TC-N 22A
TC-N 22A is a potent, selective, orally active and brain-permeable mGlu4 PAM with an EC50 of 9 nM in human mGlu4-expressing BHK cells. TC-N 22A is less active (EC50>10 μM) in agonist and PAM model at mGlu 1, 2, 3, 5, and 7 receptors. TC-N 22A has the potential for research of CNS disease in vivo.
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- CAS No.: 1314140-00-5
- 화학식: C14H13N5S
- 분자량:283.35
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
IC50 & Target
EC50: 9 nM (mGlu4 receptor)EC50: >10 μM (mGlu 1, 2, 3, 5, and 7 receptors)[1]
In Vitro
TC-N 22A is selected for mGlu4 and has an EC50 of 9 nM in human mGlu4-expressing BHK cells. This compound is less active in agonist and PAM modelinactive (EC50>10 μM), and is inactive in negative allosteric modulator (NAM) model at mGlu 1, 2, 3, 5, and 7 receptors (IC50 >10 μM) and shows low potential for hERG channel inhibition[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 1314140-00-5
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분자량 283.35
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화학식 C14H13N5S
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SMILES
C1(NC2=NC3=C(CCCC4=NNC=C43)S2)=CC=CC=N1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
용액&용해도
In Vivo:
The following protocol is derived from the literature and is for reference only. It is recommended to first try a small sample.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Working solution concentration: 0.22 mg/mL
Protocol
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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
TC-N 22A Related Classifications
HY-18679 Related Classifications
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