Cat. No.: HY-129440

N-(p-Coumaroyl) Serotonin

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N-(p-Coumaroyl) Serotonin is an orally active polyphenol found in safflower seeds with potent anti-inflammatory, antioxidant, and antitumor activities. N-(p-Coumaroyl) Serotonin suppresses NF‑κB, TLR4/MyD88 and MAPK signaling, activates NQO1/HO‑1 pathways, and inhibits pro‑inflammatory cytokines, iNOS and COX‑2 and ROS production. N-(p-Coumaroyl) Serotonin induces S‑phase arrest and apoptosis in glioblastoma cells, reduces atherosclerotic lesions, and alleviates renal and vascular injuries. N-(p-Coumaroyl) Serotonin acts as a vasodilator, regulates calcium dynamics. N-(p-Coumaroyl) Serotonin can be used for the research of neurodegenerative diseases, atherosclerosis, glioblastoma, and acute renal failure.

For research use only. We do not sell to patients.

Purity: 99.03%
CAS No.: 68573-24-0
Formula: C₁₉H₁₈N₂O₃
Molecular Weight:322.36

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

N-(p-Coumaroyl) Serotonin Chemical Structure

CAS No.: 68573-24-0

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Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]^[2]

NF-κB

p38 MAPK

TLR4

COX-2

iNOS

ERK1

ERK2

Caspase-8

PDGFRβ

All NF-κB Isoforms :

All Toll-like Receptor (TLR) Isoforms :

All p38 MAPK Isoforms :

All NO Synthase Isoforms :

All COX Isoforms :

All ERK Isoforms :

All Caspase Isoforms :

All PDGFR Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
RAW264.7	IC₅₀	164.43 μM Compound: 9; CS	Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production measured after 24 hrs by Griess assay Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production measured after 24 hrs by Griess assay	[PMID: 29102229]
RAW264.7	IC₅₀	43.22 μM Compound: 9; CS	Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced PGE2 production pretreated for 1 hr followed by LPS addition measured after 24 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced PGE2 production pretreated for 1 hr followed by LPS addition measured after 24 hrs	[PMID: 29102229]

In Vitro

N-(p-Coumaroyl) Serotonin (CS) (12.5-100 μM, 1 h pre-incubation + 20 h LPS challenge) dose-dependently suppresses LPS-induced IL-6, TNF-α, MCP-1 secretion and NO production in BV2 microglia^[1].
N-(p-Coumaroyl) Serotonin (12.5-100 μM) significantly inhibits LPS-induced signaling cascades in murine BV2 microglial cells. At 60 min post-LPS challenge, it dose-dependently suppresses the phosphorylation of p38, JNK, and ERK MAPKs, as well as the protein levels of TLR4 and MyD88. Furthermore, at 20 h post-LPS challenge, it robustly reduces the phosphorylation of IκBα and NF-κB p65 and inhibits the nuclear translocation of p65, thereby blocking the activation of the IκB/NF-κB signaling axis^[1].
N-(p-Coumaroyl) Serotonin (12.5-100 μM; 20 h) dose-dependently upregulates HO-1 and NQO1 protein levels in murine BV2 microglial cells^[1].
N-(p-Coumaroyl) Serotonin (1-100 μM, 15 s pre-treatment) concentration-dependently suppresses KCl- and 5-HT-induced [Ca²⁺] increases in A7r5 cells^[2].
N-(p-Coumaroyl) Serotonin (1-100 μM; 24 hours) concentration-dependently inhibits FBS- and PDGF-BB-induced proliferation and PDGF-BB-induced migration in A7r5 cells^[2].
N-(p-Coumaroyl) Serotonin (10-66 μM; 5 minutes (PDGF receptor β phosphorylation); 5, 10 minutes (ERK1/2 phosphorylation)) inhibits PDGF-BB-induced PDGF receptor β phosphorylation at 5 minutes and ERK1/2 phosphorylation at 5 and 10 minutes in A7r5 cells^[2].
N-(p-Coumaroyl) Serotonin (50-1000 μM; 72 h) dose-dependently reduces viability in U251MG, A172, D54, U87MG and T98G glioblastoma cells (IC₅₀: 48–81 μM), with T98G cells being more sensitive than U251MG cells; it shows markedly lower cytotoxicity in MRC-5 and HFL1 non-cancer fibroblasts^[3].
N-(p-Coumaroyl) Serotonin (50-200 μM; 72 h) induces dose-dependent S-phase cell cycle arrest and sub-G0/G1 phase accumulation (apoptosis) in U251MG and T98G glioblastoma cells^[3].
N-(p-Coumaroyl) Serotonin (77 μM; 24 h) activates caspase-8 in U251MG glioblastoma cells^[3].
N-(p-Coumaroyl) Serotonin (150-200 μM; 24 h) induces mitochondrial membrane depolarization in U251MG glioblastoma cells^[3].
N-(p-Coumaroyl) Serotonin (50-200 μM; 72 h) induces dose-dependent increases in CD71 and CD15 expression in U251MG and T98G glioblastoma cells after 72 hours of treatment, while leaving CD24, CD44, and CD56 expression unchanged^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cytotoxicity Assay^[1]

Cell Line:

murine BV2 microglial cells
Concentration:

6.25, 12.5, 25, 50, 100 ,200 μM
Incubation Time:

24 h
Result:

Remained unaffected at concentrations up to 100 μM.
Reduced cellular viability at 200 μM.

ELISA Assay^[1]

Cell Line:

LPS-challenged murine BV2 microglial cells
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

1 h pre-incubation, followed by 20 h LPS challenge
Result:

Attenuated LPS-induced IL-6, TNF-α, and MCP-1 levels by 65.20%, 46.44%, and 30.36%, respectively.

Western Blot Analysis^[1]

Cell Line:

LPS-challenged murine BV2 microglial cells
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

1 h pre-incubation, followed by 20 h LPS challenge
Result:

Reduced LPS-induced increases in iNOS and COX-2 protein levels dose-dependently.

Western Blot Analysis^[1]

Cell Line:

LPS-challenged murine BV2 microglial cells
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

1 h pre-incubation, followed by 60 min LPS challenge
Result:

Reduced LPS-induced phosphorylation of p38, JNK, and ERK dose-dependently. Showed significant inhibition at all tested concentrations for p38 and JNK compared to LPS-only treated cells, and significant inhibition at 50 and 100 μM for ERK.
Reduced LPS-induced increases in TLR4 and MyD88 protein levels dose-dependently.
Reduced LPS-induced phosphorylation of IκBα and NF-κB p65 dose-dependently, with significant inhibition observed at 25, 50, and 100 μM compared to LPS-only treated cells.

Immunofluorescence^[1]

Cell Line:

LPS-challenged murine BV2 microglial cells
Concentration:

100 μM
Incubation Time:

1 h pre-incubation, followed by 60 min LPS challenge (Immunocytochemistry)
Result:

Inhibited LPS-induced nuclear translocation of NF-κB p65 robustly at 100 μM, sequestering the protein in the cytoplasm.

Western Blot Analysis^[1]

Cell Line:

murine BV2 microglial cells
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

20 h
Result:

Increased protein levels of HO-1 and NQO1 dose-dependently.

Cell Proliferation Assay^[2]

Cell Line:

A7r5 rat aortic vascular smooth muscle cells
Concentration:

1, 10, 100 μM
Incubation Time:

24 hours (with 10% FBS stimulation)
Result:

Inhibited 10% FBS-induced proliferation in a concentration-dependent manner.
Achieved 40% inhibition at 100 μM.

Cell Proliferation Assay^[2]

Cell Line:

A7r5 rat aortic vascular smooth muscle cells
Concentration:

10, 100 μM
Incubation Time:

24 hours (with PDGF-BB stimulation)
Result:

Inhibited 10 ng/mL PDGF-BB-induced proliferation in a concentration-dependent manner.
Reduced proliferation activity to ~80% of control at 10 μM.
Reduced activity to ~40% of control at 100 μM.

Cell Migration Assay ^[2]

Cell Line:

A7r5 rat aortic vascular smooth muscle cells
Concentration:

1, 10, 66 μM
Incubation Time:

4 hours (with PDGF-BB stimulation)
Result:

Attenuated 10 ng/mL PDGF-BB-induced migration in a concentration-dependent manner, reducing migration absorbance to ~40%, ~35%, and ~30% of the PDGF-BB-only control at 1, 10, and 66 μM, respectively.

Western Blot Analysis^[2]

Cell Line:

A7r5 rat aortic vascular smooth muscle cells
Concentration:

10, 66 μM
Incubation Time:

5 minutes (PDGF receptor β phosphorylation); 5, 10 minutes (ERK1/2 phosphorylation) (with PDGF-BB stimulation)
Result:

Attenuated PDGF-BB-induced PDGF receptor β and ERK1/2 phosphorylation in a concentration-dependent manner, with stronger inhibition observed at 5 minutes than at 10 minutes.

Cell Viability Assay^[3]

Cell Line:

U251MG, A172, D54, U87MG, T98G (glioblastoma); MRC-5, HFL1 (non-cancer fibroblast)
Concentration:

50, 150, 250, 500, 1000 μM
Incubation Time:

72 h
Result:

Reduced viability in all glioblastoma cell lines with IC₅₀ values of 77 μM (U251MG), 62 μM (A172), 81 μM (D54), 48 μM (U87MG), and 68 μM (T98G).
Exhibited far lower cytotoxicity in non-cancer fibroblasts with an IC₅₀ of 197 μM (MRC-5) and 181 μM (HFL1).
Showed dose-dependent sensitivity in both U251MG and T98G cells, with T98G cells more sensitive than U251MG cells.
Showed T98G cells greater sensitivity than U251MG cells.

Cell Cycle Analysis^[3]

Cell Line:

U251MG, T98G (glioblastoma)
Concentration:

50, 150, 200 μM
Incubation Time:

72 h
Result:

Induced a dose-dependent increase in the percentage of cells in the sub-G0/G1 phase, indicative of apoptosis, in both cell lines.
Caused dose-dependent S-phase cell cycle arrest in both U251MG and T98G cells.

Apoptosis Analysis^[3]

Cell Line:

U251MG (glioblastoma)
Concentration:

150, 200 μM
Incubation Time:

24 h
Result:

Induced mitochondrial membrane depolarization in a concentration‑dependent manner.

In Vivo

N-(p-Coumaroyl) Serotonin (oral; continuous; 16 weeks) significantly reduces aortic wall thickening, attenuates atherosclerosis, and improves vascular distensibility in KHC rabbits^[2].
N-(p-Coumaroyl) Serotonin (100-1000 μM; immersion; continuous; 96 hours) exhibits no acute toxicity in zebrafish embryos^[3].
N-(p-coumaroyl) serotonin (7.5 mg/kg body weight per day; oral gavage; daily; 2 days) exerts a potent renoprotective effect against Cisplatin (HY-17394)-induced acute renal failure in male BALB/c mice, as evidenced by normalization of renal function biomarkers, reduction in oxidative stress, modulation of inflammatory and apoptotic protein expression, and improved renal histology^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Danio rerio (embryos, 24 hours post fertilization)^[3]
Dosage:

100 μM, 250 μM, 500 μM, 1000 μM
Administration:

immersion; continuous; 96 hours
Result:

Showed zero mortality at all tested concentrations up to 1 mM at 5 days post fertilization.

Animal Model:

BALB/c (male, 7-week-old, acute renal failure model via cisplatin injection)^[4]
Dosage:

7.5 mg/kg body weight per day
Administration:

oral gavage; daily; 2 days
Result:

Attenuated cisplatin-induced body weight loss (mean change of -3.33 g over 3 days).
Prevented cisplatin-induced reduction in kidney weight (mean kidney weight of 0.44 g).
Significantly reduced serum urea nitrogen level to 22.7 mg/dl.
Significantly reduced serum creatinine level to 0.86 mg/dl.
Markedly decreased cisplatin-induced renal reactive oxygen species (ROS) production to near-normal levels.
Significantly upregulated cisplatin-reduced glutathione peroxidase (GPx) protein expression in the kidney.
Significantly decreased cisplatin-induced overexpression of p-p38, p-ERK1/2, and p-JNK proteins.
Significantly reduced cisplatin-induced overexpression of nuclear factor-kappa Bp65 (NF-κBp65), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) proteins.
Significantly suppressed cisplatin-induced upregulation of pro-apoptotic Bax protein and increased expression of anti-apoptotic Bcl-2 protein.
Showed significant reduction in cisplatin-induced renal histological damage, including less tubular necrosis, desquamation, and parenchymal degeneration compared to vehicle-treated cisplatin-exposed mice.

Chemical Information

CAS No. 68573-24-0
Appearance Solid
Molecular Weight 322.36
Formula C₁₉H₁₈N₂O₃
Color Off-white to light yellow
SMILES

O=C(NCCC1=CNC2=C1C=C(O)C=C2)/C=C/C3=CC=C(O)C=C3
Structure Classification
- Phenols
- Polyphenols
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL (310.21 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.1021 mL

15.5106 mL

31.0212 mL

5 mM

0.6204 mL

3.1021 mL

6.2042 mL

10 mM

0.3102 mL

1.5511 mL

3.1021 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.08 mg/mL (6.45 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.08 mg/mL (6.45 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.08 mg/mL (6.45 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (294 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Jeon CH, et al. N-(p-Coumaroyl) Serotonin Ameliorates LPS-Induced Inflammation in BV2 Microglia via MAPK/NF-κB Inactivation and HO-1/NQO1 Upregulation. Curr Issues Mol Biol. 2026;48(2):232. Published 2026 Feb 21. [Content Brief]

[2]. Takimoto T, et al. Effect of N-(p-coumaroyl)serotonin and N-feruloylserotonin, major anti-atherogenic polyphenols in safflower seed, on vasodilation, proliferation and migration of vascular smooth muscle cells. Mol Nutr Food Res. 2011;55(10):1561-1571. [Content Brief]

[3]. Lazari D, et al. N-(p-coumaroyl) serotonin inhibits glioblastoma cells growth through triggering S-phase arrest and apoptosis. J Neurooncol. 2017;132(3):373-381. [Content Brief]

[4]. Park CH, et al. Protective Effects of Serotonin and its Derivatives, N-Feruloylserotonin and N-(p-Coumaroyl) Serotonin, Against Cisplatin-Induced Renal Damage in Mice. Am J Chin Med. 2019;47(2):369-383. [Content Brief]

[5]. Katsuda S, et al. Safflower seed polyphenols (N-(p-coumaroyl)serotonin and N-feruloylserotonin) ameliorate atherosclerosis and distensibility of the aortic wall in Kurosawa and Kusanagi-hypercholesterolemic (KHC) rabbits. Hypertens Res. 2009;32(11):944-949. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.1021 mL	15.5106 mL	31.0212 mL	77.5530 mL
	5 mM	0.6204 mL	3.1021 mL	6.2042 mL	15.5106 mL
	10 mM	0.3102 mL	1.5511 mL	3.1021 mL	7.7553 mL
	15 mM	0.2068 mL	1.0340 mL	2.0681 mL	5.1702 mL
	20 mM	0.1551 mL	0.7755 mL	1.5511 mL	3.8777 mL
	25 mM	0.1241 mL	0.6204 mL	1.2408 mL	3.1021 mL
	30 mM	0.1034 mL	0.5170 mL	1.0340 mL	2.5851 mL
	40 mM	0.0776 mL	0.3878 mL	0.7755 mL	1.9388 mL
	50 mM	0.0620 mL	0.3102 mL	0.6204 mL	1.5511 mL
	60 mM	0.0517 mL	0.2585 mL	0.5170 mL	1.2926 mL
	80 mM	0.0388 mL	0.1939 mL	0.3878 mL	0.9694 mL
	100 mM	0.0310 mL	0.1551 mL	0.3102 mL	0.7755 mL

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N-(p-Coumaroyl) Serotonin

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