5-HT2C agonist-13
5-HT2C agonist-13 is an orally active, selective and brain-penetrant 5-HT2C receptor agonist with human 5-HT2C receptor EC50 of 16 nM, Ki of 20 nM. 5-HT2C agonist-13 functionally activates 5-HT2C receptors, reduces food intake, reduces body weight gain, and exhibits effects reversible by a selective 5-HT2C antagonist. 5-HT2C agonist-13 can be used for the research of obesity.
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- CAS No.: 850033-84-0
- Formule: C14H15F3N2O
- Masse moléculaire:284.28
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
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- Pureté et documentation
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Activité biologique
Description
IC50 & Target
[1]|
Human 5-HT2C Receptor 16 nM (EC50) |
Human 5-HT2C Receptor 20 nM (Ki) |
5-HT2A Receptor 4926 nM (EC50) |
5-HT2A Receptor 153 nM (Ki) |
5-HT2B Receptor 1170 nM (EC50) |
5-HT2B Receptor 431 nM (Ki) |
In Vitro
5-HT2C agonist-13 (compound 58) (10 pM-10 μM; 45 min) binds potently to human recombinant 5-HT2C receptors expressed in HEK293E cell membranes with a Ki of 20 nM, and shows selective binding over human 5-HT2B and 5-HT2A receptors[1].
5-HT2C agonist-13 (90 s-18 h) potently activates human recombinant 5-HT2C receptors expressed in HEK293E cells with an EC50 of 16 nM, and exhibits high functional selectivity over human 5-HT2B and 5-HT2A receptors, acting as a partial agonist at the latter two[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
5-HT2C agonist-13 (10 mg/kg; p.o.; single dose; co-administered with SB-243213) has its food intake-reducing effect in male Sprague Dawley rats fully reversed by co-administration of a selective 5-HT2C antagonist, confirming mediation via the 5-HT2C receptor[1].
5-HT2C agonist-13 (3-30 mg/kg; p.o.; daily; 4 days) reduces body weight gain in lean Sprague Dawley rats in a dose-dependent manner, with a statistically significant 6% reduction at 30 mg/kg on day 4[1].
5-HT2C agonist-13 (300 mg/kg; p.o.; single dose) does not cause gastric parietal cell necrosis or stomach lesions in mice after 24 hours[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague Dawley (male, 250 g)[1]
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Dosage:3 mg/kg; 10 mg/kg; 30 mg/kg
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Administration:p.o.; single dose
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Result:Caused a 12% reduction in food pellet consumption compared to vehicle.
Caused a statistically significant 32% reduction in food pellet consumption compared to vehicle.
Caused a statistically significant 41% reduction in food pellet consumption compared to vehicle.
Left water consumption and locomotor activity within normal ranges, and no overt physical or behavioral abnormalities were observed.
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Animal Model:Sprague Dawley (male, 250 g)[1]
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Dosage:10 mg/kg
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Administration:p.o.; single dose; co-administered with SB-243213
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Result:Caused a 30% reduction in food intake that was completely reversed in a dose-dependent manner by co-administration of SB-243213.
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Animal Model:Sprague Dawley (lean)[1]
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Dosage:3 mg/kg; 30 mg/kg
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Administration:p.o.; daily; 4 days
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Result:Caused a 1.6% reduction in body weight gain compared to vehicle on day 4.
Caused a statistically significant reduction in body weight gain as early as day 2, with a 6% reduction compared to vehicle on day 4.
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Animal Model:Mice[1]
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Dosage:300 mg/kg
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Administration:p.o.; single dose
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Result:Did not cause gastric parietal cell necrosis or stomach lesions after 24 hours.
Chemical Information
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CAS No. 850033-84-0
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Masse moléculaire 284.28
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Formule C14H15F3N2O
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SMILES
FC(F)(C1=C2C([C@@]3([H])N(CCNC3)C2=O)=CC(CC)=C1)F
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Livraison
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.
Protocole
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
5-HT2C agonist-13 Related Classifications
HY-182373 Related Classifications
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