VCU-1012
VCU-1012 is a serotonin 2A receptor (5-HT2AR) agonist, with a pEC50 of 5.81 and a pKi of 5.75 against human receptors. VCU-1012 binds to the canonical orthosteric binding pocket of 5-HT2AR, triggers intracellular calcium release and Gαq protein dissociation, and its agonistic activity depends on specific amino acid residues in the receptor binding pocket. VCU-1012 can be used in research related to depression, anxiety disorders, and chemotherapy-induced mood disorders.
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- Formel: C12H15ClN4
- Molecular Weight:250.73
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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5-HT2A Receptor 5.75 (pKi) |
5-HT2A Receptor 5.81 (pEC50) |
VCU-1012 (compound 15) displaces [3H]ketanserin in HEK293 cells stably expressing human 5-HT2AR, with a pKi of 5.75 for 5-HT2AR[1].
VCU-1012 induces Ca2+ mobilization in HEK293 cells stably expressing 5-HT2AR, with a pEC50 of 5.81 and an Emax of 46.25%, exhibiting partial agonist activity; Volinanserin (HY-14940) completely blocks VCU-1012-induced Ca2+ mobilization[1].
VCU-1012 induces concentration-dependent dissociation of Gαq in HEK293 cells expressing 5-HT2AR, exhibiting partial agonist activity relative to 5-HT; this effect is reversed by the 5-HT2AR antagonist volinanserin and is absent in parental HEK293 cells[1].
VCU-1012 (10 μM) does not induce significant 5-HT3R-mediated inward currents in Flp-In T-REx HEK293 cells expressing 5-HT3R, indicating that VCU-1012 has no detectable 5-HT3R agonist activity[1].
VCU-1012 exhibits low binding affinity for 5-HT1BR, 5-HT2CR and 5-HT7R, with Ki values all > 1000 nM; it shows overall low off-target activity in screening against more than 40 receptors and transporters[1].
VCU-1012 (100 μM) displaces < 50% of [3H]LSD; it can completely displace [3H]LSD binding at lower [3H]LSD concentrations, but its apparent affinity is lower than that observed in the [3H]ketanserin displacement assay[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
VCU-1012 (1 mg/kg; i.p.; 24 h after a single administration) reduces immobility time in the forced swim test of WT mice, but exerts no such effect in 5-HT2AR KO mice; it does not significantly alter spontaneous horizontal activity or the time spent in the central area of the open field in WT mice during the same period[1].
VCU-1012 (1 mg/kg; i.p.; administered on day 15 after the final dose of paclitaxel, with tests conducted 24 h later) abolishes the light-avoiding phenotype observed in Paclitaxel (HY-B0015)-treated mice in the light-dark box test; administration of VCU-1012 alone does not alter anxiety-like behaviors, and no significant changes are observed in the number of light-dark box crossings among all groups[1].
VCU-1012 (1 mg/kg; i.p.; 24 h after a single administration) increases the total dendritic spine density and mature mushroom-shaped dendritic spine density in the prefrontal cortex of WT mice, with an effect comparable to that of psilocybin; VCU-1012 does not significantly alter stubby or thin spines, and the increases in total dendritic spines and mushroom-shaped dendritic spines are abolished in 5-HT2AR KO mice[1].
VCU-1012 (1 mg/kg; i.p.; single administration) does not significantly alter charcoal meal propulsion in the small intestine of mice, whereas Quipazine (HY-W028142) (5 mg/kg; i.p.) significantly inhibits small intestinal propulsion[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:wild-type; 5-HT2A receptor knockout[1]
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Dosage:1 mg/kg
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Administration:i.p.; single dose
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Result:Showed charcoal transit similar to vehicle-treated animals.
Did not produce significant reduction in gastrointestinal motility.
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Animal Model:wild-type[1]
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Dosage:0.1 mg/kg; 0.5 mg/kg; 1.0 mg/kg
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Administration:i.p.; single dose
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Result:Produced a dose-dependent robust increase in head-twitch response (HTR) counts that peaked during the first 15 minutes post-administration and lasted for more than 45 minutes.
Showed significantly higher cumulative HTR counts over the first 30 minutes at 0.5 mg/kg and 1.0 mg/kg compared to vehicle.
Had HTR induced by 1.0 mg/kg fully blocked by pretreatment with Volinanserin.
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Animal Model:wild-type; 5-HT2A receptor knockout[1]
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Dosage:1 mg/kg
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Administration:i.p.; single dose
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Result:Reduced immobility time in the forced-swim test compared to vehicle in wild-type mice.
Did not affect immobility time in 5-HT2A receptor knockout mice.
Showed locomotor activity and time spent in the center of an open field arena 24 hours post-treatment similar to vehicle-treated wild-type mice.
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Animal Model:wild-type[1]
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Dosage:1 mg/kg
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Administration:i.p.; single dose
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Result:Reversed the reduced time spent in the light compartment (indicative of anxiety-like behavior) induced by Paclitaxel, 24 hours post-administration.
Did not affect anxiety-like behavior when administered alone.
Showed no alteration in the number of compartment crosses, indicating no change in locomotor activity.
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Animal Model:wild-type; 5-HT2A receptor knockout[1]
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Dosage:1 mg/kg
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Administration:i.p.; single dose
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Result:Increased overall dendritic spine density in the frontal cortex of wild-type mice, comparable to the effect induced by psilocybin.
Drove the increase via a rise in mature mushroom spine density, with no changes in stubby or immature thin spine density in wild-type mice.
Did not increase overall dendritic spine density or mushroom spine density in 5-HT2A receptor knockout mice.
Chemical Information
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Molecular Weight 250.73
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Formel C12H15ClN4
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SMILES
C1(N2CCNCC2)=NC=C3C=CC=CC3=N1.Cl
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)