5-Methoxytryptoline
5-Methoxytryptoline acts as a modulator of the Serotonin transporter complex, as well as a ligand for the 5-HT2A and 5-HT2C receptors, with Ki values of 130 nM and 140 nM for the 5-HT2A and 5-HT2C receptors, respectively. 5-Methoxytryptoline inhibits the active uptake of Serotonin (HY-B1473A) and Tryptamine (HY-B2132) in platelets. 5-Methoxytryptoline induces behavioral excitation, cortical electroencephalographic desynchronization, and dose-dependent elevation of plasma prolactin, followed by behavioral sedation and partial recovery of cortical electroencephalographic voltage. 5-Methoxytryptoline antagonizes Reserpine (HY-N0480)-induced sedation, reduced locomotor activity, and hypothermia. 5-Methoxytryptoline exerts dose-dependent effects on behavior and cortical electroencephalographic activity in freely moving rats. 5-Methoxytryptoline can be used in depression-related research.
For research use only. We do not sell to patients.
- CAS No.: 30439-19-1
- Formula: C12H14N2O
- Molecular Weight:202.26
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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
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
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5-HT2A Receptor 130 nM (Ki) |
5-HT2C Receptor 140 nM (Ki) |
5-Methoxytryptoline (Compound 22) binds to cloned rat 5-HT2A receptors with a Ki value of 130 nM, and its affinity is 30-fold higher than that of the unsubstituted parent compound[2].
5-Methoxytryptoline binds to cloned rat 5-HT2C receptors with a Ki value of 140 nM, showing significantly higher affinity compared with the unsubstituted parent compound[2].
5-Methoxytryptoline significantly increases the Kd value of [3H]Imipramine (HY-B1490A) binding to platelet membranes from 0.61 nM to 2.30 nM without altering Bmax, confirming that it acts as a competitive inhibitor[3].
5-Methoxytryptoline potently displaces 3H-Imipramine from 5-hydroxytryptamine (5-HT) reuptake-associated binding sites in synaptosomal preparations from rat or mouse cerebral cortex, with an IC50 of 150 nM[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
5-Methoxytryptoline (50-100 μmol; i.v.; single injection) induces rapid, short-lasting behavioural stimulation and electrocortical desynchronization in freely moving Wistar rats when administered intravenously, with duration dependent on dose[1].
5-Methoxytryptoline (104 nmol; i.c.v.; single injection) administered via intraventricular microinjection antagonizes reserpine-induced sedation in Wistar rats; 5-Methoxytryptoline (70-210 nmol; i.c.v.; single injection) reverses reserpine-induced hypothermia in Wistar rats, with hypothermia reversal occurring within 60-90 seconds[1].
5-Methoxytryptoline (12.5-50 mg/kg; i.v.; single dose; 3.125-50 mg/kg; i.p.; single dose) induces dose-dependent increases in plasma PRL and dose-dependent reductions in plasma GH in healthy adult male Sprague-Dawley rats after acute iv or ip administration, with a threshold ip dose of 6.25 mg/kg for both effects[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar rats (adult male, 200-250 g, stereotaxically implanted with third cerebral ventricle guide cannulas)[1]
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Dosage:4 nmol; 21 nmol; 42 nmol; 105 nmol; 210 nmol; 335 nmol
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Administration:i.c.v.; single injection at 0.2 μl/min
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Result:Induced dose-dependent behavioural stimulation (increased exploratory/locomotor activity, stereotyped movements, wet dog shakes, rearing, heightened tactile reactivity) followed by 1-2 hours of sedation.
Caused behavioural stimulation with durations of 5 minutes (4 nmol), 22 minutes (21 nmol), 35 minutes (42 nmol), 57 minutes (105 nmol), 68 minutes (210 nmol), and 75 minutes (335 nmol).
Caused electrocortical desynchronization with a significant (P < 0.05) decrease in total voltage, most pronounced in the 0.25-3 Hz, 3-6 Hz, and 6-9 Hz frequency bands.
Produced dose-dependent duration of electrocortical desynchronization.
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Animal Model:Wistar rats (adult male, 200-250 g, chronic jugular vein polyethylene tube implantation)[1]
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Dosage:50 μmol; 100 μmol
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Administration:i.v.; single injection
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Result:Induced behavioural stimulation and electrocortical desynchronization similar to intraventricular administration.
Produced effects that started immediately after infusion and lasted 5 minutes (50 μmol) to 15 minutes (100 μmol).
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Animal Model:Wistar rats (adult male, 200-250 g, reserpine-induced sedation and hypothermia model)[1]
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Dosage:104 nmol (sedation antagonism); 70-210 nmol (hypothermia reversal)
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Administration:i.c.v.; single injection
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Result:Antagonized reserpine-induced sedation and reduced motor activity when administered 5, 15, or 30 minutes before reserpine at 104 nmol.
Reversed reserpine-induced hypothermia (which caused a mean body temperature decrease of -1.2°C) within 60-90 seconds of administration at 70 nmol, 140 nmol, and 210 nmol doses.
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Animal Model:Sprague-Dawley (Crl:CD(SD)BR) (adult male, 175-200 g)[4]
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Dosage:12.5-50 mg/kg (i.v.); 3.125-50 mg/kg (i.p.)
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Administration:i.v.; single dose; i.p.; single dose
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Result:Induced a rapid, transient dose-dependent increase in plasma PRL levels, with peak values at 15 minutes; levels returned to baseline by 45-60 minutes.
Induced a dose-dependent increase in plasma PRL levels at 20 minutes, with a threshold effective dose of 6.25 mg/kg; the correlation coefficient between log-dose and hyperprolactinemic effect was 0.97.
Induced a dose-dependent inhibition of GH pulsatory peaks; the 50 mg/kg dose completely abolished GH peaks.
The area under the GH concentration-time curve was significantly reduced in a dose-dependent manner relative to controls.
Induced a dose-dependent reduction in plasma GH levels at 20 minutes: 6.25 mg/kg reduced GH to 7.64 ng/mL (p < 0.05 vs saline control of 30.82 ng/mL); 12.5 mg/kg, 25 mg/kg, and 50 mg/kg reduced GH to 5.20 ng/mL, 5.56 ng/mL, and 2.58 ng/mL respectively (all p < 0.01 vs saline).
The correlation coefficient between log-dose and plasma GH levels was -0.79.
Chemical Information
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CAS No. 30439-19-1
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Molecular Weight 202.26
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Formula C12H14N2O
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SMILES
O(C1=CC=CC=2NC3=C(C12)CCNC3)C
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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.
Purity & Documentation
References
[1]. Nistico G, et al. Behavioural and electrocortical power spectrum effects of 5-methoxytryptoline and other analogs after intraventricular administration in rats. European journal of pharmacology. 1987 Oct 06;142(1):121-8. [Content Brief]
[2]. Grella B, et al. Binding of beta-carbolines at 5-HT(2) serotonin receptors. Bioorg Med Chem Lett. 2003 Dec 15;13(24):4421-5. [Content Brief]
[3]. Segonzac A, et al. 5-Methoxytryptoline, a competitive endocoid acting at [3H]imipramine recognition sites in human platelets. Journal of neurochemistry. 1985 Jul;45(1):249-56. [Content Brief]
[4]. Rovescalli AC, et al. Endocrine effects of 5-methoxytryptoline, 5-hydroxytryptoline and tryptoline, putative modulators of rat serotonergic system. Journal of endocrinological investigation. 1987 Feb;10(1):65-72. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
5-Methoxytryptoline Related Classifications
HY-177797 Related Classifications
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