AM12814
AM12814 is a potent and partial CB1 and CB2 agonist with Ki values of 0.7 nM and 3.4 nM. AM12814 can inhibit cAMP accumulation and recruitse β-arrestin 2. AM12814 exhibits cannabimimetic effects. AM12814 can be used for the research of neurological disease, suah as catalepsy.
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- CAS. Nr.: 3054511-18-8
- Formel: C24H38F3NO2
- Molecular Weight:429.56
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
rCB1-R 0.7 nM (Ki) |
hCB2-R 3.4 nM (Ki) |
In Vitro
AM12814 (Compound 12) binds to cannabinoid receptors with high affinity, with Ki values of 0.7 nM (rCB1) and 3.4 nM (hCB2)[1].
AM12814 (30 mins) inhibits Forskolin (HY-15371)-stimulated cAMP accumulation in 3xHA-hCB1-CHO and 3xHA-hCB2-CHO cells with EC50 values of 8.75 nM and 22 nM[1].
AM12814 (90 mins) recruitses β-arrestin 2 in hCB1-DRx-CHO and hCB2-DRx-U2OS cells with EC50 values of 25 nM and 5.6 nM[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.
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Animal Model:CD1 mice[1]
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Dosage:0.3, 1 and 3 mg/kg
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Administration:Intraperitoneally injection
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Result:Increased immobility time in the ring test.
Reduced core body temperature.
Prolonged tail-flick latency in the hot water test.
Alleviated CFA (HY-153808)-induced mechanical hypersensitivity.
Chemical Information
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CAS. Nr. 3054511-18-8
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Molecular Weight 429.56
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Formel C24H38F3NO2
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SMILES
O=C(N[C@H](C)CO)CCC/C=C\C/C=C\C/C=C\[C@@H](C)/C=C\CCCCC(F)(F)F
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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.
Protokoll
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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
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)