α-Synuclein (61-75) is a peptide fragment derived from the larger protein α-Synuclein. α-Synuclein is predominantly found in presynaptic nerve terminals and is considered to be a biomarker candidate for Parkinson's disease (PD).
Synucleozid is a potent the SNCA mRNA inhibitor that encodes α-synuclein protein (IC50=1.5 μM), has the potential for the investigation of Parkinson’s disease.
tau Protein α-synuclein-IN-2 (Compound 14T) 是一种可以穿透血脑屏障的tau和α-syn抑制剂。tau Protein α-synuclein-IN-2 通过硫脲连接子结构以剂量依赖方式减少α-syn的寡聚。该化合物在生物传感器细胞中阻止tau聚集的种子效应,并在M17D神经母细胞瘤模型中显示出抗包涵体效应。此外,tau Protein α-synuclein-IN-2 能够抑制Aβ斑块的形成,展示了其在阿尔茨海默病和帕金森病研究中的潜力。
Rasagiline-13C3is intended for use as an internal standard for the quantification of rasagiline by GC- or LC-MS. Rasagiline is an inhibitor of monoamine oxidase B (MAO-B; IC50= 4.43 nM for the rat brain enzyme).1It is selective for MAO-B over MAO-A (IC50= 412 nM for the rat brain enzyme). It inhibits serum and NGF withdrawal-induced apoptosis of PC12 cells when used at concentrations ranging from 0.01 to 100 μM.2Rasagiline inhibits rat brain MAO-Bin vivo(ED50= 0.1 mg kg).1It reduces cerebral edema in a mouse model of traumatic brain injury.2Rasagiline (0.1 mg kg) reduces cortical and hippocampal levels of full-length and soluble amyloid precursor protein (APP) in rats and mice. It also reduces α-synuclein-induced substantia nigral neuron loss and improves motor dysfunction in a mouse model of Parkinson's disease.3Formulations containing rasagiline have been used in the treatment of Parkinson's disease. 1.Youdim, M.B.H., Gross, A., and Finberg, J.P.Rasagiline [N-propargyl-1R(+)-aminoindan], a selective and potent inhibitor of mitochondrial monoamine oxidase BBrit. J. Pharmacol.132(2)500-506(2001) 2.Youdim, M.B.H., and Weinstock, M.Molecular basis of neuroprotective activities of rasagiline and the anti-Alzheimer drug TV3326 [(N-propargyl-(3R) aminoindan-5-YL)-ethyl methyl carbamate]Cell. Mol. Neurobiol.21(6)555-573(2001) 3.Kang, S.S., Ahn, E.H., Zhang, Z., et al.α-Synuclein stimulation of monoamine oxidase-B and legumain protease mediates the pathology of Parkinson's diseaseEMBO J.37(12)e98878(2018)
DOPAL is an aldehyde product of the oxidative deamination of dopamine by monoamine oxidase.[1] It can be further oxidized to 3,4-dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase (ALDH) and, to a lesser extent reduced to 3,4-dihydroxyphenyl ethanol (DOPET). DOPAL is toxic to neurons.[2],[3] It can also oligomerize and precipitate α-synuclein, an event associated with Parkinson's disease.[2] Mice lacking cytosolic and mitochondrial forms of ALDH display increased levels of DOPAL as well as neurodegeneration and motor dysfunction characteristic of Parkinson’s disease.[4]
α-Synuclein inhibitor 3 (Compound 7g) is a potent inhibitor of α-synuclein (α -Syn) aggregation. It has potential applications in Parkinson's disease research [1].
α-Synuclein inhibitor 4 (compound 3gh) is a highly effective and blood-brain barrier-permeable inhibitor of α-Synuclein aggregation. It displays potent activity, with an IC50 value of 0.98 μM, and exhibits a remarkable inhibition ratio of 91.2% at a concentration of 30 μM [1].
α-Synuclein inhibitor 6 (compound 3ge) is a highly effective and blood-brain barrier-permeable inhibitor that targets the aggregation of α-Synuclein (α-Syn). It exhibits a potent inhibitory activity, with an IC50 value of 1.70 μM, leading to a remarkable inhibition ratio of 94.4% at 30 μM [1].
CLR01 is a molecular tweezer. CLR01 reduces aggregated, pathologic, and seeding-competent α-synuclein in experimental multiple system atrophy. CLR01 inhibits aberrant superoxide dismutase 1 (SOD1) self-assembly in vitro and in the G93A-SOD1 mouse model of ALS. CLR01 inhibits Ebola and Zika virus infection. CLR01 Stabilizes a Disordered Protein-Protein Interface. CLR01, Modulates Aggregation of the Mutant p53 DNA Binding Domain and Inhibits Its Toxicity.