FGFR1 inhibitor (IC50 for kinase inhibition: ~3.78 μM). [1]
Weak inhibitor of FGFR2 (IC50 for kinase inhibition: ~12.5 μM; inhibition rate at 1 μM: 64%). [1]
Minimal inhibitory activity against VEGFR2 (4% at 1 μM), PDGFR-α (1% at 1 μM), PDGFR-β (2% at 1 μM), and a panel of other 15 kinases. [1]

The fibroblast growth factor receptor 1 (FGFR1) conjugate ferulic acid (FA) has IC50 values of 3.78 and 12.5 μM for FGFR1 and FGFR2, respectively. At 1 μM, ferulic acid demonstrates a 92% inhibition rate of FGFR1 core inhibitory action. Ferulic acid at 5 to 40 μM was treated for 24 hours, which resulted in a substantial reduction in the proliferation of FGF1-stimulated HUVEC. In HUVEC cells, ferulic acid up to 20 μM had no discernible influence on cell viability; however, over 30 μM, ferulic acid showed hazardous effects when compared to controls. In a dose-dependent manner, ferulic acid blocks the migration of HUVECs triggered by FGF1 as well as their transitory migration. Ferulic acid dramatically reduced the phosphorylation of PI3K and Akt that was generated by FGF1. FGF1 induction was markedly suppressed by ferulic acid. MMP-2 and MMP-9 expression [1].

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In a radiometric kinase inhibition profile assay against 20 kinases, ferulic acid at 1 μM exhibited potent inhibitory activity on FGFR1 (92% inhibition). It showed moderate inhibition on FGFR2 (64%) and minimal inhibition on others like VEGFR2 (4%), PDGFR-α (1%), PDGFR-β (2%), c-Met (11%), PI3K (20%), and c-RAF (18%). [1]
In a direct in vitro kinase assay, ferulic acid inhibited FGFR1 kinase activity in a dose-dependent manner with an IC50 of approximately 3.78 μM. It also inhibited FGFR2 kinase activity but with a higher IC50 of approximately 12.5 μM, indicating selectivity for FGFR1. [1]
In an FGF1 binding assay, ferulic acid decreased the binding of FGFR1 to immobilized FGF1 in a dose-dependent manner. It had a less significant effect on FGF1-FGFR2 binding. [1]
In FGF1-stimulated HUVEC, ferulic acid treatment (5-40 μM for 24h) significantly inhibited cell proliferation in a dose-dependent manner. It did not significantly affect HUVEC proliferation stimulated by other angiogenic factors (VEGF-A, FGF2, PDGF-α, PDGF-β, PIGF). [1]
In HUVEC without FGF1 stimulation, ferulic acid showed no significant cytotoxicity up to 20 μM. Cytotoxic effects were observed at concentrations above 30 μM, as determined by MTT assay. This was confirmed by LDH release assay, where ferulic acid (up to 10 μM) caused little LDH release compared to control, while Triton X-100 caused significant release. [1]
In FGF1-stimulated HUVEC, ferulic acid significantly inhibited cell migration in a wound-healing assay and cell invasion in a Transwell Matrigel invasion assay in a dose-dependent manner. [1]
In a 2D Matrigel tube formation assay, ferulic acid (2.5, 5, 10 μM) dose-dependently suppressed the FGF1-stimulated capillary-like tube formation by HUVEC. [1]
Western blot analysis on HUVEC showed that ferulic acid treatment significantly inhibited FGF1-induced phosphorylation of FGFR1 (at Tyr154), PI3K (p85 subunit at Tyr458), and Akt (at Thr308) in a dose-dependent manner, without affecting total protein levels. The phosphorylation of ERK and mTOR was not greatly affected. [1]
Immunoprecipitation-Western blot and immunofluorescence analysis in HUVEC confirmed that ferulic acid decreased FGF1 binding to FGFR1 and reduced FGF1-induced p-FGFR1 (Tyr154) expression. [1]
In HUVEC, ferulic acid treatment in the presence of FGF1 significantly inhibited the expression and activity of matrix metalloproteinases MMP-2 and MMP-9, as shown by Western blot and fluorogenic activity assays. [1]
siRNA-mediated knockdown experiments showed that the anti-proliferative effect of ferulic acid on HUVEC was abolished by FGFR1 siRNA but not by control siRNA, indicating the effect is FGFR1-dependent. [1]
In four melanoma cell lines (A375, CHL-1, SK-MEL-2, B16F10) and normal melanocyte NHEM-a, ferulic acid and the FGFR1 inhibitor SSR128129E inhibited cell proliferation in a dose-responsive manner. The inhibitory effect on normal NHEM-a cells required higher concentrations compared to melanoma cells. [1]
In a soft agar colony formation assay, ferulic acid dose-dependently decreased the number and size of colonies formed by B16F10 melanoma cells. [1]
In B16F10 melanoma cells, Western blot analysis showed that ferulic acid administration significantly reduced the phosphorylation of PI3K (p85 Tyr458) and Akt (Thr308) in a dose-dependent manner. [1]
siRNA experiments in B16F10 cells showed that the anti-proliferative effect of ferulic acid was abolished by FGFR1 siRNA but not by FGFR2 siRNA, confirming the dependency on FGFR1 for its anti-tumor growth effects. [1]

Ferulic acid (FA) treatment successfully prevented FGF1-induced neovascularization. Comparing intragastric ferulic acid formulations to those treated with dimethyl sulfoxide (DMSO), it was observed that the former greatly inhibited tumor volume and tumor weight. Furthermore, the administration of ferulic acid was well tolerated, and no discernible variation in body weight was seen between the vehicle and FA-treated groups [1]. in the open field test, but had no impact on immobility time in the TST. The formulation of ferulic acid (0.001 mg/kg, po) improved the antidepressant-like action of fluoxetine (5 mg/kg, po) in TST, according to the data [2].

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In a rat aortic ring assay (ex vivo), ferulic acid dose-dependently and almost completely inhibited FGF1-induced microvessel sprouting from the aortic rings. [1]
In a chick chorioallantoic membrane (CAM) assay (in vivo), ferulic acid potently inhibited FGF1-induced neovascularization. No dead embryos were observed at the tested doses, indicating the anti-angiogenic effect was not due to toxicity. [1]
In a B16F10 melanoma xenograft model in C57BL/6 mice, intragastric administration of ferulic acid (10, 30, 50 mg/kg daily) for 25 days significantly inhibited tumor growth. The average tumor volumes were 714 ± 96 mm³ (10 mg/kg), 500 ± 36 mm³ (30 mg/kg), and 328 ± 56 mm³ (50 mg/kg), compared to the vehicle group. The positive control dacarbazine also dramatically suppressed tumor volumes. [1]
Immunohistochemistry analysis of tumor tissues from the xenograft model showed that ferulic acid treatment significantly reduced the number of p-FGFR1 (Tyr154)-positive cells and the expression of CD31 (a marker of microvessel density), indicating inhibition of tumor angiogenesis. It also resulted in downregulation of p-PI3K (p85 Tyr458) and p-Akt (Thr308) in the tumor tissues. [1]
The ferulic acid treatment was well tolerated in mice, with no significant difference in body weight between the vehicle-treated group and the FA-treated groups throughout the experiment. [1]

Kinase Inhibition Profiling: The inhibitory activity of ferulic acid against a panel of 20 kinases was determined using radiometric assays. The assays were performed at a concentration of 1 μM of the test compound. The results were expressed as the percentage of kinase activity inhibition compared to a vehicle control. [1]
FGFR1 and FGFR2 IC50 Determination: The half-maximal inhibitory concentration (IC50) values for the inhibition of FGFR1 and FGFR2 by ferulic acid were determined using a Z'-lyte kinase assay. The kinase domains of FGFR1 or FGFR2 were assayed in a reaction buffer containing 50 mM HEPES pH 7.5, 0.01% BRIJ-35, 10 mM MgCl2, 2 mM MnCl2, 1 mM EGTA, and 1 mM DTT. The assay was performed in triplicate in 384-well plates according to the manufacturer's instructions. [1]
FGF1-FGFR Binding Assay: The effect of ferulic acid on the binding of FGF1 to its receptors FGFR1 and FGFR2 was evaluated. Recombinant FGF1 protein was immobilized. Then, FGFR1 or FGFR2 protein was added in the presence of varying concentrations of ferulic acid. The amount of receptor bound to the immobilized FGF1 was then quantified, allowing the assessment of how ferulic acid disrupts this protein-protein interaction. [1]
MMP Activity Assay: The activity of MMP-2 and MMP-9 in cell culture supernatants was determined using a commercial activity assay kit. After treatment, cell medium was collected and centrifuged. The supernatant was added to a 96-well strip coated with an antibody specific for MMP-9 or MMP-2 and incubated overnight. After washing, assay buffer and a detection reagent were added. Following incubation at 37°C for 1 hour, the optical density at 405 nm was measured with a microplate reader, which is proportional to MMP activity. [1]

Cell Proliferation (MTT) Assay: Cells (HUVEC or melanoma cells) were seeded in plates. For HUVEC, they were cultured with or without various angiogenic stimuli (VEGF-A, FGF1, FGF2, PDGF-α, PDGF-β, PIGF). Cells were treated with ferulic acid at concentrations ranging from 2.5 to 40 μM for 24 hours. Cell viability was determined by adding MTT reagent. After 4 hours of incubation, the absorbance at 450 nm was measured. The results were used to calculate the percentage of viable cells relative to a vehicle control (0.1% DMSO). [1]
Lactate Dehydrogenase (LDH) Cytotoxicity Assay: HUVEC were seeded in a 96-well plate and incubated with vehicle (0.1% DMSO), 1% Triton X-100 (positive control), or various concentrations of ferulic acid for 24 hours. Cell supernatants were collected, and LDH activity was measured using a commercial LDH cytotoxicity assay kit. The absorbance of the formed formazan was read at 490 nm, with higher absorbance indicating higher LDH release and cytotoxicity. [1]
Wound Healing Migration Assay: HUVEC were grown to confluence in plates. A uniform wound was made in the cell layer with a pipette tip, and cell debris was washed away. Cells were then treated with ferulic acid in the presence of FGF1. Wound closure was evaluated at 24 hours using bright-field microscopy. [1]
Transwell Invasion Assay: The assay was performed using Matrigel-coated chambers. HUVEC in serum-free medium with or without ferulic acid and FGF1 were added to the upper chamber. Complete medium was added to the lower chamber as a chemoattractant. After 24 hours of incubation, non-invasive cells on the upper surface of the membrane were removed, and cells that had invaded to the lower surface were fixed, stained, and counted. [1]
Tube Formation Assay: 12-well plates were coated with Matrigel. HUVEC suspended in medium with 2% FBS were plated on the Matrigel. Ferulic acid (2.5, 5, 10 μM) and FGF1 were then added. After 6 hours, the formation of capillary-like tube structures was photographed. The extent of angiogenesis was evaluated by measuring the total tube length per microscopic field. [1]
Soft Agar Colony Formation Assay: B16F10 melanoma cells were mixed with growth medium and 0.5% agarose containing vehicle or ferulic acid. This mixture was layered on top of a 0.5% base agar in culture dishes. Culture medium was added and replaced weekly. After 21 days, colonies larger than 2 mm in diameter were stained with crystal violet and counted. [1]
Western Blotting: Cell lysates were prepared from treated HUVEC or B16F10 cells. Proteins were separated by SDS-PAGE and transferred to membranes. Membranes were incubated with primary antibodies against proteins of interest (e.g., p-FGFR1, total-FGFR1, p-PI3K, total-PI3K, p-Akt, total-Akt, MMP-2, MMP-9, GAPDH as loading control) followed by HRP-conjugated secondary antibodies. Immunoreactive bands were visualized using an enhanced chemiluminescence (ECL) detection system. [1]
Immunofluorescence Analysis: HUVEC were treated with or without ferulic acid in the presence of FGF1. Cells were then fixed and labeled with a primary antibody against p-FGFR1 (Tyr154). A FITC-conjugated secondary antibody was used for detection (green fluorescence). Nuclei were counterstained with Hoechst 33258 (blue fluorescence). Fluorescent cells were observed and photographed under a laser scanning confocal microscope. [1]
siRNA Knockdown Experiment: HUVEC or B16F10 cells were transfected with siRNA targeting FGFR1, FGFR2, or a control siRNA. The effect of gene knockdown on cell proliferation in the presence or absence of ferulic acid was then assessed using an MTT assay to determine the dependency of FA's activity on these receptors. [1]

Rat Aortic Ring Assay:** Aortas were isolated from 6-week-old male Sprague-Dawley rats, cleaned of fat and connective tissue, and cut into rings. 48-well plates were coated with Matrigel. Aortic rings were placed in the wells and sealed with an additional overlay of Matrigel. FGF1 in serum-free M199 medium, with or without ferulic acid, was added to the wells. The medium was changed every 2 days. After 6 days, microvessel sprouting was fixed, photographed, and quantified. [1]
* **Chick Chorioallantoic Membrane (CAM) Assay:** Fertilized chicken eggs were incubated. A window was made in the shell to expose the CAM. FGF1, alone or in combination with ferulic acid, was applied to the CAM. After further incubation, neovascularization was observed and photographed. The absence of dead embryos was noted to rule out general toxicity. [1]
* **B16F10 Melanoma Xenograft Model:** Female C57BL/6 mice were subcutaneously implanted with 3 × 10⁶ B16F10 melanoma cells. On day 7, when tumors reached an appropriate size (150-300 mm³), mice were randomly divided into six groups: a control group, a positive drug group (dacarbazine), a vehicle-treated group (carboxymethyl cellulose), and three ferulic acid dosage groups (10, 30, 50 mg/kg). Mice were treated daily by intragastric administration with ferulic acid or vehicle. Tumor volume and body weight were measured every 3 days. Tumor volume was calculated as mm³ = 0.5 × length (mm) × width (mm)². On day 25, mice were euthanized, and tumor tissues were excised for further analysis, including immunohistochemistry. [1]
* **Immunohistochemistry:** Deparaffinized tumor sections from the xenograft model were stained with specific antibodies against CD31, p-FGFR1 (Tyr154), p-PI3K (p85 Tyr458), and p-Akt (Thr308). Detection was performed using an avidin-biotin-HRP complex and diaminobenzidine as the chromogen. Nuclei were counterstained with hematoxylin. [1]

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Rat Aortic Ring Assay: Aortas were isolated from 6-week-old male Sprague-Dawley rats, cleaned of fat and connective tissue, and cut into rings. 48-well plates were coated with Matrigel. Aortic rings were placed in the wells and sealed with an additional overlay of Matrigel. FGF1 in serum-free M199 medium, with or without ferulic acid, was added to the wells. The medium was changed every 2 days. After 6 days, microvessel sprouting was fixed, photographed, and quantified. [1]
Chick Chorioallantoic Membrane (CAM) Assay: Fertilized chicken eggs were incubated. A window was made in the shell to expose the CAM. FGF1, alone or in combination with ferulic acid, was applied to the CAM. After further incubation, neovascularization was observed and photographed. The absence of dead embryos was noted to rule out general toxicity. [1]
B16F10 Melanoma Xenograft Model: Female C57BL/6 mice were subcutaneously implanted with 3 × 10⁶ B16F10 melanoma cells. On day 7, when tumors reached an appropriate size (150-300 mm³), mice were randomly divided into six groups: a control group, a positive drug group (dacarbazine), a vehicle-treated group (carboxymethyl cellulose), and three ferulic acid dosage groups (10, 30, 50 mg/kg). Mice were treated daily by intragastric administration with ferulic acid or vehicle. Tumor volume and body weight were measured every 3 days. Tumor volume was calculated as mm³ = 0.5 × length (mm) × width (mm)². On day 25, mice were euthanized, and tumor tissues were excised for further analysis, including immunohistochemistry. [1]
Immunohistochemistry: Deparaffinized tumor sections from the xenograft model were stained with specific antibodies against CD31, p-FGFR1 (Tyr154), p-PI3K (p85 Tyr458), and p-Akt (Thr308). Detection was performed using an avidin-biotin-HRP complex and diaminobenzidine as the chromogen. Nuclei were counterstained with hematoxylin. [1]

Absorption, Distribution and Excretion
This study investigated the bioavailability of ferulic acid in humans after tomato consumption by monitoring the relationship between intake and excretion pharmacokinetics. Results showed that peak urinary ferulic acid excretion occurred approximately 7 hours later, and the recovery rate of urinary ferulic acid was 11-25% of the intake, based on the total amount of free ferulic acid and feruloyl glucuronide excreted. …This study examined the excretion of free and conjugated ferulic acid in urine after oral administration of Pinus maritima bark extract (PBE). Eleven healthy adult subjects (4 women and 7 men) received a single dose of 200 mg PBE or two doses of 100 mg and 200 mg PBE within 48 hours. Subjects followed a low-polyphenol diet for two days prior to oral PBE administration and during urine sample collection. All urine samples were collected within 24 hours. The levels of free and bound ferulic acid in urine were determined using high-performance liquid chromatography-diode array detector (HPLC-DAD). Results showed a close correlation between dietary PBE intake and urinary ferulic acid excretion. Furthermore, the results indicated that a significant portion of ferulic acid was excreted as glucuronide or sulfate after PBE administration, with inter-individual differences ranging from 2% to 20%. The excretion kinetics after 100 mg PBE administration were very similar to those after 200 mg PBE administration. Excretion exhibited a biphasic trend in some subjects. All subjects showed significant but differential ferulic acid excretion levels after PBE supplementation. Therefore, the data suggest that at least a portion of the phenolic components in PBE can be absorbed, metabolized, and eliminated by the human body. Hydroxycinnamate, an intermediate in the phenylpropanoid synthesis pathway, effectively enhances the antioxidant capacity of low-density lipoprotein (LDL), with the effects following those of caffeic acid, ferulic acid, and p-coumaric acid. It remains unclear whether the mechanism of action of ferulic acid as an antioxidant is based on its activity in the aqueous or lipophilic phase. Under optimal water solubility conditions, the partitioning of 14C-labeled ferulic acid in plasma and its components (LDL and albumin-rich fractions) was investigated. Results showed that most ferulic acid bound to the albumin-rich fraction in plasma, but some also partitioned between the LDL and aqueous phases. However, ferulic acid did not bind to the lipid portion of low-density lipoprotein (LDL) particles, indicating that it exerts its antioxidant activity in the aqueous phase. This is particularly noteworthy because the results suggest that ferulic acid inhibits LDL oxidation more effectively than the hydrophilic antioxidant ascorbic acid. The main components of artichoke extract are hydroxycinnamic acid compounds, such as chlorogenic acid, dicaffeoylquinic acid compounds (such as caffeic acid and ferulic acid), and flavonoids, such as luteolin and apigenin glycoside. …Multiple studies have shown the effects of artichoke extract on animal models…Results showed that chlorogenic acid peaked at 6.4 (SD 1.8) ng/mL in plasma 1 hour after administration and disappeared within 2 hours (P<0.05). The peak plasma concentration of total caffeic acid reached 19.5 (SD 6.9) ng/mL within 1 hour, while the plasma concentration of ferulic acid showed a biphasic change, reaching 6.4 (SD 1.5) ng/mL and 8.4 (SD 4.6) ng/mL within 1 hour and 8 hours, respectively. …After 8 hours, the total levels of dihydrocaffeic acid and dihydroferulic acid were significantly increased (P<0.05). Luteolin and apigenin were not detected in circulating plasma.

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Metabolism/Metabolites
This study investigated the bioavailability of ferulic acid and its metabolites in plasma and urine of rats after short-term oral administration of 5.15 mg/kg ferulic acid (FA; 3-methoxy-4-hydroxycinnamic acid). Within 30 minutes of ingestion, free ferulic acid, glucuronide conjugates, and sulfonate conjugates were rapidly detected in plasma, reaching peak concentrations. Sulfonate conjugates were the main derivatives (approximately 50%). 1.5 hours after ingestion, the cumulative excretion of total metabolites in urine reached a plateau, with approximately 40% of metabolites excreted via urine. Free ferulic acid recovered in urine accounted for only 4.9 ± 1.5% of the naturally ingested ferulic acid in rats. Glucuronide conjugates and sulfonate conjugates accounted for 0.5 ± 0.3% and 32.7 ± 7.3%, respectively. These results indicate that some of the ferulic acid ingested in the diet is rapidly absorbed and primarily metabolized into sulfonate conjugates before being excreted in urine. Ferulic acid (FA) is a phytochemical commonly found in fruits and vegetables such as tomatoes, sweet corn, and rice bran. Ferulic acid is a product of the metabolism of phenylalanine and tyrosine in plants via the shikimic acid pathway.
It is known that ferulic acid has metabolites in the human body including (2S,3S,4S,5R)-6-[4-[(E)-2-carboxyvinyl]-2-methoxyphenoxy]-3,4,5-trihydroxyoxacyclohexane-2-carboxylic acid.

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Interactions
This study evaluated the effects of topical application of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal ornithine decarboxylase activity, epidermal DNA synthesis, and promotion of skin tumorigenesis in female CD-1 mice. Topical application of 0.5, 1, 3, or 10 μmol curcumin inhibited 5 nmol TPA-induced epidermal ornithine decarboxylase activity by 31%, 46%, 84%, and 98%, respectively. In another study, topical application of 10 μmol curcumin, chlorogenic acid, caffeic acid, or ferulic acid inhibited 5 nmol TPA-induced ornithine decarboxylase activity by 91%, 25%, 42%, and 46%, respectively. Topical application of 10 μmol curcumin in combination with 2 nmol or 5 nmol TPA inhibited TPA-dependent [3H]-thymidine incorporation into epidermal DNA by 49% and 29%, respectively, while lower doses of curcumin had little or no effect. Chlorogenic acid, caffeic acid, and ferulic acid, as inhibitors of TPA-dependent DNA synthesis stimulation, were all less effective than curcumin. In mice pre-injected with 7,12-dimethylbenzo[a]anthracene, topical application of 1, 3, or 10 μmol curcumin twice weekly, along with 5 nmol TPA, for 20 weeks, resulted in a 39%, 77%, and 98% inhibition of TPA-induced tumor numbers per mouse, respectively. Similar treatment with 10 μmol chlorogenic acid, caffeic acid, or ferulic acid in combination with 5 nmol TPA resulted in a 60%, 28%, and 35% inhibition of TPA-induced tumor numbers per mouse, respectively, with higher doses of phenolic acids showing more significant tumor-inhibiting effects. To assess the potential of curcumin in inhibiting arachidonic acid, we investigated the effect of curcumin on arachidonic acid-induced ear edema in mice. Topical application of 3 μmol or 10 μmol curcumin 30 minutes before the application of 1 μmol arachidonic acid inhibited arachidonic acid-induced edema by 33% and 80%, respectively. A series of in vivo experiments were conducted to evaluate the ability of caffeic acid and ferulic acid to reduce UVB-induced skin erythema in healthy volunteers, and the results were monitored by reflectance spectrophotometry. Caffeic acid and ferulic acid dissolved in a saturated aqueous solution at pH 7.2 were shown to significantly protect the skin from UVB-induced erythema. Various synthetic and dietary polyphenols protect mammalian and bacterial cells from cytotoxicity induced by hydrogen peroxide (especially hydrogen peroxide (H₂O₂)). The cytotoxicity of H₂O₂ to Chinese hamster V79 cells was assessed using a colony formation assay. The cytotoxicity and mutagenicity of H₂O₂ against Salmonella TA104 were assessed using the Ames assay. The H₂O₂-induced SOS response was investigated using the SOS chromogenic assay with Escherichia coli PQ37 as a model. The results showed that polyphenolic compounds containing the o-dihydroxy (catechol) structure, such as nordihydroguaiac acid, caffeic acid esters, gallic acid esters, quercetin, and catechins, effectively inhibited H₂O₂-induced cytotoxicity in these assay systems. Conversely, ferulic acid esters and α-tocopherol containing the o-methoxyphenol structure were ineffective, indicating that the o-dihydroxy structure or its equivalent in flavonoids is crucial for protective effects. Many reports have indicated that polyphenolic compounds exhibit pro-oxidative effects in the presence of metal ions. However, these results suggest that they act as antioxidants intracellularly when no metal ions are added to the culture medium. This review describes the radiation injury models induced by soft X-ray irradiation in mice under different conditions, and the protective effects of several substances against these injuries. The radiation injury models in this study included bone marrow death after lethal dose irradiation, skin damage caused by long-wavelength soft X-ray irradiation, and peripheral blood leukopenia after sublethal dose irradiation. Two bioassays were established to evaluate survival rates after lethal dose irradiation and protective efficacy against skin damage induced by soft X-ray irradiation. The protective efficacy of various sulfur compounds, ferulic acid-related compounds, nucleic acid constituent compounds, traditional Chinese medicines, and other traditional Chinese medicines was determined, and several effective drugs were screened. The effective components with radioprotective effects in the methanol extracts of Cnidium monnieri and Aloe vera were isolated. These results indicate that the active components in Cnidium monnieri are ferulic acid and adenosine. The study also evaluated its radioprotective mechanisms, including scavenging reactive oxygen species and protecting DNA and superoxide dismutase from in vitro soft X-ray damage. For more complete data on interactions of ferulic acids (8 in total), please visit the HSDB record page.

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In HUVEC, ferulic acid showed no significant cytotoxicity up to a concentration of 20 μM, as determined by MTT and LDH release assays. Cytotoxic effects were observed at concentrations above 30 μM. [1]
In the chick CAM assay, no dead embryos were observed at the tested dose ranges of ferulic acid, indicating that its anti-angiogenic effect in vivo was not due to overt toxicity. [1]
In the B16F10 mouse xenograft model, ferulic acid treatment at doses up to 50 mg/kg was well tolerated, with no significant difference in body weight between the vehicle-treated group and the FA-treated groups throughout the experiment. [1]
In a cell proliferation assay on normal human epidermal melanocytes (NHEM-a), the inhibitory effect of ferulic acid was observed at higher concentrations compared to its effect on melanoma cell lines, suggesting a degree of selectivity for cancer cells. [1]

[1]. Ferulic Acid Exerts Anti-Angiogenic and Anti-Tumor Activity by Targeting Fibroblast Growth Factor Receptor 1-Mediated Angiogenesis. Int J Mol Sci. 2015 Oct 12;16(10):24011-31.

[2]. Ferulic acid exerts antidepressant-like effect in the tail suspension test in mice: evidence for the involvement of the serotonergic system. Eur J Pharmacol. 2012 Mar 15;679(1-3):68-74.

Ferulic acid is formed by adding methoxy and hydroxy substituents at the 3 and 4 positions of the benzene ring, respectively, to trans-cinnamic acid. It possesses antioxidant, MALDI matrix material, plant metabolite, anti-inflammatory, apoptosis inhibitor, and cardioprotective effects. It is the conjugate acid of ferulic acid.
It has been reported that ferulic acid is found in rosemary, camellia, and some other organisms with relevant data.
Ferulic acid is a metabolite of or produced by Saccharomyces cerevisiae.
See also: Angelica sinensis root (part).
Therapeutic Uses

Ferulic acid (FA) is an effective free radical scavenger and has been approved as a food additive in some countries for preventing lipid peroxidation.
Sodium ferulate (SF), or sodium 3-methoxy-4-hydroxycinnamate, is an active ingredient in plants such as Angelica sinensis, Cimicifuga foetida, and Ligusticum chuanxiong. It has been used in traditional Chinese medicine and has been approved by the China National Medical Products Administration for the treatment of cardiovascular and cerebrovascular diseases. Sodium ferulate (SF) exhibits antithrombotic, platelet aggregation-inhibiting, and antioxidant activities in both animals and humans. For decades, SF has been widely used in China to treat cardiovascular and cerebrovascular diseases and prevent thrombosis…/Sodium ferulate/
/EXPL THER/ Ligusticum chuanxiong and its active ingredients are used to treat ischemic stroke, a common sudden-onset disease in China. Several injectable formulations, including Ligusticum chuanxiong, ligustrazine, ligustrazine alcohol, and ferulic acid, have undergone clinical and experimental testing. Results show that these drugs are as effective as or even better than control groups (such as papaverine, dextran, and aspirin-dipyridamole). They can improve cerebral microcirculation by inhibiting thrombus formation, platelet aggregation, and blood viscosity.
/EXPL THER/ While more definitive research is needed, some natural remedies show promise in treating hot flashes without the risks associated with traditional therapies. Soy and other phytoestrogens, black cohosh, evening primrose oil, vitamin E, bioflavonoids hesperidin and vitamin C, ferulic acid, acupuncture, and regular aerobic exercise have been shown to be effective in treating hot flashes in menopausal women. For more complete data on the therapeutic uses of ferulic acid (6 types), please visit the HSDB record page.

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Ferulic acid (4-hydroxy-3-methoxycinnamic acid) is a ubiquitous phenolic acid found in many plants. It is an effective component of several Chinese medicinal herbs, such as Cimicifuga heracleifolia, Angelica sinensis, and Ligusticum chuangxiong. [1]
It exhibits a broad range of physiological functions, including antioxidant, antimicrobial, anti-thrombosis, anti-inflammatory, anti-hypercholesterolemic, and anti-cancer activities. [1]
Previous studies have reported conflicting roles for ferulic acid in angiogenesis, with some showing pro-angiogenic effects and others anti-angiogenic effects. This study clarifies its role as an anti-angiogenic agent in the context of melanoma by specifically targeting the FGF1/FGFR1 pathway. [1]
The study demonstrates for the first time that ferulic acid is a potent and selective inhibitor of FGFR1, with an IC50 of ~3.78 μM. It shows much weaker inhibition against FGFR2 and minimal activity against other tested receptor tyrosine kinases like VEGFR2 and PDGFR. [1]
The anti-angiogenic and anti-tumor effects of ferulic acid in melanoma are mediated through the suppression of the FGFR1-mediated PI3K-Akt signaling pathway, leading to reduced endothelial cell migration, invasion, and tube formation, as well as direct inhibition of melanoma cell proliferation. [1]

C10H10O4

194.186

194.057

1135-24-6

Ferulic acid sodium;24276-84-4;(E)-Ferulic acid;537-98-4;Ferulic acid-13C3;1261170-81-3

445858

Off-white to yellow solid powder

1.3±0.1 g/cm3

372.3±27.0 °C at 760 mmHg

168 - 171 °C

150.5±17.2 °C

0.0±0.9 mmHg at 25°C

1.627

1.64

2

4

3

14

224

0

COC1=C(C=CC(=C1)/C=C/C(=O)O)O

KSEBMYQBYZTDHS-HWKANZROSA-N

InChI=1S/C10H10O4/c1-14-9-6-7(2-4-8(9)11)3-5-10(12)13/h2-6,11H,1H3,(H,12,13)/b5-3+

(E)-3-(4-hydroxy-3-methoxyphenyl)prop-2-enoic acid

Methyl ferulateFerulic AcidNSC2821Coniferic acidNSC 2821trans-Ferulic acidNSC-2821

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~514.99 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (12.87 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (12.87 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (12.87 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)