SK-129
SK-129 is a blood-brain barrier-permeable inhibitor of α-synuclein (αS) oligomers with a Kd of 221 nM. SK-129 preferentially binds to neurotoxic αS oligomers over physiological αS monomers, inhibits αS aggregation, blocks the interaction and co-aggregation of αS with tau protein, and prevents the maturation of αS-tau condensates into amyloid aggregates. SK-129 reduces ROS production, rescues dopaminergic neuron degeneration, improves motor function, restores endogenous dopamine synthesis, increases the number of Tyrosine Hydroxylase-positive neurons, prevents brain histopathological changes, alleviates neuroinflammation, and improves survival rates in relevant models. SK-129 can be used in research related to Parkinson's disease (PD) and Lewy body dementia (LBD).
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 1919889-97-6
- 分子式: C51H42N8O15
- 分子量:1006.92
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保管条件:
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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生物活性
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化学情報
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
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生物活性
SK-129 (SK-129F; 100 nM; until signal saturation) preferentially binds pathological αS oligomers and fibrils over physiological αS monomers, with a Kd value of 221 nM for αS oligomers[1].
SK-129 (10 μM; 12 h pre- or post-treatment) potently inhibits αS aggregation in αSA53T-YFP-expressing HEK293T cells mediated by NDE derived from Parkinson's disease (PD)[1].
SK-129 (1 μM) binds to αS-tau liquid condensates and inhibits their transition to toxic amyloid-like co-aggregates, instead inducing the formation of non-amyloid gel-like aggregates[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
| Species | Dose | Route | T1/2 | Cmax | Brain-to-Plasma Ratio |
|---|---|---|---|---|---|
| Mice[1] | 20 mg/kg | i.v. | 1.78 (blood plasma) h | 139.8 (blood plasma) μg/mL | 9.4 % |
SK-129 (20 mg/kg; i.v.; every other day; 21 days) confers 100% survival up to 270 days, prevents PD-related weight loss, eliminates α-synuclein and α-synuclein-tau pathology, reduces neuroinflammation, and shows no systemic toxicity in the M83(A) mouse PD model[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:UA196 (expresses human α-synuclein and GFP in DA neurons)[1]
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Dosage:25 μM; 50 μM
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Administration:administered on days 2 and 4 (early treatment); administered on day 5 (postdisease treatment)
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Result:Restored healthy DA neuron counts to 58.2 on day 5, 56.8 on day 10, and 56.5 on day 15 at 50 μM early treatment (untreated: 42.1, 20.5, 15.2 respectively).
Restored healthy DA neuron counts to 40 on day 5, 20 on day 10, and 15 on day 15 at 25 μM early treatment.
Restored motility to levels comparable to healthy N2 worms.
Reduced ROS-dependent fluorescence intensity compared to untreated worms.
Prevented further motility enhancement by dopamine supplementation, indicating restored endogenous dopamine synthesis.
Increased healthy DA neuron counts to 38.4 on day 15 at 50 μM postdisease treatment (untreated: 13.2).
Increased healthy DA neuron counts to 31.8 on day 15 at 25 μM postdisease treatment.
Improved motility and reduced ROS levels compared to untreated worms.
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Animal Model:M83(A) (transgenic expressing human A53T mutant α-synuclein; 8-week-old; stereotactic injection of postmortem PD brain-derived α-synuclein aggregates)[1]
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Dosage:20 mg/kg
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Administration:i.v.; every other day; 21 days (10 total doses)
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Result:Achieved weight gain comparable to control mice, whereas vehicle-treated mice exhibited progressive weight loss.
Conferred 100% survival up to 270 days with no motor impairment.
Eliminated detectable phosphorylated α-synuclein (αS-129), p62 aggregation, and microglial activation (Iba1 staining) at 6 and 9 months, whereas vehicle-treated mice had extensive pathology across multiple brain regions.
Showed no abnormalities in major organs via hematoxylin and eosin staining.
Prevented α-synuclein-tau coaggregates in the substantia nigra at 9 months, whereas vehicle-treated mice had clear coaggregation.
化学情報
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CAS 番号 1919889-97-6
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分子量 1006.92
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分子式 C51H42N8O15
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SMILES
O=C(C1=NC2=C(NC(C3=NC4=C(NC(C5=NC6=C([N+]([O-])=O)C=CC=C6C(OC(C)C)=C5)=O)C=CC=C4C(OCC(O)=O)=C3)=O)C=CC=C2C(OC(C)C)=C1)NC7=C8C(C(OCC(O)=O)=CC(C(OC)=O)=N8)=CC=C7
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
SK-129 関連分類
HY-182893 関連分類
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- SK-129
- 1919889-97-6
- SK129
- SK 129
- α-synuclein
- Reactive Oxygen Species (ROS)
- Tyrosine Hydroxylase
- mouse brain homogenate
- blood-brain barrier
- α-synuclein oligomers
- iPSC midbrain dopaminergic neurons
- HEK293T cells
- parkinson’s disease
- C. elegans
- dopaminergic neuron
- human liver microsomes
- mouse plasma
- Inhibitor
- inhibitor
- inhibit