion)
Result: Increased the proportion of SNpc cells rescued, increased there was a trend to improved turning behavior, significantly increased varicosity abundance, prevented the decline in levels of the presynaptic marker synaptophysin (SYNP) in a dose-dependent manner.
Molecular Weight

383.07

Formula

C12H14BrCl2N3O2

CAS No.
SMILES

O=C1N(C)C(CNCC)=NC2=C1C(Cl)=CC(Cl)=C2O.Br

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Storage

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Purity & Documentation
References
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PBT434 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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PBT434
Cat. No.:
HY-120475
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