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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.
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[1][2][3][4][5].
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
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.
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.
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.
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.
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.
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.
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.
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.
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)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
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
View the Complete Stock Solution Preparation Table
*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.
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.
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μLDMSO 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.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
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 μLDMSO stock solution (20.8 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*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.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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