- Rat Lens Aldose Reductase (RLAR): Fucosterol exhibits inhibitory activity (kinetic study showed mixed inhibition). [1]
- Human Recombinant Aldose Reductase (HRAR): Fucosterol exhibits inhibitory activity (kinetic study showed mixed inhibition). [1]
- Protein Tyrosine Phosphatase 1B (PTP1B): Fucosterol exhibits inhibitory activity (kinetic study showed non-competitive inhibition). [1]
- Butyrylcholinesterase (BChE): IC50 = 421.72 ± 1.43 μM. [1]
- Acetylcholinesterase (AChE): Fucosterol showed less potent inhibition compared to BChE. [1]

- Anti-adipogenic Activity: In 3T3-L1 pre-adipocytes, fucosterol (3.125-50 μM for 8 days) reduced lipid contents in a concentration-dependent manner without affecting cell viability (up to 50 μM). It decreased the expression of the adipocyte marker proteins peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα). [1]
- Anti-inflammatory Activity: In LPS-stimulated RAW 264.7 macrophages, fucosterol inhibited the production of nitric oxide (NO) and reactive oxygen species (ROS). It suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Fucosterol also suppressed the LPS-induced DNA binding and transcriptional activity of nuclear factor-κB (NF-κB) and attenuated the phosphorylation of MKK3/6 and MK2, which are involved in the p38 MAPK pathway. [1]
- Cytotoxicity in Cancer Cell Lines: Fucosterol showed cytotoxic effects against various cancer cell lines. - Against T47D (breast ductal carcinoma) and HT-29 (colon carcinoma) cells, IC50 values were 27.94 ± 9.3 μg/mL and 70.41 ± 7.5 μg/mL, respectively. It showed no toxic effect on Caco-2 and NIH 3T3 cells up to 70 μg/mL. [4] - Against KB (oral carcinoma), Hep-2 (laryngeal carcinoma), MCF-7 (breast adenocarcinoma), and SiHa (cervix adenocarcinoma) cells, fucosterol showed CC50 (cytotoxic concentration) values of 20.9 μg/mL, 14.8 μg/mL, 25.6 μg/mL, and 18.6 μg/mL, respectively. [5] - The compound 24ζ-hydroperoxy-24-vinylcholesteral (a related sterol) showed higher potency with CC50 values of 3.1 μg/mL (KB), 10.5 μg/mL (Hep-2), 12.1 μg/mL (MCF-7), and 18.9 μg/mL (SiHa). [5] - Fucosterol from Sargassum angustifolium showed an IC50 of 166.42 ± 26.7 μg/mL against T47D and 190.24 ± 52.8 μg/mL against HT-29 cell lines. [4] - Antiproliferative Activity: In MCF-7 and SiHa cell lines, fucosterol showed antiproliferative activity (IC50) of 43.3 μg/mL and 34.0 μg/mL, respectively. [5] - Induction of Apoptosis in HL-60 Cells: Fucosterol inhibited the growth of HL-60 cells and induced apoptosis, showing morphological changes like cell protuberance, concentrated cytoplasm, and apoptotic bodies. It reduced the mitochondrial membrane potential, induced the release of cytochrome c, and activated caspase-9 and caspase-3. Fucosterol also increased the protein expression of Fas, FasL, Fadd, and caspase-8, indicating involvement of the death receptor pathway. [1]
- Cell Cycle Arrest: Fucosterol arrested the cell cycle of HL-60 cells at the G2/M phase. [1]
- Anti-leishmanial Activity: Fucosterol was identified as a constituent in active fractions, but its specific activity was not detailed. [3]

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In comparison to fully differentiated control adipocytes, fumasterol (0-50 μM; 7 days) inhibits the expression of C/EBPα and PPARα [1]. With IC50 values of 27.94 and 70.41 μg/ml, respectively, fumonisin is cytotoxic to T47D and HT29 cell lines[3]. With IC50 values of 185.4, 43.3, and 34.0 μg/ml, respectively, fumonisin inhibits the proliferation of HEK293, MCF-7, and SiHa cells [4].

- Antidiabetic Activity (STZ-induced diabetic rats): Oral administration of fucosterol (30 mg/kg) to streptozotocin-induced diabetic rats caused a significant decrease in serum glucose concentrations (to 404.00 ± 21.24 g/L compared to diabetic control 474.20 ± 15.15 g/L) and exhibited an inhibition of sorbitol accumulation in the lenses (1.42 ± 0.08 vs. 1.83 ± 0.14 nmol/mg dry wt. for control). No significant inhibition was observed in RBC or sciatic nerve sorbitol levels. [2]
- Antidiabetic Activity (Epinephrine-induced diabetic mice): Oral administration of fucosterol (300 mg/kg) to epinephrine-induced diabetic mice inhibited the blood glucose level (by 33% compared to control) and glycogen degradation (by 29% compared to control). [2]
- Antioxidant and Hepatoprotective Activity (CCl4-intoxicated rats): In rats with carbon tetrachloride-induced liver damage, fucosterol (30 mg/kg body weight for 3 days) downregulated elevated serum transaminase activities (sGOT and sGPT) by 25.57% and 63.16%, respectively. It enhanced the activities of hepatic antioxidant enzymes: superoxide dismutase (33.89%), catalase (21.56%), and glutathione peroxidase (39.24%). [1]
- Anti-osteoporotic Activity (OVX rats): In ovariectomized (estrogen-deficient) rats, fucosterol treatment enhanced bone mineral density of the femoral bone, increased bone volume/total volume, decreased trabecular separation, and upregulated serum osteocalcin level (more than triple the OVX control) while downregulating serum CTx level. It also promoted osteoblast proliferation and suppressed osteoclast differentiation in in vitro assays using MG63 cells. [1]
- Anti-hyperlipidemic Activity: In hyperlipidemic rats, dietary supplementation with sea tangle extract residue (containing fucosterol) at 200 mg/kg body weight substantially decreased total lipid and triglyceride levels in serum, and modified total cholesterol and LDL-cholesterol levels. The atherosclerosis index was also significantly smaller. [1]
- Anti-atopic Activity (DNCB-induced atopic dermatitis in NC/Nga mice): Oral administration of fucosterol (200 mg/kg/day) reduced the frequency of scratching, epidermal thickness, and the number of degranulated mast cells. It decreased serum immunoglobulin E (IgE) levels and inhibited IL-4 and TNF-α levels while upregulating IFN-γ secretion in cultured splenocytes. [1]

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Oral treatment of 30 mg/kg of fumosterol significantly lowers serum glucose levels and prevents the build-up of sorbitol in the lens [2].

- Aldose Reductase (AR) Inhibition Kinetics: The inhibitory activity of fucosterol against rat lens aldose reductase (RLAR) and human recombinant aldose reductase (HRAR) was evaluated. In a kinetic experiment, fucosterol displayed mixed inhibition against both RLAR and HRAR. Docking simulations provided negative binding energies for fucosterol (-8.2 kcal/mol for RLAR and -8.5 kcal/mol for HRAR), suggesting a higher affinity for the active site of the enzyme. [1]
- Protein Tyrosine Phosphatase 1B (PTP1B) Inhibition: Fucosterol showed inhibitory effects against PTP1B. In a kinetic experiment, it displayed non-competitive inhibition. [1]
- Cholinesterase Inhibition Assay: Fucosterol was tested for its ability to inhibit acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). The IC50 value against BChE was determined to be 421.72 ± 1.43 μM. [1]

- Cell Viability (MTT Assay): 3T3-L1 cells were seeded in 96-well plates, treated with various concentrations of fucosterol for 24 hours, then MTT solution was added for 3 hours. The formazan product was dissolved in DMSO, and absorbance was measured at 540 nm. Fucosterol showed no cytotoxicity up to 50 μM. [1] For cancer cell lines (KB, Hep-2, MCF-7, SiHa), cells were seeded in 96-well plates, incubated with compounds for 72 hours, then MTT solution was added for 4 hours. The formazan was solubilized with acidified isopropanol, and absorbance was measured at 590 nm. [5] For other cancer cell lines (T47D, HT-29, Caco-2, NIH 3T3), cells were treated for 72-120 hours, MTT reagent was added for 4 hours, and the formazan was dissolved in DMSO for absorbance measurement at 550 nm. [4]
- Antiproliferative Assay (Sulforhodamine B - SRB): Cells were seeded in 96-well plates, treated with compounds for 48 hours, then fixed with 10% trichloroacetic acid. After staining with SRB solution, the bound dye was solubilized, and absorbance was measured at 540 nm. [5]
- Oil Red O Staining for Adipogenesis: Differentiated 3T3-L1 cells were fixed with formaldehyde and stained with Oil Red O solution. Stained oil droplets were photographed, extracted with isopropanol, and quantified by absorbance at 510 nm. [1]
- Western Blot Analysis: 3T3-L1 cells were treated with fucosterol, lysed, and proteins were separated by SDS-PAGE, transferred to PVDF membranes, and probed with specific antibodies for PPARγ and C/EBPα. [1] For RAW 264.7 macrophages, expression of iNOS and COX-2 was detected. [1]
- Apoptosis Assay (HL-60 cells): HL-60 cells were treated with fucosterol, and apoptosis was assessed by morphological changes, mitochondrial membrane potential (using a fluorescent dye), and activation of caspases (using colorimetric substrates or Western blot for cleaved forms). [1]

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Cell viability assay [1]
Cell Types: 3T3-L1 adipocyte
Tested Concentrations: 0 μM; 25 μM; 50 μM
Incubation Duration: 7 days
Experimental Results: Inhibition of PPARα and C/EBPα expression.

- STZ-induced Diabetic Rat Model: Male Sprague-Dawley rats were made diabetic by a single intravenous injection of streptozotocin (85 mg/kg) dissolved in acidified citrate buffer (pH 4.5). Fucosterol (30 mg/kg) or epalrestat (50 mg/kg) were administered via an intragastric tube at 4, 7, and 24 hours. Three hours after the last administration, blood samples were collected, and lenses and sciatic nerves were removed. [2]
- Epinephrine-induced Diabetic Mouse Model: Groups of 8 mice were administered i.p. with fucosterol (100 or 300 mg/kg) dissolved in olive oil or vehicle alone. Four hours later, epinephrine (0.6 mg/kg i.p.) was administered. Blood samples were withdrawn by decapitation 1 hour post-dosing, and livers were removed for glycogen content measurement. [2]
- CCl4-intoxicated Rat Model (Hepatoprotective): Rats were treated with fucosterol (30 mg/kg body weight for 3 days) before or after CCl4 intoxication. Blood and liver samples were collected for biochemical analysis. [1]
- OVX Rat Model (Anti-osteoporotic): Female ovariectomized (OVX) rats were used as a model for postmenopausal osteoporosis. Fucosterol was administered, and bone mineral density, bone volume, and serum biomarkers (osteocalcin, CTx) were analyzed. [1]
- DNCB-induced Atopic Dermatitis Mouse Model: NC/Nga mice were treated with DNCB to induce atopic dermatitis-like lesions. Fucosterol was administered orally (200 mg/kg/day). Scratching frequency, epidermal thickness, mast cell degranulation, serum IgE, and cytokine levels (IL-4, TNF-α, IFN-γ) were assessed. [1]

- Cytotoxicity in Normal Cells: Fucosterol showed no toxic effect on normal Caco-2 and NIH 3T3 cell lines up to 70 μg/mL. [4] Against the normal HEK-293 cell line, the CC50 (cytotoxic concentration) of fucosterol was 147.9 μg/mL. [5]
- General Safety: In animal studies, no specific toxic effects were reported at the doses used (e.g., 30 mg/kg in rats, 300 mg/kg in mice). [1][2]

[1]. Anti-adipogenic activity of the edible brown alga Ecklonia stolonifera and its constituent fucosterol in 3T3-L1 adipocytes. Arch Pharm Res. 2014 Jun;37(6):713-20.

[2]. Anti-diabetic activities of fucosterol from Pelvetia siliquosa. Arch Pharm Res. 2004 Nov;27(11):1120-2.

[3]. Health benefit of fucosterol from marine algae: a review. J Sci Food Agric. 2016 Apr;96(6):1856-66.

[4]. Cytotoxicity of fucosterol containing fraction of marine algae against breast and colon carcinoma cell line. Pharmacogn Mag. 2012 Jan;8(29):60-4.

[5]. Cytotoxic and antiproliferative constituents from Dictyota ciliolata, Padina sanctae-crucis and Turbinaria tricostata. Pharm Biol. 2014 Oct;52(10):1244-8.

- Source: Fucosterol is a characteristic sterol of brown algae (Phaeophyceae) and can be isolated from species such as Ecklonia stolonifera, Pelvetia siliquosa, Sargassum angustifolium, Turbinaria tricostata, Dictyota ciliolata, Padina sanctae-crucis, and Hizikia fusiformis. [1][2][3][4][5]
- Mechanism of Anti-adipogenic Effect: Fucosterol inhibits adipocyte differentiation in 3T3-L1 cells by downregulating the expression of key adipogenic transcription factors PPARγ and C/EBPα, leading to reduced lipid accumulation. [1]
- Mechanism of Anti-inflammatory Effect: The anti-inflammatory activity of fucosterol in macrophages is primarily related to the suppression of the NF-κB and p38 MAPK signaling pathways, leading to reduced expression of iNOS, COX-2, and pro-inflammatory cytokines. [1]
- Mechanism of Antidiabetic Effect: Fucosterol exhibits antidiabetic activity by inhibiting aldose reductase (a key enzyme in the polyol pathway implicated in diabetic complications) and protein tyrosine phosphatase 1B (a negative regulator of insulin signaling). It also lowers blood glucose and inhibits glycogen degradation in epinephrine-induced hyperglycemia. [1][2]
- Mechanism of Cytotoxic Effect: Fucosterol induces apoptosis in HL-60 leukemia cells through both the mitochondrial pathway (involving loss of MMP, cytochrome c release, and caspase-9 activation) and the death receptor pathway (involving Fas/FasL and caspase-8 activation). It also causes G2/M cell cycle arrest. [1]

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Isofucosterol is a 3β-sterol composed of stigmasterane-3β-ol, with double bonds at positions 5 and 24(28). The double bond at position 24(28) has a Z configuration. It is found in animals, plants, algae, and marine organisms as a metabolite. It is a 3β-sterol, 3β-hydroxy-Δ(5)-steroid, C29-steroid, belonging to the phytosterol class of compounds. It is derived from the hydride of stigmasterane. Fucosterol has been reported to be found in horsetail, potato, and other organisms with relevant data. See also: Fucosterol (note moved to).

C29H48O

412.702

412.371

C, 84.40; H, 11.72; O, 3.88

17605-67-3

5281326

White to off-white solid powder

0.98 g/cm3

504.2ºC at 760 mmHg

118-120ºC

220.3ºC

2.8E-12mmHg at 25°C

1.53

7.944

1

1

5

30

687

8

C/C=C(/CC[C@@H](C)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2CC=C4[C@@]3(CC[C@@H](C4)O)C)C)\C(C)C

OSELKOCHBMDKEJ-WGMIZEQOSA-N

InChI=1S/C29H48O/c1-7-21(19(2)3)9-8-20(4)25-12-13-26-24-11-10-22-18-23(30)14-16-28(22,5)27(24)15-17-29(25,26)6/h7,10,19-20,23-27,30H,8-9,11-18H2,1-6H3/b21-7-/t20-,23+,24+,25-,26+,27+,28+,29-/m1/s1

(3S,8S,9S,10R,13R,14S,17R)-10,13-dimethyl-17-[(Z,2R)-5-propan-2-ylhept-5-en-2-yl]-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol

28-Isofucosterol; Fucosterin; 17605-67-3; (24E)-24-N-Propylidenecholesterol; trans-24-Ethylidenecholesterol; Fucosterol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

Ethanol : ~16.67 mg/mL (~40.39 mM)
DMSO :< 1 mg/mL

Solubility in Formulation 1: ≥ 1.67 mg/mL (4.05 mM) (saturation unknown) in 10% EtOH + 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 16.7 mg/mL clear EtOH + stock solution to 900 μL of corn oil and mix well.

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Solubility in Formulation 2: 10 mg/mL (24.23 mM) in Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution; Need ultrasonic and warming and heat to 45°C.

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Solubility in Formulation 3: 6.25 mg/mL (15.14 mM) in 17% Polyethylene glycol 12-hydroxystearate in Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; Need ultrasonic and warming and heat to 42°C.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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