MAO-B-IN-64
MAO-B-IN-64 is an orally active, blood-brain barrier-permeable reversible competitive inhibitor of monoamine oxidase B, with an IC50 of 0.35 nM against human MAO-B and a Ki of 0.22 nM for human MAO-B. MAO-B-IN-64 exhibits antioxidant effects by scavenging free radicals. MAO-B-IN-64 exerts anti-neuroinflammatory effects by inhibiting the release of pro-inflammatory factors. MAO-B-IN-64 acts as an H2S donor by releasing hydrogen sulfide. MAO-B-IN-64 can be applied in the research of Parkinson's disease.
For research use only. We do not sell to patients.
- Formula: C18H15F2NO2S
- Molecular Weight:347.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
hMAO-B 0.35 nM (IC50) |
hMAO-B 0.22 nM (Ki) |
In Vitro
MAO-B-IN-64 (30 min) is a highly potent and selective inhibitor of recombinant human MAO-B, with an MAO-B IC50 value of 0.35 nM[1].
MAO-B-IN-64 acts as a reversible MAO-B inhibitor, as the MAO-B activity of the inhibited enzyme is largely recovered after dialysis[1].
MAO-B-IN-64 is a competitive inhibitor of recombinant human MAO-B with a Ki value of 0.22 nM[1].
MAO-B-IN-64 (100 μg/mL) possesses excellent in vitro blood-brain barrier permeability and is predicted to successfully penetrate the central nervous system[1].
MAO-B-IN-64 (compound 12d) has the highest antioxidant activity among all tested target derivatives, reaching 0.59 Trolox equivalent[1].
MAO-B-IN-64 (2.5-50 μM) shows no cytotoxicity in PC12 cells up to 50 μM, and exerts significant neuroprotective effects to improve the viability of H2O2-injured PC12 cells[1].
MAO-B-IN-64 (2.5-10.0 μM) potently and dose-dependently reduces LPS-triggered intracellular ROS production in BV2 microglial cells[1].
MAO-B-IN-64 (2.5-10.0 μM) exerts potent anti-neuroinflammatory effects in in vitro LPS-activated BV2 microglial cells by suppressing multiple inflammatory mediators including NO, TNF-α, IL-6, and iNOS[1].
MAO-B-IN-64 (5.0-10 μM) effectively alleviates MPP+-induced neuronal apoptosis and rescues cell viability in SH-SY5Y cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
MAO-B-IN-64 (30 mg/kg; i.g.; single administration) exhibits favorable pharmacokinetic properties, good BBB penetration with an AUCbrain/plasma ratio of 0.83, and in vivo metabolic cleavage that generates the active metabolite 9a for sustained action[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Balb/C mice[1]
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Dosage:8.3 mg/kg; 17.5 mg/kg; 43.7 mg/kg
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Administration:p.o.; once daily; 12 consecutive days
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Result:Mitigated MPTP-induced deficits in the climbing exploration test, with the 43.7 mg/kg dose producing effects slightly superior to the equimolar positive control.
Reduced the prolonged beam transit time observed in the MPTP model in the beam walking test.
Improved motor function scores in a dose-dependent manner in the traction test, with the 43.7 mg/kg group showing the best performance.
Reduced both T-turn and T-total times in the pole test at 43.7 mg/kg relative to the model group.
Moderately recovered striatal dopamine content at 8.3 mg/kg and 17.5 mg/kg, with the 43.7 mg/kg group exhibiting a significant increase in dopamine levels.
Produced a 56.4% reduction in striatal malondialdehyde content at 43.7 mg/kg relative to the model group.
Restored striatal sulfide (H2S) concentration in a dose-dependent manner, reaching 22.7 nmol/mg protein at 43.7 mg/kg.
Increased the number of tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra and striatum, preserving this neuronal population against MPTP-induced damage.
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Animal Model:Balb/C mice[1]
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Dosage:30 mg/kg
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Administration:i.g.; single administration
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Result:Reached a peak plasma concentration of 1262.8 ng/mL at 1.0 hour, with an AUC0-ₜ of 3501.0 ng/mL/h and plasma half-life of 3.04 h.
Reached a maximum brain concentration of 813.3 ng/mL at 2.0 hours, with an AUC0-ₜ of 2916.1 ng/mL/h and brain half-life of 3.29 h.
Achieved an AUCbrain/plasma ratio of 0.83, confirming excellent central nervous system penetrability.
Generated active metabolite 9a detected in both plasma and brain, with plasma T1/2 of 3.65 h and brain T1/2 of 3.89 h.
Chemical Information
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Molecular Weight 347.38
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Formula C18H15F2NO2S
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SMILES
O=C1SC(NCC=C)C2=CC=C(OCC3=CC(F)=C(F)C=C3)C=C21
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Human pluripotent stem cell midbrain dopaminergic neuron differentiation
Human pluripotent stem cells are directed toward midbrain dopaminergic neurons by first inducing a neural floor-plate-like progenitor state, then patterning cells with ventralizing SHH signaling and midbrain/WNT-FGF cues, and finally maturing progenitors into neurons expressing dopaminergic markers such as TH, NURR1/NR4A2, PITX3, DAT/SLC6A3, VMAT2/SLC18A2, GIRK2/KCNJ6, FOXA2, LMX1A, and EN1. The main readouts are loss of pluripotency, acquisition of FOXA2+/LMX1A+ midbrain floor-plate progenitors, emergence of βIII-tubulin+/MAP2+ neurons, and production of TH+ dopaminergic neurons with molecular, dopamine-release, and electrophysiological features of midbrain dopaminergic identity.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
MAO-B-IN-64 Related Classifications
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