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

SK-129 Chemical Structure

CAS No. : 1919889-97-6

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Description

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].

In Vitro

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.

SK-129 Related Antibodies
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 %
In Vivo

SK-129 (25-50 μM; administered on days 2 and 4, day 5) rescues DA neuron degeneration, motor deficits, oxidative stress, and behavioral deficits in both early and postdisease UA196 C. elegans PD models in a dose-dependent manner[1].
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.

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.
Molecular Weight

1006.92

Formula

C51H42N8O15
CAS No.
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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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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