LY-272015
LY-272015 is an orally active and selective 5-HT2B receptor antagonist. LY-272015 blocks 5-HT2 receptors and inhibits Fluoxetine (HY-B0102)-induced PDGFβ receptor transactivation. LY-272015 attenuates 5-HT-induced smooth muscle cell migration and proliferation, and inhibits downstream mTOR/p70S6K phosphorylation. LY-272015 reduces 5-HT-induced vasoconstriction. LY-272015 reverses the excitatory effect of BW-723C86 (HY-101369) on NTS neurons. LY-272015 lowers mean arterial blood pressure in severely hypertensive DOCA-salt rats. LY-272015 can be used in research related to diseases such as hypertension and cardiovascular calcification.
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- No. CAS: 159730-07-1
- Fòrmula: C21H24N2O2
- Peso molecular:336.43
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Actividad biológica
Descripciòn
IC50 & Target
[1]|
5-HT2B Receptor |
PDGFRβ |
mTOR |
In Vitro
LY-272015 (LY) (0-5 μM; 5 min) inhibits Fluoxetine (HY-B0102)-induced PDGFβ receptor transactivation in SH-SY5Y cells[1].
LY-272015 (100 nmol/L; 0-24 h) attenuates 5-HT-induced migration and proliferation of rat aortic SMCs[2].
LY-272015 (10 nmol/L; 2 h) antagonizes 5-HT-induced activation of the mTOR/p70S6K pathway in rat aortic SMCs[2].
LY 272015 (2.87 μg/mL; 5 min) had no significant effect on the amplitude or frequency of phrenic nerve discharge in isolated perfused brainstem preparations from Sprague-Dawley rats[3].
LY-272015 right-shifted the BW-723C86 (HY-101369)-induced contraction curve in endothelium-denuded mesenteric arteries of DOCA-salt rats, confirming the involvement of vascular 5-HT2B receptors in the increase[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SH-SY5Y
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Concentration:0, 0.01, 0.1, 0.5, 5 μM
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Incubation Time:5 min
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Result:Did not significantly abrogate fluoxetine-induced PDGFβ receptor phosphorylation at lower concentrations.
Inhibited fluoxetine-induced PDGFβ receptor phosphorylation at 5 μM.
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Cell Line:Rat aortic smooth muscle cells (SMCs)
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Concentration:100 nmol/L
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Incubation Time:0, 24 h
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Result:Mitigated the 5-HT-induced migration of SMCs.\nLargely abrogated the enhancing effect of 5-HT on PDGF-BB-induced SMC migration.
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Cell Line:Rat aortic smooth muscle cells (SMCs)
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Concentration:100 nmol/L
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Incubation Time:24 h
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Result:Mitigated the 5-HT-induced proliferation of SMCs.
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Cell Line:Rat aortic smooth muscle cells (SMCs)
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Concentration:10 nmol/L
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Incubation Time:2 h (pre-treatment); 0, 2, 5, 15, 30, 60 min (5-HT stimulation)
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Result:Antagonized the 5-HT-induced phosphorylation of mTOR and p70S6K.
In Vivo
LY-272015 (30-50 nA) reverses the excitatory effect of BW-723C86 on active Group 2 and Group 3 (active and inactive) NTS neurons, but does not reverse the inhibitory effect of BW-723C86 on inactive Group 2 cells[5].
LY-272015 (3 mg/kg; intraperitoneal injection; 3 days per week; 8 weeks) did not inhibit the progression of aortic calcification or reduce atherosclerotic lipid/lesion area in diet-induced calcific atherosclerosis Apoe−/− mice, and did not affect bone density[6].
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, 300-350 g, DOCA-salt hypertension model)[4]
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Dosage:0.3, 1.0, and 3.0 mg/kg
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Administration:i.v.; once per week; 4 weeks
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Result:Did not reduce blood pressure in sham-treated rats at any time or dose.
Did not cause blood pressure reduction in any group during weeks 1 and 2.
Reduced blood pressure by ~20 mmHg with 1.0 and 3.0 mg/kg in DOCA-S group at week 3.
Reduced blood pressure with 1.0 mg/kg and caused a significant fall in blood pressure (>40 mmHg) with 3.0 mg/kg after 30 min in week 4 DOCA-S rats.
Abolished the residual pressor response to α-methyl-5-HT after ketanserin in DOCA-S rats.
Did not alter the pressor response to phenylephrine in sham rats.
Abolished 5-HT-induced contraction in stomach fundus.
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Animal Model:Apoe−/− (C57BL/6 background, male, 25 weeks old)[6]
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Dosage:3 mg/kg
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Administration:i.p.; 3 days/week; 8 weeks
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Result:Did not inhibit aortic calcification progression, and produced no effects on lipid area, lesion area, or infiltration of CD68‑positive inflammatory cells.
Blocked the significant rise in systolic posterior left‑ventricular wall thickness, while leaving systolic‑diastolic left‑ventricular anterior wall thickness and diastolic posterior wall thickness unaffected; preserved week‑8 cardiac parameters including ejection fraction (67 %), fractional shortening (37 %), corrected LV mass (109 mg), LVAW systole (1.59 mm), LVAW diastole (1.09 mm), LVPW systole (1.34 mm), LVPW diastole (0.85 mm), and terminal body weight (40 g).
Reduced aortic HTR‑2A protein levels and exerted no influence on HTR‑2B protein abundance.
Displayed bone loss at study endpoint that showed no statistical differences relative to other experimental groups.
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Animal Model:Apoe−/− (C57BL/6 background, female, 23 weeks old)[6]
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Dosage:3 mg/kg
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Administration:i.p.; 3 days/week; 8 weeks
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Result:Did not inhibit the progression of aortic calcification and failed to reduce lipid content or atherosclerotic lesion area, and exerted no observable influence on the infiltration of CD68‑positive inflammatory cells.
Blocked the increases in systolic and diastolic anterior left‑ventricular wall thickness, while leaving systolic and diastolic posterior‑wall thickness unchanged; maintained stable cardiac functional indices including ejection fraction, fractional shortening, corrected LV mass and ventricular wall dimensional parameters at week 8.
Reduced aortic HTR‑2A protein expression levels but produced no change in HTR‑2B protein abundance.
Did not trigger bone loss in experimental animals at the end of the 8‑week experimental period.
- Scratch/Wound-Healing Migration Assay
- Western Blot
- Cell migration
- Neural Crest/Neuronal Cell Migration Explant Assay
- Research Protocol for Cardiovascular Diseases
- Cell Viability Determination by MTT Colorimetric Assay
- Kinase activity and phosphorylation assays
- Chemotaxis Gradient Chamber Assay 1
- Under-Agarose Cell Migration Assay
- Transwell/Boyden Chamber Migration Assay
- 3D Collagen/Hydrogel Matrix Migration Assay
- Protocol for Kinase activity and phosphorylation assays
- Cell-Exclusion Zone Migration Assay
- Chemotaxis Gradient Chamber Assay 2
Chemical Information
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No. CAS 159730-07-1
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Peso molecular 336.43
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Fòrmula C21H24N2O2
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SMILES
CC1=CC2=C(NC3=C2CCNC3CC4=CC=C(OC)C(OC)=C4)C=C1
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
LY-272015 Related Classifications
HY-100851 Related Classifications
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