BPR1M492
BPR1M492 is a brain-penetrant μ-opioid receptor (MOR) agonist an in vitro EC50 of 0.93 nM in the cAMP inhibition assay and 0.004 nM in the FLIPR Ca2+ assay without a clear signaling bias between cAMP and β-arrestin-2 pathway. BPR1M492 is a cAMP-biased nociceptin-orphanin FQ opioid peptide agonist. BPR1M492 is a weak cAMP-biased δ/κ-opioid receptor agonist. BPR1M492 demonstrates potent in vivo antinociception and can be used for pain research.
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- CAS No.: 3118558-91-8
- Formule: C21H24N2O
- Masse moléculaire:320.43
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
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Activité biologique
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μ Opioid Receptor/MOR 0.93 nM (EC50, the cAMP inhibition assay) |
μ Opioid Receptor/MOR 0.004 nM (EC50, the FLIPR Ca2+ assay) |
NOP Receptor/ORL1 52.89 nM (EC50, the cAMP inhibition assay) |
κ Opioid Receptor/KOR 2410 nM (EC50, the FLIPR Ca2+ assay) |
δ Opioid Receptor/DOR 730 nM (EC50, the cAMP assay) |
BPR1M492 (compound 56) (336 s) activates MOR of CHO-K1 cells expressing human MOR and Gα15 (CHO-K1/hMOR/Gα15) with 91.7% maximum efficacy[1].
BPR1M492 fully agonizes MOR with an EC50 of 0.93 nM by the cAMP assay and NOP with an EC50 of 52.89 nM by the cAMP assay[1].
BPR1M492 weakly agonizes DOR with an EC50 of 730 nM by the cAMP assay and KOR with an EC50 of 2410 nM by the FLIPR Ca2+ assay[1].
BPR1M492 (CHO-K1 cell) effectively recruits β-arrestin-2 on MOR with an EC50 of 161 nM[1].
BPR1M492 (CHO-K1 cell) exhibits nearly no effect on β-arrestin-2 recruitment for NOP and KOR, and a partial effect for DOR with an EC50 of 2883 nM[1].
BPR1M492 fails to block the NMDAR ion channel at 3 μM and inhibits CYP1A, 2B6, 2C8, 2C9, and 3A with IC50s > 100 μM[1].
BPR1M492 inhibits CYP2C19 with an IC50 of 26 μM and 2D6 with an IC50 of 2.1 μM[1].
BPR1M492 inhibits hERG with an IC50 of 1.92 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
| Species | Dose | Route | T1/2 (Plasma) | T1/2 (Brain) | Cmax (Brain) | Tmax (Plasma) | Tmax (Brain) | AUC0-∞ (Plasma) | AUC0-∞ (Brain) |
|---|---|---|---|---|---|---|---|---|---|
| Mice[1] | 1 mg/kg | s.c. | 0.2 h | 0.3 h | 1457 ng/g | 0.1 h | 0.3 h | 181 ng·h/mL | 856 h·ng/g |
BPR1M492 (0.168 mg/kg; s.c.; 12 min) takes effect within approximately 5 minutes after subcutaneous (s.c.) administration in hMOR+ and mMOR-/- mice which indicates that BPR1M492 shows potential as an analgesic for postoperation[1].
BPR1M492 (0.054 mg/kg-0.162 mg/kg; s.c.; 30-120 min) produces potent antinociception and shows smaller reductions in oxygen saturation and respiratory rate in the incisional pain model in hMOR+ and mMOR-/- mice than TRV130 under the present dosing conditions[1].
BPR1M492 retains effective antinociception in the incisional pain model in hMOR+ and mMOR-/- mice and shows the clearest improvement in withdrawal-related behaviors in hMOR+ and mMOR-/- mice relative to TRV130[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mice with pharmacological treatments targeting acute thermal pain[1].
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Dosage:0.054 mg/kg, 0.108 mg/kg, 0.162 mg/kg
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Administration:s.c.; 120 min
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Result:Increased pain thresholds in a dose-dependent manner in response to thermal.
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Animal Model:The hMOR+ and mMOR-/- mice in the incisional pain model[1].
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Dosage:0.054 mg/kg, 0.108 mg/kg, 0.162 mg/kg
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Administration:s.c.; 120 min
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Result:Increased pain thresholds in a dose-dependent manner in response to mechanical stimuli.
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Animal Model:Mice were anesthetized with a cocktail of ketamine (100 mg/kg) and xylazine (10 mg/kg) administered intraperitoneally[1].
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Dosage:0.054 mg/kg, 0.108 mg/kg
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Administration:s.c.; 30 min
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Result:Showed smaller reductions in oxygen saturation and respiratory rate than TRV130 under the present dosing conditions and compensatoryly increased heart rate.
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Animal Model:Male hMOR+; mMOR -/- mice[1].
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Dosage:0.270 mg/kg
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Administration:s.c.; 30 min
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Result:Demonstrated that adverse effects were abolished in MOR knockout (mMOR-/-) mice, suggesting that the side effects are indeed mediated through the MOR.
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Animal Model:Male C57BL/6J mice[1].
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Dosage:0.270 mg/kg, 0.054 mg/kg, 0.108 mg/kg, 0.216 mg/kg
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Administration:s.c.; 24 h
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Result:Showed lower CPP responses than TRV130 at some of the tested dose levels (1 × and 8 × ED50) and elicited significant place preference only at medium to high doses (2 × and 4 × ED50).
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Animal Model:Male C57BL/6J mice[1].
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Dosage:0.054 mg/kg, 0.108 mg/kg, 0.162 mg/kg, 0.216 mg/kg, 0.270 mg/kg
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Administration:twice a day; 5 days
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Result:Elicited only mild withdrawal signs.
Chemical Information
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CAS No. 3118558-91-8
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Masse moléculaire 320.43
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Formule C21H24N2O
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SMILES
CN1CC2=CC=CC=C2C[C@@H]1CNC(C3CC(C=CC=C4)=C4C3)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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