KDS12025
KDS12025 is a blood-brain barrier-permeable, orally active H2O2-decomposing peroxidase enhancer. KDS12025 enhances the H2O2-decomposing pseudoperoxidase activity of Hb without altering oxygen transport function, and reduces intracellular H2O2 load. KDS12025 reduces abnormal H2O2 levels and inhibits the production of COL1. KDS12025 restores cerebral blood flow, maintains neuronal excitability, membrane properties, synaptic connections and corticospinal tract fibers, reduces cerebral edema and exerts neuroprotective effects. KDS12025 improves motor function and overall neurological function. KDS12025 can be used in the research of ischemic stroke, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, aging-related neurodegenerative diseases and rheumatoid arthritis.
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- CAS. Nr.: 2769053-56-5
- Formel: C16H20N2O
- Molecular Weight:256.34
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Speicherung:
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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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
Beschreibung
In Vitro
KDS12025 significantly protects primary cortical neurons against astrocyte-mediated in vitro neurotoxicity induced by H2O2[1].
KDS12025 (1 μM; 30 min) potently enhances the H2O2-decomposing pseudoperoxidase activity of purified hemoglobin, with an EC50 of 0.04 μM, and effectively achieves H2O2 decomposition even at extremely low Hb concentrations[2].
KDS12025 (10 μM; 24 h) effectively reduces H2O2 levels induced by Aβ, putrescine and 6-OHDA (HY-B1081) in primary cultured hippocampal astrocytes, with an EC50 of 0.5 μM, and its antioxidant effect depends on Hbβ in astrocytes[2].
KDS12025 binds strongly to the proximal heme site of the hemoglobin β subunit with a binding energy of −16.5 kcal/mol, thereby enhancing the pseudoperoxidase activity of Hb[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
KDS12025 (1 mg/kg/day; p.o.; ad libitum in drinking water; 4 weeks) fully restores motor function and reverses Parkinson's disease-related pathology in A53T α-synuclein mice, with efficacy dependent on both astrocytic and neuronal Hbβ[2].
KDS12025 (0.1-1 mg/kg/day; p.o.; ad libitum in drinking water; 22 months) increases median survival by ~14%, restores locomotor function, prevents neuronal loss, reverses astrocytic atrophy, and restores astrocytic Hbβ levels in aging C57BL/6J mice[2].
KDS12025 (0.1-10 mg/kg/day; i.p., p.o.; daily, ad libitum in drinking water; 7 days, 2 weeks, 16 days) potently reverses Alzheimer's disease-related memory impairment, neurodegeneration, astrogliosis, oxidative stress, and neuronal dysfunction in APP/PS1 mice, with efficacy dependent on astrocytic Hbβ[2].
KDS12025 (1 mg/kg/day) mitigates rheumatoid arthritis pathology and systemic inflammation in collagen-induced arthritis mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:APP/PS1 mice (10-18 months old, both sexes)[2]
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Dosage:3 mg/kg/day; 10 mg/kg/day; 0.1 mg/kg/day
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Administration:i.p.; daily; 16 days, 7 days; p.o.; ad libitum in drinking water; 2 weeks, 16 days
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Result:Improved memory impairment.
Reduced hippocampal reactive astrocyte (GFAP) and microglia (Iba1) levels.
Reversed astrogliosis.
Normalized aberrant tonic GABA currents.
Restored astrocytic hemoglobin β (Hbβ) levels.
Reduced oxidative stress marker 8-OHdG levels.
Normalized astrocytic GABA levels.
Restored neuronal spike probability.
Abolished all effects following astrocytic Hbβ gene silencing.
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Animal Model:A53T α-synuclein overexpression mice[2]
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Dosage:1 mg/kg/day
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Administration:p.o.; ad libitum in drinking water; 4 weeks
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Result:Rescued motor impairment.
Reversed tyrosine hydroxylase (TH)-positive dopaminergic neuronal loss.
Reduced astrogliosis.
Normalized abnormally elevated astrocytic GABA levels.
Restored astrocytic and neuronal Hbβ levels.
Partially abolished effects following either astrocytic or neuronal Hbβ gene silencing.
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Animal Model:C57BL/6J mice (14 months old, female)[2]
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Dosage:0.1 mg/kg/day; 1 mg/kg/day
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Administration:p.o.; ad libitum in drinking water; 22 months
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Result:Increased median survival by ~14% in both dose groups.
Enabled 46.7% of female mice to survive to 31 months when all control mice had died.
Restored locomotor function in 26-month-old mice to levels comparable to 12-month-old mice.
Prevented neuronal loss in the hippocampal CA1 region.
Preserved TH-positive dopaminergic neurons in the substantia nigra pars compacta.
Reversed astrocytic atrophy, restoring astrocytic arborization to 18-month-old control levels.
Restored reduced astrocytic Hbβ levels to exceed those in 18-month-old mice.
Chemical Information
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CAS. Nr. 2769053-56-5
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Molecular Weight 256.34
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Formel C16H20N2O
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SMILES
CNC(C=C1)=CC=C1NCCC2=C(C=CC=C2)OC
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
KDS12025 Related Classifications
HY-186316 Related Classifications
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