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α-Synuclein is an abundant neuronal protein that is highly enriched in presynaptic nerve terminals. α-synuclein regulates synaptic vesicle trafficking and subsequent neurotransmitter release. Genetics and neuropathology studies link α-synuclein to Parkinson's disease (PD) and other neurodegenerative disorders. Accumulation of misfolded oligomers and larger aggregates of α-synuclein defines multiple neurodegenerative diseases called synucleinopathies, but the mechanisms by which α-synuclein acts in neurodegeneration are unknown.
Semaglutide is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
6PPD-Q (6PPD-Quinone) is an environmental pollutant that can be detected in human urine and is widely present in the environment. 6PPD-Q targets and binds to CNR2, CNR1, AA2AR, LCAT, and TRPA1, with CNR2 exhibiting the highest binding affinity, potentially acting as a CNR2 receptor agonist to activate cannabinoid receptors. 6PPD-Q induces intestinal inflammation and barrier damage by disrupting mitochondrial function, reducing neuronal glycolysis metabolites and TCA cycle intermediates, and exacerbating α-synuclein (α-syn) aggregation.
6PPD-Q is applicable in research on environmental toxicology, neurodegenerative diseases, and inflammation-related disorders.
Semaglutide TFA is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide TFA promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide TFA also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide TFA has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide TFA can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
Fast Green FCF is a sea green triarylmethane food dye, with absorption maximum ranging from 622 to 626 nm. Fast Green FCF inhibits α-synuclein aggregation, as well as Aβ and P2X4 receptor, and TLR4/Myd88/NF-κB. Fast Green FCF is widely used as a staining agent like quantitative stain for histones at alkaline pH after acid extraction of DNA, and as a protein stain in electrophoresis. Fast Green FCF improves cognitive impairment, depression, relieves pain allergies, and promotes reproductive function.
Buntanetap ((+)-Phenserine) is a multiple neurotoxic protein translation inhibitor with oral activity, including amyloid precursor protein (APP), α-synuclein (αSYN) and huntingtin protein (HTT). Buntanetap has anti-inflammatory effects and can be used in the study of Alzheimer's disease and Parkinson's disease.
ZPD-2 inhibits the aggregation of C-terminally truncated and full-length α-synuclein. ZPD-2 inhibits the formation and fibrillation of α-Syn, thereby preventing its propagation. ZPD-2 can be used in research of Parkinson's disease.
Tau Protein/α-synuclein-IN-2 (Compound 14T) is a blood-brain barrier penetrating tau and α-syn inhibitor. Through its thiourea linker structure, Tau Protein/α-synuclein-IN-2 dose-dependently reduces α-syn oligomerization. In biosensor cells, Tau Protein/α-synuclein-IN-2 prevents the seeding effect of tau aggregation. In the M17D neuroblastoma model, Tau Protein/α-synuclein-IN-2 exhibits anti-inclusion effects. Additionally, Tau Protein/α-synuclein-IN-2 reduces Aβ plaque formation. Tau Protein/α-synuclein-IN-2 holds promise for Alzheimer's disease and Parkinson's disease research.
HUP-55 is a prolyl endopeptidase inhibitor (IC50 = 5 nM). HUP-55 reduces the dimerization of α-synuclein in Neuro2a cells and induces autophagy (Autophagy) in HEK293 cells. It also decreases the increase in reactive oxygen species (ROS) production induced by hydrogen peroxide in SH-SY5Y cells at a concentration of 10 μM. In a mouse Parkinson’s disease model, HUP-55 (10 mg/kg) improves motor function (reduces the use frequency of the impaired paw) and decreases the levels of harmful oligomers of α-synuclein in the striatum caused by overexpression of α-synuclein.
Beta-asarone is an orally active and BBB-penatrable anti-inflammatory agent and neuroprotective agent, which is the major ingredient of Acorus tatarinowii Schott. Beta-asarone can protect nerve cells from apoptosis and autophagy, inhibit expression of α-synuclein, as well as myocardial protection. Beta-asarone can be used in the study of neurological and cardiovascular diseases.
Semaglutide, FITC labeled is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide, FITC labeled promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide, FITC labeled also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide, FITC labeled has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide, FITC labeled can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
SynuClean-D (SC-D) is an inhibitor of α-synuclein aggregation, disrupts mature amyloid fibrils, prevents fibril propagation, and abolishes the degeneration of dopaminergic neurons in an animal model of Parkinson’s disease.
Harmol is an orally active β-carboline alkaloid. Harmol is a TFEB activator and monoamine oxidase inhibitor. Harmol can induce cell mitosis, Autophagy and Apoptosis. Harmol promotes the degradation of α-synuclein by regulating the autophagy-lysosomal pathway. Harmol has anti-tumor, anti-depressant and anti-aging activities. Harmol improves motor impairment in a mouse Parkinson's disease model.
Utreloxastat (PTC857) is an orally active and blood-brain barrier-permeable 15-lipooxygenase inhibitor. Utreloxastat is a weak inhibitor of CYP1A2 and 2B6 with an IC50 of >5.3 μM. Utreloxastat reduces oxidative stress and inhibits the consumption of reduced glutathione and ferroptosis. Utreloxastat can be used in the study of neurodegenerative diseases characterized by high levels of oxidative stress and mitochondrial pathology, such as amyotrophic lateral sclerosisc.
Prasinezumab (PRX 002) is a humanized IgG1 monoclonal antibody directed against aggregated α-synuclein. Prasinezumab has the potential for Parkinson's disease research.
PROTACα-synuclein degrader 6 (compound T3) is a PROTAC degrader of α-synuclein and tau, with EC50 of 1.57 μM and 4.09 μM, respectively. PROTACα-synuclein degrader 6 plays an important role in neurodegenerative diseases (NDs) research (Blue:ubiquitin E3 ligasecereblon ligand (HY-14658), Black: linker (HY-128803); Pink: Ligand for target protein (HY-151035)).
Semaglutide acetate is a long-acting, selective, competitive, orally active GLP-1R agonist that can penetrate the blood-brain barrier. After activating GLP-1R, Semaglutide acetate promotes insulin secretion, inhibits gastric emptying and appetite, and at the same time enhances autophagy, inhibits oxidative stress and apoptosis. Semaglutide acetate also regulates mitochondrial function and lipid metabolism (such as reducing de novo lipogenesis in the liver). Semaglutide acetate has activities such as lowering blood sugar, reducing weight, neuroprotection (such as improving motor function in Parkinson's disease models, reducing α-synuclein aggregation) and improving hepatic steatosis. Semaglutide acetate can be used for the study of neurodegenerative diseases and liver diseases such as type 2 diabetes, obesity, Parkinson's disease, metabolic associated fatty liver disease (MASLD), and cancer.
PBT434 methanesulfonate is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 methanesulfonate can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 methanesulfonate inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 methanesulfonate prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 methanesulfonate has the potential for the research of Parkinson’s disease (PD).
Senkyunolide A is a phthalide, anti-tumor cell proliferation agent with anticancer activity. Senkyunolide A protects neurons from corticosterone (HY-B1618)-induced apoptosis by decreasing protein phosphatasePP2A and α-synuclein phosphorylation and protein level. Senkyunolide A also inhibits osteoarthritis through the NLRP3 signaling pathway and suppresses the expression of CD137, a diagnostic biomarker for atherosclerosis.
Cuminaldehyde is the main component of Cuminum cyminum and has multiple biological activities, including anti-inflammatory, anti-cancer, anti-diabetic, anti-injury, anti-neuropathy and antibacterial effects. Cuminaldehyde is an inhibitor of aldose reductase (IC50= 0.00085 mg/mL), α-glucosidase (IC50=0.5 mg/mL) and lipoxygenase (IC50=1370 μM). Cuminaldehyde also inhibits the fibrillation of α-synuclein and prevents its aggregation. Cuminaldehyde has potential application value in the research of neurodegenerative diseases, cancer, diabetes and neuropathic pain diseases.
