Methoctramine
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Methoctramine is an M2 subtype-preferring muscarinic acetylcholine receptor (mAChR) antagonist. Methoctramine blocks presynaptic inhibitory M2 autoreceptors, relieves negative feedback inhibition, increases acetylcholine release, and enhances neuromuscular transmission. Methoctramine can be used in research on amyotrophic lateral sclerosis, breast cancer, central cholinergic hypertension, and psychostimulant use disorder.
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- CAS No.: 104807-40-1
- Formule: C36H62N4O2
- Masse moléculaire:582.90
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Description
Methoctramine is an M2 subtype-preferring muscarinic acetylcholine receptor (mAChR) antagonist. Methoctramine blocks presynaptic inhibitory M2 autoreceptors, relieves negative feedback inhibition, increases acetylcholine release, and enhances neuromuscular transmission. Methoctramine can be used in research on amyotrophic lateral sclerosis, breast cancer, central cholinergic hypertension, and psychostimulant use disorder[1][2][3][4][5][6].
IC50 & Target
[4]|
mAChR2 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Thymocyte | IC50 |
> 100 μM
Compound: 1, methoctramine
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Cytotoxicity against rat thymocytes assessed as cell survival after 24 hrs by trypan blue exclusion assay
Cytotoxicity against rat thymocytes assessed as cell survival after 24 hrs by trypan blue exclusion assay
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[PMID: 23887056] |
| HeLa | IC50 |
> 100 μM
Compound: 1, methoctramine
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Cytotoxicity against human HeLa cells assessed as cell survival after 24 hrs by trypan blue exclusion assay
Cytotoxicity against human HeLa cells assessed as cell survival after 24 hrs by trypan blue exclusion assay
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[PMID: 23887056] |
| Astrocyte | EC50 |
0.0845 μM
Compound: 31
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Antiproliferative activity against mouse astrocyte cells by MTT assay
Antiproliferative activity against mouse astrocyte cells by MTT assay
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[PMID: 17417631] |
| Oocyte | IC50 |
138 nM
Compound: 1
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Antagonist activity at recombinant GluN1/GluN2A receptor (unknown origin) expressed in Xenopus laevis oocytes assessed as inhibition of glycine/glutamate-induced inward current at -70mV by two-electrode voltage clamp assay
Antagonist activity at recombinant GluN1/GluN2A receptor (unknown origin) expressed in Xenopus laevis oocytes assessed as inhibition of glycine/glutamate-induced inward current at -70mV by two-electrode voltage clamp assay
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[PMID: 23692871] |
In Vitro
Innate ImmunityCytokines & ChemokinesLipid mediators of inflammationLocal Vascular RegulationOthers
Innate Immunity
Cytokines & Chemokines
Methoctramine (10 μM; 30 min before LPS and 12 h of LPS stimulation) does not inhibit LPS-induced or Pilocarpine (HY-B0726A)-induced TNF-α release from NR8383 alveolar macrophages, indicating that M2 mAChR blockade does not suppress this response[4].
Lipid mediators of inflammation
Local Vascular Regulation
Methoctramine (1 µM; 1 h) does not alter carbachol-induced PGE2 release in TMps, with PGE2 levels at 2,799 pg/106 cells[1].
Local Vascular Regulation
Others
Methoctramine (1 µM) partially attenuates carbamoylcholine chloride (HY-B1208)-stimulated arginase activity[1].
Methoctramine (increasing concentrations; 5 h at 25°C) affinity for the M3 receptor is increased more than 6-fold by K523N and restored by S519P combined with K523N to a value close to that of M2, whereas M2 P415S reduces the affinity 10-fold[5].
Methoctramine (10 pM-1 mM; preincubated for 1 h at 25°C) binds the M2 receptor occupied by [3H]NMS with a pKD of 5.2 and slows [3H]NMS dissociation by more than 50-fold at 100 µM, whereas no allosteric effect is detected at the M3 receptor unless K523 is mutated[5].
Methoctramine (increasing concentrations; 5 h at 25°C) affinity for the M3 receptor is increased more than 6-fold by K523N and restored by S519P combined with K523N to a value close to that of M2, whereas M2 P415S reduces the affinity 10-fold[5].
Methoctramine (10 pM-1 mM; preincubated for 1 h at 25°C) binds the M2 receptor occupied by [3H]NMS with a pKD of 5.2 and slows [3H]NMS dissociation by more than 50-fold at 100 µM, whereas no allosteric effect is detected at the M3 receptor unless K523 is mutated[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
ELISA Assay[5]
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Cell Line:NR8383 alveolar macrophage cell line
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Concentration:10 μM
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Incubation Time:30 min (before LPS); 12 h (LPS stimulation)
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Result:At 10 μM, no significant inhibitory effect was observed on LPS-induced TNF-α release from NR8383 alveolar macrophages.
At 10 μM, no inhibitory effect was observed on pilocarpine-induced TNF-α release.
In Vivo
Cardiovascular RegulationGlutamate Release or ReceptorsOthers
Cardiovascular Regulation
Methoctramine (10-30 nmol/rat; i.c.v.; once; administered 10 minutes before physostigmine 60 µg/kg i.v.) produces dose-dependent bidirectional modulation of Physostigmine (HY-N6608)-induced central cholinergic cardiovascular responses in Sprague-Dawley rats, with low doses inhibiting and high doses enhancing these responses[3].
Methoctramine (10-30 nmol/rat; i.c.v.; once; administered 10 min before oxotremorine 20 µg/kg i.v.) partially inhibits oxotremorine (HY-170032)-induced central cholinergic pressor responses at low doses, whereas high doses do not alter these responses in Sprague-Dawley rats[3].
Methoctramine (10-30 nmol/rat; i.c.v.; once; administered 10 min before oxotremorine 20 µg/kg i.v.) partially inhibits oxotremorine (HY-170032)-induced central cholinergic pressor responses at low doses, whereas high doses do not alter these responses in Sprague-Dawley rats[3].
Glutamate Release or Receptors
Methoctramine (2 mg/kg; i.p.; once; administered immediately after acquisition shock) impairs passive avoidance memory retention in Wistar rats and increases CA1 fEPSP amplitude 24 hours after injection[2].
Methoctramine (12.5 µg/rat; i.c.v.; once) impairs passive avoidance memory retention and enhances CA1 fEPSP amplitude in Wistar rats[2].
Methoctramine (12.5 µg/rat; i.c.v.; once) impairs passive avoidance memory retention and enhances CA1 fEPSP amplitude in Wistar rats[2].
Others
Methoctramine (0.1-3.2 mg/kg; s.c.; administered 15 minutes before training) alone produces a limited training-compound-like response and attenuates the discriminative stimulus effects at low doses, while this effect disappears at higher doses[6].
Methoctramine (0.032 mg/kg; s.c.; administered 15 minutes before the training compound) attenuates the discriminative stimulus effects through M2 receptors, possibly with the involvement of M1 receptors[6].
Methoctramine (0.032 mg/kg; s.c.; administered 15 minutes before the training compound) attenuates the discriminative stimulus effects through M2 receptors, possibly with the involvement of M1 receptors[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, adult, 250-300 g)[3]
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Dosage:2 mg/kg
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Administration:i.p.; once; immediately after acquisition shock
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Result:Reduced retention latency to enter the dark chamber to 91.1 sec (n = 8), compared with 228.6 sec (n = 19) in saline controls.
Did not change CA1 fEPSP amplitude at 90 min after injection.
At 24 hours, untrained rats showed increased fEPSP amplitude before placement into the light-dark chamber, at 115.7% of baseline.
In trained rats, fEPSP amplitude before the camera session was 120.1% of baseline.
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Animal Model:Wistar (male, adult, 250-300 g)[3]
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Dosage:12.5 µg/rat
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Administration:i.c.v.; once; 2 µl at 0.2 µl/min
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Result:Reduced retention latency to enter the dark chamber to 98.1 sec (n = 8), compared with 228.6 sec (n = 19) in saline controls.
Rats had higher CA1 fEPSP amplitude compared with controls, and the amplitude increased over time independently of training conditions.
A persistent enhancement of fEPSP amplitude occurred immediately after injection.
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Animal Model:Sprague-Dawley (both sexes, 200-300 g)[4]
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Dosage:10 nmol/rat; 30 nmol/rat
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Administration:i.c.v.; once; 10 min before physostigmine 60 µg/kg i.v.
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Result:Did not alter mean arterial pressure or heart rate alone at 10 and 30 nmol/rat.
In physostigmine-treated rats, 10 nmol/rat reduced the pressor response and slightly attenuated the heart rate response.
30 nmol/rat increased both the pressor and tachycardiac effects of physostigmine.
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Animal Model:Sprague-Dawley (both sexes, 200-300 g)[4]
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Dosage:10 nmol/rat; 30 nmol/rat
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Administration:i.c.v.; once; 10 min before oxotremorine 20 µg/kg i.v.
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Result:10 nmol/rat partially inhibited oxotremorine-induced elevations in mean arterial pressure.
30 nmol/rat did not affect oxotremorine-induced mean arterial pressure changes.
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Animal Model:C57BL/6NTac (wild-type and M1−/−, M2−/−, M4−/− knockout; male; acquired at 4-8 weeks; trained no earlier than 7 weeks of age)[7]
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Dosage:0.032 mg/kg
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Administration:s.c.; 15 min before training compound
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Result:At 0.032 mg/kg, no effect on discrimination occurred in M2−/− mice.
A moderate rightward shift of the training compound dose-effect function was confirmed in wild-type mice and remained intact in M4−/− mice.
The rightward shift was diminished in M1−/− mice.
Related Protocols :
Chemical Information
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CAS No. 104807-40-1
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Masse moléculaire 582.90
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Formule C36H62N4O2
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SMILES
COC1=CC=CC=C1CNCCCCCCNCCCCCCCCNCCCCCCNCC2=CC=CC=C2OC
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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.
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Ethanolic Extracts of Cupressaceae Species Conifers Provide Rapid Protection against Barium Chloride-Induced Cardiac Arrhythmia. [Abstract]2024 Jul 29;17(8):1003. PMID: 39204108
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Methoctramine Related Classifications
HY-116294 Related Classifications
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