2. Neuronal Signaling Metabolic Enzyme/Protease Immunology/Inflammation NF-κB
  3. α-synuclein Reactive Oxygen Species (ROS) Tyrosine Hydroxylase
  4. SK-129

SK-129 是一种可穿过血脑屏障 α-突触核蛋白 (αS) 寡聚体抑制剂，其 Kd 为 221 nM。SK-129 相较于生理性 αS 单体，优先结合具有神经毒性的 αS 寡聚体，可抑制 αS 聚集，阻断 αS 与 tau 蛋白的相互作用及共聚集，阻止 αS-tau 凝聚体成熟为淀粉样聚集体。SK-129 可减少 ROS 生成，挽救多巴胺能神经元变性，改善运动能力，恢复内源性多巴胺合成，增加 Tyrosine Hydroxylase 阳性神经元数量，阻止脑部组织病理学改变，减轻神经炎症，并提高相关模型的存活率。SK-129 可用于帕金森病 (PD)、路易体痴呆 (LBD) 的相关研究 。

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SK-129

SK-129 Chemical Structure

CAS No. : 1919889-97-6

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SK-129 相关抗体

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α-synuclein α-synuclein Aggregation α-synuclein/CHMP2B

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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)[1].

体外研究
(In Vitro)

SK-129 (SK-129F; 100 nM; until signal saturation) 相较于生理性 αS 单体，优先结合病理性 αS 寡聚体和纤维，其与 αS 寡聚体的 Kd 值为 221 nM[1]。
SK-129 (10 μM; 12 h pre- or post-treatment) 可强效抑制帕金森病 (PD) 来源的 NDE 介导的、表达 αSA53T-YFP 的 HEK293T 细胞中的 αS 聚集[1]。
SK-129 (1 μM) 可结合 αS- tau 液态凝聚物并抑制其向毒性类淀粉样共聚集体转变，使其转而形成非淀粉样凝胶状聚集体[1]。

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

SK-129 相关抗体:
药代动力学
(Parmacokinetics)
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 %
体内研究
(In Vivo)

SK-129 (25-50 μM; 于第 2、4、5 天给) 可呈剂量依赖性地逆转早期及发病后 UA196 秀丽隐杆线虫帕金森病模型中的多巴胺能神经元退变、运动障碍、氧化应激及行为缺陷[1]。
SK-129 (20 mg/kg；静脉注射；每 2 天 1 次；共 21 天) 在 M83 (A)小鼠帕金森病 (PD) 模型中可使 270 天内的存活率达到 100%，预防 PD 相关的体重下降，清除 α-突触核蛋白及 α-突触核蛋白- tau 病理，减轻神经炎症，且无全身毒性[1]。

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

Animal Model: UA196 (expresses human α-synuclein and GFP in DA neurons)[1]
Dosage: 25 μM; 50 μM
Administration: administered on days 2 and 4 (early treatment); administered on day 5 (postdisease treatment)
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.
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]
Dosage: 20 mg/kg
Administration: i.v.; every other day; 21 days (10 total doses)
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.
分子量

1006.92

Formula

C51H42N8O15
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

SK-129 相关分类

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Keywords:

SK-1291919889-97-6SK129SK 129α-synucleinReactive Oxygen Species (ROS)Tyrosine Hydroxylaseα-SynTyrH, THmouse brain homogenateblood-brain barrierα-synuclein oligomersiPSC midbrain dopaminergic neuronsHEK293T cellsparkinson’s diseaseC. elegansdopaminergic neuronhuman liver microsomesmouse plasmaInhibitorinhibitorinhibit

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