Ledasorexton
Ledasorexton is an orally active OX2R agonist (EC50: 0.99 nM). Ledasorexton has awakening effect in mice. Ledasorexton can be used for research of neurological disease.
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- CAS No.: 2758363-88-9
- 화학식: C22H32FN5O2
- 분자량:417.52
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Orexin Receptor (OX Receptor) Isoforms
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Biological Activity
제품 설명
IC50 & Target
[1]|
OX2 Receptor 0.99 nM (EC50) |
OX1 Receptor >100 nM (EC50) |
In Vitro
Ledasorexton (Example 1) exhibits potent agonist activity against hOX2R with an EC50 of 0.99 nM, while showing weak activity against hOX1R (EC50 > 100 nM) in HEK293 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Orexin/ataxin-3 Tg mice (10-14 weeks old)[1]
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Dosage:0.3, 1, and 3 mg/kg
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Administration:i.g., single dose
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Result:Significantly prolonged sleep latency at 1 and 3 mg/kg.
Significantly suppressed cataplexy-like symptoms at 3 mg/kg.
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Animal Model:Male wild-type (WT) C57BL/6 mice (13 weeks old)[1]
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Dosage:1, 3 and 10 mg/kg
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Administration:i.g., single dose
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Result:Significantly increased spontaneous activity in mice.
Significantly increased sleep latency at 3 or 10 mg/kg.
Chemical Information
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CAS No. 2758363-88-9
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분자량 417.52
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화학식 C22H32FN5O2
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SMILES
NC([C@@H](C1CC1)N2[C@@]3([H])C[C@]([C@]4([H])[C@@H](CN(C5=NC=C(F)C=N5)CC4)OC)([H])C[C@]2([H])CC3)=O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)