E-6837
E-6837 is a selective and orally active 5-HT6 receptor ligand. E-6837 demonstrates partial agonism at a presumably silent rat 5-HT6 receptor and full agonism at a constitutively active human 5-HT6 receptor by monitoring the cAMP signaling pathway. E-6837 induces hypophagia, reduces fat mass and body weight, and improves glycemic control. E-6837 can be used for the research of obesity.
For research use only. We do not sell to patients.
- CAS No.: 528859-61-2
- Formula: C22H22ClN3O2S
- Molecular Weight:427.95
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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
All 5-HT Receptor Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Human 5-HT6 Receptor 9.13 (pKi) |
Rat 5-HT6 Receptor 8.37 (pIC50) |
Rat 5-HT6 Receptor 9.19 (pEC50) |
Human 5-HT6 Receptor 9.53 (pEC50) |
In Vitro
E-6837 binds selectively and with high affinity (pKi = 9.13 ± 0.17) to the recombinant human 5-HT6 receptor in HEK-293 membrane preparations[1].
E-6837 acts as a potent partial agonist (Emax = 67 ± 4%, pEC50 = 9.19 ± 0.11) and partial antagonist (Imax = 41 ± 3%, pIC50 = 8.37 ± 0.09) at the presumably silent rat 5-HT6 receptor stably expressed in HEK-293F cells[1].
E-6837 acts as a potent, nearly full agonist (Emax = 96 ± 4%, pEC50 = 9.53 ± 0.09) at the constitutively active human 5-HT6 receptor stably expressed in HEK-293F cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
E-6837 (60 mg/kg; p.o.; single dose) does not induce conditioned taste aversion or kaolin consumption in male Sprague-Dawley rats, indicating no emetic or aversive effects at these doses[1].
E-6837 (30 mg/kg; p.o.; twice daily; 28 days) induces a maximal 15.7% body weight loss in diet-induced obese female Wistar rats[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 rats (male, 190 g at study start)[1]
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Dosage:5 mg/kg; 30 mg/kg
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Administration:p.o.; single dose
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Result:Reduced food intake transiently, with onset of suppression ~2 hours into the nightly feeding session, lasting ~6 hours (30 mg/kg dose).
Had no effect on food intake (5 mg/kg dose).
Did not alter locomotor activity (both doses) both.
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Animal Model:Sprague-Dawley rats (male, 6 weeks old, ~190 g at study start)[1]
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Dosage:60 mg/kg
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Administration:p.o.; single dose
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Result:Did not elicit conditioned taste aversion, with a saccharin preference ratio of 77.0 ± 10.7% (72-84 h) similar to vehicle (up to 60 mg/kg dose).
Had no effect on kaolin consumption at tested doses.
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Animal Model:Wistar rats (female, 250-300 g at study start, diet-induced obese via 12-week high-calorie cafeteria diet)[1]
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Dosage:30 mg/kg
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Administration:p.o.; twice daily; 28 days
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Result:Induced a maximal body weight loss of -15.7% over 28-day treatment period, with sustained weight loss for 3 weeks.
Reduced fat mass by 31.7%, with no significant changes in water, protein, or ash content.
Reduced plasma leptin levels by 49.6% (from 166 ± 19 ng/mL to 83 ± 19 ng/mL).
Improved glycemic control, with a significant reduction in plasma glucose excursion during glucose tolerance test and a trend toward reduced plasma insulin levels.
Resulted in transient rebound hyperphagia after treatment withdrawal, but body weight remained -6.6% lower than vehicle controls on day 71, with no profound rebound weight gain.
Decreased cumulative food intake by 31.7% during treatment period, with preferential reduction in chocolate intake.
Chemical Information
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CAS No. 528859-61-2
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Molecular Weight 427.95
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Formula C22H22ClN3O2S
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SMILES
O=S(=O)(NC=1C=CC=2NC=C(C2C1)CCN(C)C)C=3C=CC=4C(Cl)=CC=CC4C3
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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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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
E-6837 Related Classifications
HY-14341 Related Classifications
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