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.
For research use only. We do not sell to patients.
- CAS No.: 3118558-91-8
- Formula: C21H24N2O
- Molecular Weight:320.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Opioid Receptor Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
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) |
In Vitro
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. Further protocols information, click here.
Parmacokinetics
| 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 |
In Vivo
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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Molecular Weight 320.43
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Formula C21H24N2O
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SMILES
CN1CC2=CC=CC=C2C[C@@H]1CNC(C3CC(C=CC=C4)=C4C3)=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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Formalin-Induced Paw Inflammation/Nociceptive Inflammation
The formalin-induced paw inflammation/nociceptive test is a chemical persistent pain model in rodents in which subcutaneous injection of formalin into the hind paw produces spontaneous nocifensive behaviors such as flinching and licking. The response is classically biphasic, consisting of an early acute phase (Phase I) reflecting direct activation of peripheral nociceptors (particularly C-fiber afferents), followed by a later prolonged phase (Phase II) associated with central sensitization in the spinal dorsal horn driven by sustained afferent input and inflammatory signaling. This model is widely used to evaluate analgesic and anti-inflammatory interventions because it captures both peripheral nociception and central sensitization processes within a single assay system.
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Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)