FMJ-01-054
FMJ-01-054 is a selective dopamine D4 Receptor (D4R) antagonist with a Ki od 77.7 nM. FMJ-01-054 shows subtype selectivity over D2R and D3R. FMJ-01-054 inhibits D4R-mediated β-arrestin recruitment and cAMP production with IC50 values of 3800 nM and 134 nM, respectively. FMJ-01-054 has desirable plasma half-life and brain exposure in rats. FMJ-01-054 can be used for the research of neurological disorders.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C19H21ClN6
- Molecular Weight:368.86
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
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Human D4 Receptor 77.7 nM (Ki) |
Human D2 Receptor >100,000 nM (Ki) |
Human D3 Receptor >100,000 nM (Ki) |
In Vitro
FMJ-01-054 (compound 17) (0.3 nM-100 μM; 1 h) binds to the human dopamine D4 receptor with high affinity (Ki = 77.7 nM) and >1287-fold selectivity over D2 and D3 receptors[1].
FMJ-01-054 acts as an antagonist at the human dopamine D4 receptor with an IC50 of 3800 nM and has no agonist activity[1].
FMJ-01-054 (30 min) inhibits dopamine D4 receptor-mediated cAMP production as an antagonist with an IC50 of 134 nM[1].
FMJ-01-054 exhibits metabolic stability in rat and human liver microsomes with half-lives of 64.77 min and 46.84 min, respectively[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Tmax | Brain-to-Plasma Ratio |
|---|---|---|---|---|
| Rat[1] | 5 mg/kg | i.p. | 0.25 h | 0.3 |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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Molecular Weight 368.86
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Formel C19H21ClN6
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SMILES
CC1=CC(N2N=NC(CN3CCN(C4=NC=C(Cl)C=C4)CC3)=C2)=CC=C1
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Keywords
- FMJ-01-054
- Dopamine Receptor
- rats
- substance use disorders
- D3R
- amide analogs
- human dopamine D? receptor
- blood-brain barrier
- D4R
- schizophrenia
- Sprague?Dawley rats
- l-dopa-induced dyskinesias
- Dopamine D4 Receptor
- D2R
- attention-deficit/hyperactivity disorder
- cAMP
- β-arrestin recruitment
- human liver microsomes
- rat liver microsomes
- Inhibitor
- inhibitor
- inhibit