M119
M119 (NSC 119910) is a Gβγ subunit and PLCβ3 inhibitor with selective activity toward μ-opioid receptor-related pathways. M119 selectively inhibits Gβγ-dependent PLCβ3 activation, reduces inositol phosphate production, and enhances μ-opioid receptor-mediated antinociception. M119 attenuates acute μ-opioid receptor agonist-induced antinociceptive tolerance and physical dependence in mice. M119 can be used for pain-related research.
For research use only. We do not sell to patients.
- CAS No.: 500533-94-8
- Formula: C20H18O7
- Molecular Weight:370.35
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Storage:
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
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
μ Opioid Receptor/MOR |
PLC |
In Vitro
M119 (10-30 µM; 30 min) concentration-dependently inhibits µ-opioid receptor (hMOR-CHO cell)-mediated inositol phosphate production, with significant inhibition observed at 10 µM and 30 µM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
M119 (100 nM; intracerebroventricular injection; single administration; given 30 minutes prior to Naloxone treatment) significantly attenuates acute Naloxone (HY-17417A)-induced physical dependence in mice, reducing the withdrawal jumping response triggered by the μ-opioid receptor antagonist by approximately 68%[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (male, 20-30 g)[1]
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Dosage:100 nM (coadministered with intracerebroventricular agonists); 100 mg/kg (administered immediately before subcutaneous μ-opioid receptor agonist)
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Administration:i.c.v.; single dose; coadministered with agonists; i.p.; single dose; administered immediately before subcutaneous μ-opioid receptor agonist
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Result:Produced a 10-fold leftward shift in μ-opioid receptor agonist's antinociceptive dose-response curve.
Produced a sevenfold leftward shift in μ-opioid receptor agonist DAMGO's dose-response curve, with DAMGO's ED50 decreasing from 0.07 nmol to 0.01 nM.
Produced a twofold leftward shift in κ-opioid receptor agonist U50,488's dose-response curve, with U50,488's ED50 decreasing from 37 nmol to 17 nM.
Had no significant effect on antinociception mediated by δ1-selective agonist DPDPE or δ2-selective agonist Deltorphin II.
Produced a fourfold leftward shift in μ-opioid receptor agonist's antinociceptive dose-response curve, with μ-opioid receptor agonist's ED50 decreasing from 5.0 mg/kg to 1.3 mg/kg.
Had no effect on baseline tail-withdrawal latencies.
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Animal Model:ICR mice (male, 20-30 g)[1]
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Dosage:100 nM
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Administration:i.c.v.; single dose; administered 30 min before Naloxone
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Result:Reduced μ-opioid receptor antagonist-induced withdrawal jumps from an average of 71 to 23.
Chemical Information
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CAS No. 500533-94-8
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Molecular Weight 370.35
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Formula C20H18O7
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SMILES
O=C(C1CCCCC1C2=C3C=CC(C(O)=C3OC4=C2C=CC(O)=C4O)=O)O
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Synonyms
NSC 119910
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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.
Purity & Documentation
References
[1]. Mathews JL, et al. A novel Gbetagamma-subunit inhibitor selectively modulates mu-opioid-dependent antinociception and attenuates acute morphine-induced antinociceptive tolerance and dependence. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2008 Nov 19;28(47):12183-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
M119 Related Classifications
HY-177218 Related Classifications
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