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.
For research use only. We do not sell to patients.
- CAS No.: 159730-07-1
- Formula: C21H24N2O2
- Molecular Weight:336.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All 5-HT Receptor Isoforms
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Biological Activity
Description
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. Further protocols information, click here.
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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.
Chemical Information
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CAS No. 159730-07-1
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Molecular Weight 336.43
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Formula C21H24N2O2
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SMILES
CC1=CC2=C(NC3=C2CCNC3CC4=CC=C(OC)C(OC)=C4)C=C1
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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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Scratch/Wound-Healing Migration Assay
The scratch/wound-healing migration assay measures collective migration of adherent cells into an experimentally created cell-free gap in a confluent monolayer. The readout is generated by imaging the gap immediately after scratching and at later time points, then quantifying reduction in wound area, wound width, or percentage closure as cells move into the denuded region. Gap closure reflects cell migration but may also include cell proliferation, so interpretation should distinguish migration-focused conditions from proliferation-driven closure when possible, such as by using short assay windows, serum-controlled conditions, cell counting, or proliferation controls reported in published protocols.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Neural Crest/Neuronal Cell Migration Explant Assay
Neural crest (NC) and neuronal cell migration explant assays are in vitro systems in which neural tube-derived tissues are cultured to allow premigratory or newly emigrated neural crest cells to undergo epithelial-to-mesenchymal transition (EMT), migrate away from the explant, and form a measurable radial outgrowth that reflects migratory capacity and environmental responsiveness. These assays typically quantify migration by measuring the expansion of cell outgrowth from neural tube or neural plate border explants over time, often comparing early and later timepoints to derive a migration index such as a radius ratio, which reflects net cell dispersal from the explant core. Neural tube explant cultures preserve key aspects of neural crest behavior, including EMT, migration, and early differentiation, making them suitable for assessing intrinsic migratory ability and extrinsic cue dependence. However, studies emphasize that migratory outgrowth from neural tube explants may include non-n
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Chemotaxis Gradient Chamber Assay 1
The chemotaxis gradient chamber assay is based on the principle of observing directional cell migration in response to a stable, linear or quasi-linear concentration gradient of a chemoattractant formed between two fluid reservoirs separated by a narrow observation chamber. Cells placed within the chamber respond to the gradient by polarized movement toward higher chemoattractant concentrations, allowing quantification of chemotactic behavior in real time under microscopy. The classic Zigmond chamber design enables simultaneous visualization of gradient formation and individual cell trajectories, making it suitable for studying leukocyte chemotaxis and other motile cell types in vitro.
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Under-Agarose Cell Migration Assay
The under-agarose cell migration assay is a classical in vitro chemotaxis method designed to evaluate directed cell movement through a semi-solid agarose matrix toward soluble chemoattractant gradients, enabling visualization and quantification of leukocyte or motile cell migration in a confined 2D-like environment. In this system, cells and chemoattractants are placed in separate wells cut into an agarose gel, allowing diffusion-driven gradient formation that guides directional migration, which is typically assessed by measuring migration distance, cell morphology changes, and accumulation toward the chemoattractant source. This assay has been widely used to study neutrophil and leukocyte chemotaxis as a simple alternative to filter-based migration systems and allows direct microscopic observation of migrating cells under near-physiological confinement conditions.
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Transwell/Boyden Chamber Migration Assay
The Transwell/Boyden chamber migration assay measures cell movement through a porous membrane separating an upper and lower chamber, usually after a chemoattractant gradient is established by placing cells in the upper chamber and chemoattractant-containing medium in the lower chamber. The readout is generated by quantifying cells that traverse the membrane and appear on the lower membrane surface or in the lower chamber, depending on whether the cell type is adherent or non-adherent. This assay reflects chemotactic or haptotactic migration rather than matrix invasion unless an extracellular-matrix barrier is added to the membrane.
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3D Collagen/Hydrogel Matrix Migration Assay
The 3D collagen/hydrogel matrix migration assay is based on embedding cells within or on top of a fibrillar collagen type I-rich three-dimensional matrix to model in vivo-like extracellular matrix (ECM) architecture, enabling analysis of cell migration through a physically and biochemically relevant scaffold. In contrast to 2D migration systems, cells in 3D matrices interact with fibrillar collagen networks, requiring coordinated adhesion remodeling and proteolytic or non-proteolytic deformation mechanisms to move through confined spaces, thereby providing a more physiologically relevant readout of invasive and migratory behavior in tissue-like environments. Cell movement in 3D collagen matrices is typically quantified by tracking single-cell trajectories, invasion depth, or matrix penetration over time, reflecting combined effects of cytoskeletal dynamics, cell-ECM adhesion turnover, and ECM remodeling. These systems are widely used to study tumor cell invasion and stromal cell motili
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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Cell-Exclusion Zone Migration Assay
The Cell-Exclusion Zone (CEZ) migration assay is an in vitro 2D cell migration method in which a defined cell-free area is created using removable physical barriers such as silicone stoppers, allowing cells to be seeded around the barrier and subsequently migrate into the cleared zone after barrier removal. This approach enables quantification of collective cell migration by monitoring repopulation of the initially cell-free region over time using microscopy-based imaging. Compared with scratch-based wound healing assays, barrier-based exclusion methods are designed to avoid mechanical damage to the extracellular matrix and reduce injury-induced effects on boundary cells, thereby improving interpretability of migration behavior in vitro. The assay readout is typically the progressive reduction in the cell-free area or the number of cells invading the exclusion zone, reflecting coordinated cell motility relevant to physiological processes such as wound healing, epithelial repair, and ca
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Chemotaxis Gradient Chamber Assay 2
Chemotaxis gradient chamber assays measure directional cell migration in response to a soluble chemical gradient by imaging cells as they move across a defined observation region; the readout is generated from time-lapse cell trajectories, displacement toward the gradient, forward migration index, trajectory plots, rose/polar plots, and statistical tests of non-random directionality. The Dunn chamber is a direct-viewing glass chamber in which cells migrate across a bridge between control and chemoattractant wells, allowing observation of cells in a linear concentration gradient; related direct-viewing formats include the Insall chamber, which supports defined unidirectional gradients and high numerical-aperture microscopy, and the μ-Slide Chemotaxis chamber, which supports long-term live-cell imaging and gradient characterization with fluorescent dye.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)