KIT-13
KIT-13 is an orally active plasmalogen derivative to inhibit neuroinflammation and mitochondrial DNA leakage associated with Mecp2 deficiency. KIT-13 significantly reduce neurological symptoms and improves the life span of the Rett Syndrome (RTT) model mice. KIT-13 can be used for the study of RTT and other neuroinflammation-related diseases.
For research use only. We do not sell to patients.
- Formula: C43H80NO7P
- Molecular Weight:754.07
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
KIT-13 (5-10 g/mL, 48 h, BV2 cells) ameliorates mitochondrial functional deficits induced by Mecp2 gene deletion and mitochondrial membrane potential in Mecp2-KD BV2 cells is restored by treatment with PK11195 (HY-19567) [1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Mecp2-knockdown BV2 cells
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Concentration:
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Incubation Time:48 h
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Result:Decreased levels of four different mtDNA-specific genes (Mt-Rnr2, MT-Co1, Mt-Nd2, Mt-Cytb).
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Cell Line:BV2 cells
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Concentration:5 µg/mL
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Incubation Time:48 h
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Result:Reduced TSPO expression.
In Vivo
KIT-13 (20 μg/kg, p.o., 6 weeks, daily) improves neurological symptoms and restores healthy microglia morphology in RTT mice brain tissue[1].
KIT-13 (p.o., 2 weeks, daily ) attenuates abnormalities in social and anxiety-like behavior in RTT model mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mecp2-KO in C57BL/6 mice (4 weeks)
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Dosage:20 μg/kg
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Administration:Daily oral administration 6 weeks
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Result:Improved the survival of Mecp2-KO mice and reduced the RTT neurological symptom score including improvement of the general condition of the Mecp2-KO mice more effectively compared with Plasmaloge, KIT-08, KIT19 or KIT20.
Reduced the soma size and increased the dendrite length in the Mecp2-KO mice, partially restoring a healthy phenotype.
Chemical Information
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Molecular Weight 754.07
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Formula C43H80NO7P
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SMILES
CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(O[C@@H](CO[P@]([O-])(OCC[NH3+])=O)COCCCCCCCCCCCCCCCCCC)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)