Fucoxanthinol
Fucoxanthinol, a carotenoid, is a deacetylated Fucoxanthin (HY-N2302) metabolite with oral activity, and inhibits rat pancreatic lipase with an IC50 of 764 nM. Fucoxanthinol reduces expression of Bcl-2, Bcl-xL, survivin, XIAP, cIAP2, cyclin D1, cyclin D2, cyclin E, CDK4, CDK6, β-catenin, JunD, PPARγ, and induces GADD45α expression. Fucoxanthinol activates caspase-3, caspase-8, caspase-9, Nrf2/Keap1/ARE pathway, and inhibits activation of Akt, NF-κB, AP-1, PDPK1, GSK3β phosphorylation. Fucoxanthinol induces apoptosis, G0/G1 cell cycle arrest, inhibits cancer cell viability, proliferation, migration, invasiveness, tumour growth, adipocyte differentiation, oxidative stress, neurotoxicity, triglyceride absorption, angiogenesis, and obesity-induced inflammation. Fucoxanthinol can be used for the research of osteosarcoma, leukemia, lymphoma, adult T-cell leukemia, prostate cancer, colon cancer, breast cancer, hypertriglyceridaemia, Alzheimer’s disease, Parkinson’s disease, obesity, insulin resistance, malignant melanoma, and type II diabetes.
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- CAS No.: 7176-02-5
- 화학식: C40H56O5
- 분자량:616.87
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Biological Activity
Fucoxanthinol exhibits anti-proliferative, pro-apoptotic, and anti-metastatic activity in human osteosarcoma cell lines (Saos-2, LM8, MNNG, 143B) via modulation of cell cycle regulators, apoptotic mediators, the PI3K-Akt-GSK3β-β-Catenin pathway, and AP-1-dependent MMP-1 expression[1].
Fucoxanthinol inhibits viability and induces apoptosis in human primary effusion lymphoma cells via G0/G1 cell cycle arrest, inhibition of pro-survival signalling pathways (NF-κB, AP-1, Akt), and downregulation of anti-apoptotic proteins[1].
Fucoxanthinol inhibits viability and induces apoptosis in HTLV-1-infected T-cell lines and adult T-cell leukemia cells via G0/G1 cell cycle arrest, modulation of apoptotic mediators, and inactivation of NF-κB and AP-1 signalling[1].
Fucoxanthinol exerts anti-proliferative and pro-apoptotic effects in human B-cell malignancies via G0/G1 cell cycle arrest, caspase activation, and inhibition of NF-κB-dependent pro-survival and cell cycle regulatory pathways[1].
Fucoxanthinol (10-20 µM) inhibits viability and induces apoptosis in human breast cancer MCF-7 and MDA-MB-231 cells; in MDA-MB-231 cells, these effects are linked to inhibition of NF-κB pathway members and reduced nuclear SOX9 levels[1].
Fucoxanthinol, alongside Fucoxanthin, induces apoptosis in human leukemia HL-60 cells via caspase and PARP cleavage and modulation of Bcl family proteins[1].
Fucoxanthinol (0-5 μM; 24 h) dose-dependently induces apoptosis in BCBL-1 and TY-1 PEL cells[4].
Fucoxanthinol (5 μM; 24 h) induces chromatin condensation and nuclear fragmentation, hallmarks of apoptosis, in BCBL-1 and TY-1 PEL cells[4].
Fucoxanthinol (0-5 μM; 24 h) dose- and time-dependently induces cleavage of PARP, caspase-3, caspase-9, and caspase-8, indicating caspase activation, in BCBL-1 and TY-1 PEL cells[4].
Fucoxanthinol (5 μM; 24 h) activates caspase-3, caspase-8, and caspase-9 in BCBL-1 and TY-1 PEL cells[4].
Fucoxanthinol (6.25-12.5 μM; 24 h) induces apoptosis in HL-60 human leukemia cells, enhancing relative DNA fragmentation to 7-fold of control at 12.5 μM after 24 h incubation[5].
Fucoxanthinol (12.5-25 μM; 48 h) induces apoptosis in MCF-7 human breast cancer cells, enhancing relative DNA fragmentation to ~11-fold of control at 25 μM after 48 h incubation[5].
Fucoxanthinol (12.5-25 μM; 48 h) induces apoptosis in Caco-2 human colon cancer cells, enhancing relative DNA fragmentation to ~5.7-fold of control at 25 μM after 48 h incubation[5].
Fucoxanthinol (6.25 μM; 36 h) downregulates the expression of the apoptosis-suppressing protein Bcl-2 in HL-60 human leukemia cells, reducing levels to ~40% of control at 6.25 μM after 36 h incubation[5].
Fucoxanthinol (0.63-10 μM; 24 h) induces apoptosis in Raji, Daudi, B95-8/Ramos, LCL-Ka, and LCL-Ku cells, with 2.5 μM fucoxanthinol yielding similar apoptotic levels to 5 μM fucoxanthin, and exerts dose-dependent pro-apoptotic effects in Daudi cells with greater potency than fucoxanthin[8].
Fucoxanthinol (0.63-5 μM; 24 h) induces dose-dependent activation of caspase-3 and caspase-9, and cleavage of PARP, in Daudi cells[8].
Fucoxanthinol (0.63-5 μM; 24 h) downregulates expression of Bcl-2, cIAP-2, XIAP, cyclin D1, and cyclin D2, and reduces IκBα phosphorylation while increasing total IκBα levels, in Daudi cells in a dose-dependent manner[8].
Fucoxanthinol (5 μM; 6 h) activates caspase-3 and caspase-9 in Daudi and KM-H2 cells, with 5 μM fucoxanthinol inducing ~15-fold and ~19-fold increases in caspase-3 activity, and ~3.5-fold and ~7-fold increases in caspase-9 activity, in Daudi and KM-H2 cells, respectively[8].
Fucoxanthinol (0-30 μM; 24 h) dose-dependently reduces cell viability of Saos-2, MNNG/HOS, 143B, and LM8 osteosarcoma cells, with complete viability loss in Saos-2 cells at 20 μM after 24 h[2].
Fucoxanthinol (0.63-1.25 μM; 6 h) significantly inhibits SDF-1α-induced migration of Saos-2 osteosarcoma cells over 6 h[2].
Fucoxanthinol (0.05-0.1 μM; 24 h) significantly inhibits invasion of Saos-2 osteosarcoma cells through type I collagen over 24 h[2].
Fucoxanthinol (20 μM; 0-12 h) time-dependently inhibits AP-1 DNA binding activity in Saos-2 osteosarcoma cells, without affecting Oct-1 binding[2].
Fucoxanthinol (0, 0.6, 3, 15, 75 μM; 24 h) exhibits cell line-dependent cytotoxicity, with an IC50 ranging from 4.565 μM in SW620 cells to 53.016 μM in Hela cells, and 3 μM fucoxanthinol does not impair HepG2 cell proliferation[3].
Fucoxanthinol (12.5-50 μM; 24-72 h) potently inhibits the proliferation of HL-60 human leukemia cells in a dose- and time-dependent manner, reducing viability to 5.7% of control at 12.5 μM after 48 h incubation[5].
Fucoxanthinol (25 μM; 48-72 h) inhibits the proliferation of MCF-7 human breast cancer cells, reducing viability to ~12% of control at 25 μM after 72 h incubation[5].
Fucoxanthinol (12.5 μM; 48-72 h) inhibits the proliferation of Caco-2 human colon cancer cells, reducing viability to ~12% of control at 12.5 μM after 72 h incubation[5].
Fucoxanthinol (0.63-10 μM; 24 h) potently inhibits cell viability of HTLV-1-infected T-cell lines (IC50: 0.86-1.83 μM) and primary ATL cells (IC50: 0.46-3.84 μM) in vitro, with minimal effects on uninfected cell lines and healthy PBMCs[6].
Fucoxanthinol (5 μM; 12 h for EMSA; 0, 6, 12, 24 h for Western blot) suppresses NF-κB activity by inhibiting IκBα phosphorylation and suppresses AP-1 activity by downregulating JunD expression in HTLV-1-infected T-cell lines (MT-2, HUT-102) in vitro[6].
Fucoxanthinol (0.63-10 μM; 24 h) potently reduces viability of LCL-Ka, LCL-Ku, Raji, Daudi, BJAB, Ramos, B95-8/BJAB, B95-8/Ramos, HDLM-2, L540, L428, and KM-H2 cells in a dose-dependent manner, with greater potency than fucoxanthin, while healthy human PBMC are less susceptible[8].
Fucoxanthinol (0.625-20 μM; 72 h) inhibits the proliferation of PC-3 human prostate cancer cells with an IC50 of 2.0 μM after 72 h of incubation[11].
Fucoxanthinol (5-20 μM; 24 h drug treatment, 6 days drug-free incubation) reduces cell viability (measured by T/C (%)) in Caco-2, WiDr, SW620, HCT116, and DLD-1 human colorectal cancer cell lines in a dose-dependent manner, with the strongest effect in Caco-2 cells (T/C (%) = 1.4% at 20 μM), but does not reduce viability in Colo205 cells[16].
Fucoxanthinol (5-20 μM; 24 h drug treatment, 6 days drug-free incubation) reduces cell viability (measured by T/C (%)) in surgically resected human colorectal cancer tissue samples in a dose-dependent manner, with 65% of samples showing T/C (%) <50% at 20 μM, and also exhibits activity against drug-resistant cancer samples and a malignant melanoma sample[16].
Fucoxanthinol (20 μM; 9 h) induces apoptosis in 34.9% of Saos-2 osteosarcoma cells as detected by Apo2.7 staining[2].
Fucoxanthinol (5-20 μM; 9 h) dose-dependently activates caspases-3/7, -8, and -9 in Saos-2 osteosarcoma cells over 9 h[2].
Fucoxanthinol (5-20 μM; 0-12 h) induces time- and dose-dependent cleavage of caspases-3, -8, -9, and PARP in Saos-2 osteosarcoma cells, confirming caspase-mediated apoptosis[2].
Fucoxanthinol (5-20 μM; 0-12 h) time- and dose-dependently reduces expression of anti-apoptotic proteins survivin, XIAP, Bcl-2, and Bcl-xL in Saos-2 osteosarcoma cells, without affecting NF-κB activation[2].
Fucoxanthinol (5-20 μM; 0-12 h) time- and dose-dependently inhibits phosphorylation of PDK1, Akt, GSK3β, and caspase-9, and reduces β-catenin levels in Saos-2 osteosarcoma cells, suppressing the Akt signaling pathway[2].
Fucoxanthinol (5-20 μM; 0-12 h) time- and dose-dependently reduces MMP-1 protein expression in Saos-2 osteosarcoma cells[2].
Fucoxanthinol (20 μM; 9 h) induces G1 cell cycle arrest in Saos-2 and LM8 osteosarcoma cells, with a corresponding reduction in S phase cells[2].
Fucoxanthinol (20 μM; 0-12 h) reduces expression of CDK4, CDK6, and cyclin E, and inhibits p130 phosphorylation in Saos-2 osteosarcoma cells over 12 h, contributing to G1 cell cycle arrest[2].
Fucoxanthinol (3 μM; 24 h post-TBT treatment) significantly restores viability and improves cell morphology in HepG2 cells treated with 0.2 μM TBT for 6 h[3].
Fucoxanthinol (10 μM; 24-57 h) accumulates in 3T3-L1 preadipocytes undergoing adipocyte differentiation, reaching 5.8 μg/mg protein at 24 h, and increasing to 11.8 μg/mg protein by 57 h at a treatment concentration of 10 μM[10].
Fucoxanthinol (10 μM; 60 min) is converted by mouse liver microsomes to amarouciaxanthin A with high efficiency, requiring NAD+ as a cofactor and an optimal pH of 9.5 to 10.0[11].
Fucoxanthinol (1.0 μM; 24 h) is converted by HepG2 human hepatoma cells to amarouciaxanthin A over 24 h, with the metabolite accumulating in both cells and culture medium[11].
Fucoxanthinol (1 μmol/L; 0-24 h) accumulates in differentiated Caco-2 cells and culture medium over a 24-hour period following incubation of cells with 1 μmol/L micellar fucoxanthin, reaching a cellular level of 167 pmol/well by 24 h[15].
Fucoxanthinol (1 μmol/L; 6-24 h) is actively secreted into the basolateral medium by differentiated Caco-2 cells grown on Transwells, reaching levels of 42 pmol/filter after 24 h incubation of cells with 1 μmol/L apical micellar fucoxanthin[15].
Fucoxanthinol (3 μM; 24 h post-TBT treatment) reduces TBT-induced oxidative damage in HepG2 cells by decreasing intracellular ROS and MDA, normalizing extracellular SOD, and increasing intracellular SOD activity[3].
Fucoxanthinol (5 µM; 1 min) exhibits significantly higher extracellular free radical scavenging activity than fucoxanthin in a cell-free ABTS assay, with a TAA of 240 µmol Trolox equivalents/mL at 5 µM[9].
Fucoxanthinol (5 µM; 2 h) enhances the antioxidant activity of SH-SY5Y cell membrane and cytoplasmic fractions, with TAAs of 440 µmol Trolox equivalents/mg protein (membrane) and 5600 µmol Trolox equivalents/mg protein (cytoplasm) at 5 µM, though its activity is lower than that of fucoxanthin[9].
Fucoxanthinol (2.5-5 µM; 30 min co-incubation/24 h pre-incubation) significantly inhibits t-BuOOH-induced ROS formation in SH-SY5Y cells when co-treated at 2.5 µM or 5 µM, and shows moderate inhibition when pre-treated at 5 µM for 24 h[9].
Fucoxanthinol (5 µM; 24 h) increases intracellular GSH levels in SH-SY5Y cells to 68 µM when treated at 5 µM for 24 h[9].
Fucoxanthinol (2.5-5 µM; 3 h) activates the Nrf2/Keap1 pathway in SH-SY5Y cells by increasing Nrf2 protein levels at 2.5 µM and 5 µM, and reducing Keap1 protein levels at 5 µM after 3 h of treatment[9].
Fucoxanthinol (5 µM; 24 h) upregulates Nrf2 and NQO1 gene expression in SH-SY5Y cells when treated at 5 µM for 24 h, but does not affect GSTP1 expression[9].
Fucoxanthinol (5 µM; 4 h co-incubation/24 h pre-incubation) significantly protects SH-SY5Y cells from AβO-induced neurotoxicity when co-treated at 5 µM for 4 h, but does not provide protection when pre-treated for 24 h[9].
Fucoxanthinol (5 µM; 2 h co-incubation/24 h pre-incubation) significantly protects SH-SY5Y cells from 6-OHDA-induced neurotoxicity both when co-treated at 5 µM for 2 h and when pre-treated at 5 µM for 24 h[9].
Fucoxanthinol (3 μM; 24 h post-TBT treatment) reduces TBT-induced apoptosis in HepG2 cells, as shown by increased normal cell percentage and decreased apoptotic cell percentage via flow cytometry[3].
Fucoxanthinol (3 μM; 24 h post-TBT treatment) increases the Bcl-2/Bax ratio in TBT-treated HepG2 cells by upregulating Bcl-2 and downregulating Bax, thereby inhibiting mitochondrial-dependent apoptosis[3].
Fucoxanthinol (5 μM; 24 h) induces caspase-dependent apoptosis in HTLV-1-infected T-cell lines (MT-2, MT-4, HUT-102, ED-40515(-)) in vitro, with minimal effects on uninfected HeLa cells and reduced effects on Jurkat cells[6].
Fucoxanthinol (0-5 μM; 24 h) potently reduces the viability of BCBL-1 and TY-1 PEL cells with an IC50 of 1.1 μM, while having weaker effects on HeLa cells and no toxic effect on healthy PBMC[4].
Fucoxanthinol (2.5 μM; 24 h) induces G1 cell cycle arrest by increasing G1-phase cell populations and reducing S-phase cell populations in BCBL-1 and TY-1 PEL cells[4].
Fucoxanthinol (1.25 μM; 24 h) induces G1 cell cycle arrest in Daudi, KM-H2, and L540 cells, reducing S-phase cell populations[8].
Fucoxanthinol (0-5 μM; 24 h) dose-dependently down-regulates anti-apoptotic proteins Bcl-xL, XIAP, and survivin, cell cycle regulatory proteins cyclin D2, CDK4, CDK6, and c-Myc, and reduces pRb and caspase-9 phosphorylation in BCBL-1 PEL cells[4].
Fucoxanthinol (0-5 μM; 24 h) dose-dependently inhibits the NF-κB, AP-1, and PI3K/Akt pathways in BCBL-1 PEL cells by reducing phosphorylation of IKKβ, IκBα, and Akt, and decreasing protein levels of IKKα, IKKβ, IKKγ, JunB, JunD, Akt, PDK1, and β-catenin[4].
Fucoxanthinol (5 μM; 0-24 h) time-dependently inhibits constitutive NF-κB and AP-1 DNA-binding activity in BCBL-1 PEL cells[4].
Fucoxanthinol (5 μM; 24 h) reduces levels of CDK4, CDK6, survivin, IKKα, IKKβ, IKKγ, Akt, PDK1, and JunD in BCBL-1 PEL cells via proteasome-dependent degradation, as this effect is reversed by co-treatment with the proteasome inhibitor LLnL[4].
Fucoxanthinol (5 μM; 0-24 h) down-regulates expression of HHV-8 latent genes v-FLIP and v-cyclin without inducing lytic gene expression in BCBL-1 PEL cells[4].
Fucoxanthinol (5 μM; 12-24 h) induces G1 phase cell cycle arrest in HTLV-1-infected T-cell lines (MT-2, MT-4, HUT-102, ED-40515(-)) in vitro, preceding apoptotic cell death[6].
Fucoxanthinol (5 μM; 12 h for primary ATL cells; 0, 6, 12, 24 h for MT-2, HUT-102 cells) modulates the expression of cell cycle and apoptosis-related proteins in HTLV-1-infected T-cell lines (MT-2, HUT-102) and primary ATL cells in vitro, downregulating pro-proliferative and anti-apoptotic factors while upregulating a cell cycle inhibitor[6].
Fucoxanthinol (0.02-1 μmol/mL; 30 min) inhibits rat pancreatic lipase activity in vitro with an IC50 of 764 nmol/l[7].
Fucoxanthinol (2.5-10 μM; 120 h) dose-dependently suppresses intercellular lipid accumulation during adipocyte differentiation of 3T3-L1 preadipocytes, with 10 μM reducing staining to 14% of control levels[10].
Fucoxanthinol (2.5-7.5 μM; 120 h) suppresses GPDH activity during adipocyte differentiation of 3T3-L1 preadipocytes, with 2.5, 5, and 7.5 μM reducing activity to levels below control differentiated cells, and 5 and 7.5 μM showing stronger inhibition than fucoxanthin[10].
Fucoxanthinol (2.5-5 μM; 120 h) down-regulates PPARγ protein expression during adipocyte differentiation of 3T3-L1 preadipocytes, with 5 μM reducing expression to 47% of control levels[10].
Fucoxanthinol (1-10 μM; duration of adipocyte differentiation) inhibits lipid accumulation and downregulates adipogenic marker gene expression in differentiating 3T3-L1 preadipocytes[17].
Fucoxanthinol (0.63-10 μM; 24 h) inhibits constitutive NF-κB-DNA binding activity in Daudi and KM-H2 cells in a dose-dependent manner[8].
Fucoxanthinol (5-10 μM; 24 h) suppresses pro-inflammatory mediator gene expression, protein secretion, and COX-2 protein expression in co-cultured 3T3-L1 adipocytes and RAW264.7 macrophages, with significant effects observed at 5 μM and 10 μM concentrations after 24 hours of incubation[13].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human osteosarcoma cell lines Saos-2, MNNG/HOS, 143B, mouse osteosarcoma cell line LM8
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Concentration:0-30 μM
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Incubation Time:24 h
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Result:Reduced cell viability of all four osteosarcoma cell lines in a dose-dependent manner.
Reduced Saos-2 cell viability to 0% relative to untreated controls at 20 μM.
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Cell Line:human osteosarcoma Saos-2 cells
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Concentration:20 μM
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Incubation Time:9 h
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Result:Increased the proportion of apoptotic Saos-2 cells detected by Apo2.7 staining from 0.3% in untreated controls to 34.9%.
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Cell Line:human osteosarcoma Saos-2 cells
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Concentration:5-20 μM
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Incubation Time:0-12 h
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Result:Induced time- and dose-dependent cleavage of caspase-3, caspase-8, caspase-9, and PARP, with increasing cleavage observed at longer incubation times and higher concentrations.\nReduced the expression of anti-apoptotic proteins survivin, XIAP, Bcl-2, and Bcl-xL in a time- and dose-dependent manner.
Had no effect on pro-apoptotic protein Bak expression.
Did not alter total or phosphorylated IκBα levels.\nReduced phosphorylation of PDK1, Akt (Thr308 and Ser473), GSK3β, and caspase-9 in a time- and dose-dependent manner.
Had no effect on total PDK1, Akt, or GSK3β expression.
Reduced β-catenin levels.\nReduced MMP-1 protein expression in a time- and dose-dependent manner.
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Cell Line:human osteosarcoma Saos-2 cells, mouse osteosarcoma LM8 cells
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Concentration:20 μM
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Incubation Time:9 h
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Result:Increased the proportion of Saos-2 and LM8 cells in the G1 phase relative to untreated controls.
Markedly reduced the proportion of Saos-2 and LM8 cells in the S phase relative to untreated controls.
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Cell Line:human osteosarcoma Saos-2 cells
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Concentration:20 μM
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Incubation Time:0-12 h
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Result:Reduced the expression of CDK4, CDK6, and cyclin E in a time-dependent manner.
Had no effect on CDK2, cyclin D1, or cyclin D2 expression.
Inhibited phosphorylation of p130.
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Cell Line:human osteosarcoma Saos-2 cells
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Concentration:0.63-1.25 μM
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Incubation Time:6 h
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Result:Inhibited SDF-1α-induced migration of Saos-2 cells in a dose-dependent manner.
Caused significant reduction in relative cell index at both tested concentrations.
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Cell Line:human osteosarcoma Saos-2 cells
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Concentration:0.05-0.1 μM
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Incubation Time:24 h
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Result:Inhibited invasion of Saos-2 cells through type I collagen in a dose-dependent manner.
Caused significant reduction in relative cell index at both tested concentrations.
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Cell Line:HepG2, Hela, SW620, SW480, MDCK cells
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Concentration:0, 0.6, 3, 15, 75 μM
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Incubation Time:24 h
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Result:Determined half-maximal inhibitory concentration (IC50) values for each cell line: HepG2 (32.508 μM), Hela (53.016 μM), SW620 (4.565 μM), SW480 (21.000 μM), MDCK (31.897 μM).
Showed no negative effect on HepG2 cell proliferation at 3 μM.
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Cell Line:TBT-treated HepG2 cells
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Concentration:3 μM (fucoxanthinol); 0.2 μM (TBT)
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Incubation Time:24 h (fucoxanthinol post-TBT treatment); 6 h (TBT)
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Result:Restored HepG2 cell viability significantly compared to TBT-only group where TBT reduced viability to 31.38% of control.
Showed more adherent cells and less cell shrinkage via microscopic observation.
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Cell Line:TBT-treated HepG2 cells
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Concentration:3 μM (fucoxanthinol); 0.2 μM (TBT)
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Incubation Time:24 h (fucoxanthinol post-TBT treatment); 6 h (TBT)
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Result:Increased the percentage of normal HepG2 cells compared to the TBT-only group.
Reduced the percentage of apoptotic HepG2 cells compared to the TBT-only group.
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Cell Line:TBT-treated HepG2 cells
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Concentration:3 μM (fucoxanthinol); 0.2 μM (TBT)
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Incubation Time:24 h (fucoxanthinol post-TBT treatment); 6 h (TBT)
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Result:Increased Bcl-2 protein expression compared to the TBT-only group.
Inhibited Bax protein expression compared to the TBT-only group.
Significantly elevated the Bcl-2/Bax ratio compared to the TBT-only group.
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Cell Line:BCBL-1 PEL cells, TY-1 PEL cells, HeLa cervical cancer cells, peripheral blood mononuclear cells (PBMC) from healthy volunteers
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Concentration:0-5 μM
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Incubation Time:24 h
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Result:Reduced cell viability in a dose-dependent manner in BCBL-1 and TY-1 PEL cells, with an IC50 of 1.1 μM.
Exerted weaker effects on HeLa cells.
Showed no toxic effect on healthy PBMC.
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Cell Line:BCBL-1 PEL cells, TY-1 PEL cells
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Concentration:0-5 μM
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Incubation Time:24 h
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Result:Increased the proportion of apoptotic cells in a dose-dependent manner.
Marked apoptosis was observed at 5 μM.
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Cell Line:BCBL-1 PEL cells, TY-1 PEL cells
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Concentration:5 μM
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Incubation Time:24 h
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Result:Caused chromatin condensation and nuclear fragmentation, confirming apoptotic cell death.
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Cell Line:BCBL-1 PEL cells, TY-1 PEL cells
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Concentration:0-5 μM (24 h incubation); 5 μM (time-course incubation)
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Incubation Time:0-24 h (time-course); 24 h (dose-response)
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Result:Induced production of cleaved PARP, cleaved caspase-3, cleaved caspase-9, and cleaved caspase-8 in a dose-dependent manner.
Induced production of cleaved PARP, cleaved caspase-3, cleaved caspase-9, and cleaved caspase-8 in a time-dependent manner.
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Cell Line:BCBL-1 PEL cells, TY-1 PEL cells
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Concentration:2.5 μM
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Incubation Time:24 h
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Result:Increased the population of cells in the G1 phase.
Markedly reduced the population of cells in the S phase relative to untreated cells.
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Cell Line:BCBL-1 PEL cells
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Concentration:0-5 μM
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Incubation Time:24 h
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Result:Did not alter expression levels of Bcl-2, Bak, or Bax.
Down-regulated anti-apoptotic proteins Bcl-xL, XIAP, and survivin in a dose-dependent manner.
Reduced phosphorylation of pRb in a dose-dependent manner.
Down-regulated cell cycle regulatory proteins cyclin D2, CDK4, CDK6, and c-Myc in a dose-dependent manner.
Reduced phosphorylation of caspase-9 in a dose-dependent manner.\nReduced phosphorylation of IKKβ and IκBα in a dose-dependent manner.
Reduced protein levels of IKKα, IKKβ, IKKγ, JunB, JunD, Akt, PDK1, and β-catenin in a dose-dependent manner.
Reduced phosphorylation of Akt at Thr308 and Ser473 in a dose-dependent manner.
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Cell Line:BCBL-1 PEL cells
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Concentration:5 μM fucoxanthinol; 5-20 μM LLnL (in combination with 5 μM fucoxanthinol)
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Incubation Time:24 h
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Result:Reduced protein levels of CDK4, CDK6, survivin, IKKα, IKKβ, IKKγ, Akt, PDK1, and JunD.
Had its protein-reducing effect blocked by co-treatment with LLnL.
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Cell Line:BCBL-1 PEL cells
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Concentration:5 μM
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Incubation Time:0-24 h
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Result:Did not increase expression levels of lytic HHV-8 genes ORF50 (Rta) and ORFK9 (v-IRF).
Down-regulated expression of latent HHV-8 genes ORFK13 (v-FLIP) and ORF72 (v-cyclin) after 6-12 hours of treatment.
Did not alter expression of latent HHV-8 gene ORF73 (LANA).
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Cell Line:HL-60 human leukemia cells
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Concentration:12.5-50 μM
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Incubation Time:24 h, 48 h, 72 h
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Result:Reduced HL-60 cell viability to 33.8% of control after 24 h, 5.7% of control after 48 h, and 2.2% of control after 72 h at 12.5 μM.
Reduced HL-60 cell viability to near 0% of control after 48 h at 25 μM and 50 μM.
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Cell Line:HL-60 human leukemia cells
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Concentration:6.25-12.5 μM
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Incubation Time:24 h
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Result:Induced apoptotic morphological changes (chromosomal condensation, DNA degradation), produced DNA laddering characteristic of apoptosis, and enhanced relative DNA fragmentation to 7-fold compared to control cells at 12.5 μM for 24 h.
Significantly induced DNA fragmentation relative to control at 6.25 μM for 24 h.
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Cell Line:MCF-7 human breast cancer cells
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Concentration:25 μM
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Incubation Time:48 h, 72 h
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Result:Reduced MCF-7 cell viability to ~28% of control after 48 h and ~12% of control after 72 h.
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Cell Line:Caco-2 human colon cancer cells
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Concentration:12.5 μM
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Incubation Time:48 h, 72 h
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Result:Reduced Caco-2 cell viability to ~22% of control after 48 h and ~12% of control after 72 h.
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Cell Line:MCF-7 human breast cancer cells
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Concentration:12.5-25 μM
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Incubation Time:48 h
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Result:Enhanced relative DNA fragmentation to ~7-fold of control at 12.5 μM for 48 h.
Enhanced relative DNA fragmentation to ~11-fold of control at 25 μM for 48 h.
Produced significantly higher DNA fragmentation than control and 25 μM fucoxanthin-treated cells at both concentrations.
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Cell Line:Caco-2 human colon cancer cells
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Concentration:12.5-25 μM
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Incubation Time:48 h
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Result:Enhanced relative DNA fragmentation to ~4-fold of control at 12.5 μM for 48 h.
Enhanced relative DNA fragmentation to ~5.7-fold of control at 25 μM for 48 h.
Produced significantly higher DNA fragmentation than control and 25 μM fucoxanthin-treated cells at both concentrations.
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Cell Line:HL-60 human leukemia cells
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Concentration:6.25 μM
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Incubation Time:36 h
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Result:Reduced Bcl-2 protein expression to ~40% of control (normalized to Actin).
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Cell Line:HTLV-1-infected T-cell lines (MT-2, MT-4, HUT-102, ED-40515(-)), uninfected cell lines (Jurkat, K562, HeLa), primary ATL cells, peripheral blood mononuclear cells (PBMCs) from healthy volunteers
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Concentration:0.63, 1.25, 2.5, 5, 10 μM
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Incubation Time:24 h
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Result:Inhibited cell viability in all 4 HTLV-1-infected T-cell lines in a dose-dependent manner, with IC50 values ranging from 0.86-1.83 μM.
Inhibited cell viability of primary ATL cells with IC50 values ranging from 0.46-3.84 μM.
Showed minimal susceptibility in uninfected cell lines (K562, HeLa), while Jurkat cells were less susceptible than HTLV-1-infected lines.
Made primary ATL cells more susceptible to viability inhibition than PBMCs from healthy volunteers.
Was approximately twice as potent as fucoxanthin across all tested cell types.
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Cell Line:HTLV-1-infected T-cell lines (MT-2, MT-4, HUT-102, ED-40515(-)), uninfected cell lines (Jurkat, HeLa)
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Concentration:5 μM
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Incubation Time:24 h
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Result:Increased the proportion of apoptotic cells in all HTLV-1-infected T-cell lines, with minimal effects on HeLa cells and reduced effects on Jurkat cells compared to infected lines.
Induced characteristic apoptotic nuclear changes in treated HUT-102 cells via Hoechst 33342 staining.
Cleaved caspase-3, -8, -9, and PARP in HUT-102 cells.
Activated caspase-3, -8, and -9 in HUT-102 and ED-40515(-) cells, with relative caspase activity increased 14-20-fold compared to untreated cells.
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Cell Line:HTLV-1-infected T-cell lines (MT-2, MT-4, HUT-102, ED-40515(-))
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Concentration:5 μM
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Incubation Time:12 h, 24 h
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Result:Increased the proportion of HUT-102 cells in G1 phase and reduced the proportion in S phase after 12 hours, indicating G1 cell cycle arrest.
Markedly increased the percentage of apoptotic HUT-102 cells after 24 hours.
Induced G1 phase arrest in all 4 HTLV-1-infected T-cell lines after 12 hours, with increased G1 cell populations and reduced S phase populations across all lines.
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Cell Line:EBV-immortalized human B-cell lines (LCL-Ka, LCL-Ku), Burkitt's lymphoma (BL) cell lines (Raji, Daudi, BJAB, Ramos, B95-8/BJAB, B95-8/Ramos), Hodgkin's lymphoma (HL) cell lines (HDLM-2, L540, L428, KM-H2), healthy human peripheral blood mononuclear cells (PBMC)
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Concentration:0.63-10 μM
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Incubation Time:24 h
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Result:Reduced cell viability in a dose-dependent manner across all tested EBV-immortalized B-cell, BL, and HL cell lines.
Showed reduced susceptibility in healthy PBMC compared to malignant B-cell lines.
Was approximately twice as potent as fucoxanthin at suppressing cell viability.
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Cell Line:EBV-immortalized human B-cell lines (LCL-Ka, LCL-Ku), Burkitt's lymphoma (BL) cell lines (Raji, Daudi, B95-8/Ramos)
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Concentration:2.5 μM (general cell lines); 0.63-10 μM (Daudi cells)
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Incubation Time:24 h
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Result:Increased the proportion of apoptotic cells in Raji, Daudi, B95-8/Ramos, LCL-Ka, and LCL-Ku cell lines to levels comparable to 5 μM fucoxanthin.
Induced apoptosis in a dose-dependent manner in Daudi cells, with greater pro-apoptotic activity than fucoxanthin.
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Cell Line:Daudi Burkitt's lymphoma (BL) cells
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Concentration:0.63-5 μM
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Incubation Time:24 h
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Result:Induced dose-dependent cleavage of caspase-3, caspase-9, and PARP, indicating activation of the caspase cascade.\nDid not alter expression levels of Bcl-xL, survivin, or Bax.
Downregulated expression of anti-apoptotic proteins Bcl-2, cIAP-2, and XIAP in a dose-dependent manner.
Downregulated expression of cell cycle regulatory proteins cyclin D1 and cyclin D2 in a dose-dependent manner.
Reduced phosphorylation of IκBα and increased levels of total IκBα in a dose-dependent manner.
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Cell Line:Daudi Burkitt's lymphoma (BL) cells, KM-H2 Hodgkin's lymphoma (HL) cells, L540 Hodgkin's lymphoma (HL) cells
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Concentration:1.25 μM
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Incubation Time:24 h
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Result:Increased the population of cells in the G1 phase relative to untreated cells.
Reduced the number of cells in the S phase relative to untreated cells.
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Cell Line:human neuroblastoma SH-SY5Y cells
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Concentration:2.5-5 µM
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Incubation Time:3 h
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Result:Significantly increased total Nrf2 protein levels (normalized to β-Actin) at both 2.5 µM and 5 µM, with a larger increase at 5 µM.
Significantly reduced Keap1 protein levels (normalized to β-Actin) only at 5 µM.
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Cell Line:human neuroblastoma SH-SY5Y cells
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Concentration:5 µM
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Incubation Time:24 h
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Result:Significantly increased Nrf2 mRNA relative expression compared to untreated cells, with a lower increase than that induced by fucoxanthin.
Significantly increased NQO1 mRNA relative expression compared to untreated cells, with a lower increase than that induced by fucoxanthin.
Had no significant effect on GSTP1 mRNA relative expression.
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Cell Line:human neuroblastoma SH-SY5Y cells
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Concentration:5 µM (co-incubated with AβO); 5 µM (pre-incubated)
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Incubation Time:4 h (co-incubated with AβO); 24 h (pre-incubated, followed by 4 h AβO exposure)
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Result:Significantly reduced AβO-induced neurotoxicity, maintaining neuronal viability at ~60% relative to untreated cells when co-treated at 5 µM for 4 h.
Did not modify AβO-induced neurotoxicity when pre-treated at 5 µM for 24 h.
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Cell Line:human neuroblastoma SH-SY5Y cells
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Concentration:5 µM (co-incubated with 6-OHDA); 5 µM (pre-incubated)
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Incubation Time:2 h (co-incubated with 6-OHDA); 24 h (pre-incubated, followed by 2 h 6-OHDA exposure)
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Result:Significantly reduced 6-OHDA-induced neurotoxicity, maintaining neuronal viability at ~90% relative to untreated cells when co-treated at 5 µM for 2 h.
Significantly reduced 6-OHDA-induced neurotoxicity, maintaining neuronal viability at ~90% relative to untreated cells when pre-treated at 5 µM for 24 h.
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Cell Line:murine 3T3-L1 preadipocytes undergoing adipocyte differentiation
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Concentration:2.5 μM, 5 μM
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Incubation Time:120 h
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Result:Down-regulated PPARγ protein expression in differentiated 3T3-L1 cells.
Decreased PPARγ expression to 47% of that in control differentiated cells at 5 μM.
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Cell Line:PC-3 human prostate cancer cells
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Concentration:0.625-20 μM
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Incubation Time:72 h
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Result:Inhibited PC-3 cell proliferation in a dose-dependent manner.
Achieved a 50% inhibitory concentration (IC50) of 2.0 μM.
Generated no amarouciaxanthin A in PC-3 cells cultured with fucoxanthinol-supplemented medium.
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Cell Line:3T3-L1 preadipocyte cells
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Concentration:1, 5, 10 μM
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Incubation Time:duration of adipocyte differentiation
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Result:Suppressed lipid accumulation in differentiating 3T3-L1 cells in a concentration-dependent manner.
Reduced intracellular lipid accumulation by approximately 50% at 10 μM compared to untreated differentiating cells.
Downregulated the mRNA expression of adipogenic marker genes peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) at 10 μM.
| Species | Dose | Route | Cmax | Tmax | T1/2 | AUC0-∞ | Plasma Concentration |
|---|---|---|---|---|---|---|---|
| Mice[14] | 3.5 mg/kg | p.o. | 132 nM | 4 h | 4.5 h | 1430 nM·h | 8.2 nM |
Fucoxanthinol (200 mg/kg; p.o.; daily; 28 days) significantly reduces tumor volume, tumor weight, and serum sIL-2Rα levels, and induces tumor cell apoptosis in SCID mice bearing subcutaneous HUT-102 ATL tumors, with no observed adverse effects[6].
Fucoxanthinol (2 mg; duodenal infusion; single dose) reduces total 4-hour lymphatic triglyceride absorption by ~53% and suppresses post-infusion lymphatic triglyceride release rates in conscious cannulated rats[7].
Fucoxanthinol (2 mg; duodenal infusion; single dose) suppresses post-infusion systemic blood triglyceride increases in conscious cannulated rats when given with non-pre-digested oil, but this effect is abolished with pre-digested oil[7].
Fucoxanthinol (0.1-0.2%; p.o.; daily; 4 weeks) increases hepatic DHA levels by 1.8-fold and hepatic arachidonic acid levels by 1.2-fold in obese/diabetic KKAy mice after 4 weeks of feeding, with no significant effect on hepatic DHA levels at the 0.1% dose[17].
Fucoxanthinol (1.5 nmol; i.v.; single dose) results in detectable plasma and liver concentrations of fucoxanthinol and its metabolite Amarouciaxanthin A (HY-N18109) at 2 hours post-injection in male ICR mice[11].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C.B-17/Icr-SCID (5-week-old female; subcutaneous inoculation with 1×107 HUT-102 HTLV-1-infected T cells)[6]
-
Dosage:200 mg/kg
-
Administration:p.o.; daily; 28 days
-
Result:Significantly reduced tumor volume compared to vehicle controls after 14 days.
Significantly lowered tumor weights at necropsy on day 28 compared to controls.
Significantly decreased serum sIL-2Rα levels compared to controls.
Induced abundant apoptotic cells in tumors, while few apoptotic cells were present in control tumors.
Achieved tumor concentrations of 3.51 μg/g (equivalent to 5.70 μM) and serum concentrations of 0.51 μg/mL.
Caused no adverse effects on general appearance, body weight, or food intake, with no pathological findings or metastatic tumors detected in major organs.
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Animal Model:Wistar ST (male, 280-300 g, lymph duct, portal vein, and duodenal cannulated)[7]
-
Dosage:2 mg
-
Administration:duodenal infusion; single dose
-
Result:Reduced total 4-hour lymphatic triglyceride absorption to 53.1 μmol, compared to 113.5 μmol in controls.
Lowered lymphatic triglyceride absorption rates at 60, 90, and 120 minutes post-infusion significantly compared to controls.
Decreased lymph flow rates at 30 and 60 minutes post-infusion significantly compared to controls, while total 4-hour lymph flow did not differ from controls.
Detected fucoxanthinol (including its isomer) in lymph fluid, reaching peak concentration at 120 minutes; total amount released into lymph over 4 hours was 0.44 μmol.
Did not detect fucoxanthinol in portal blood.
-
Animal Model:Wistar ST (male, 280-300 g, jugular vein and duodenal cannulated)[7]
-
Dosage:2 mg
-
Administration:duodenal infusion; single dose
-
Result:Lowered serum triglyceride concentrations at 30, 60, 90, and 120 minutes post-infusion significantly compared to controls when given with non-pre-digested soybean oil emulsion.
Reduced the 0-240 minute AUC for serum triglyceride significantly compared to controls when given with non-pre-digested soybean oil emulsion.
Showed no significant differences in serum triglyceride concentrations or AUC between fucoxanthinol-treated rats and controls when infused with pre-digested soybean oil emulsion.
-
Animal Model:KKAy mice (female, 4 weeks old at study start, genetically obese/diabetic)[17]
-
Dosage:0.1%; 0.2%
-
Administration:p.o.; daily; 4 weeks
-
Result:Increased hepatic docosahexaenoic acid (DHA) levels by 1.8-fold compared to control mice.
Increased hepatic arachidonic acid (20:4n-6) levels by 1.2-fold compared to control mice.
Did not significantly increase hepatic DHA levels compared to control mice at 0.1% dose.
Did not significantly alter liver weight or total liver lipid content compared to control mice at both doses.
Did not increase DHA or arachidonic acid levels in the small intestine compared to control mice at 0.2% dose.
Chemical Information
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CAS No. 7176-02-5
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분자량 616.87
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화학식 C40H56O5
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SMILES
CC(C)(C[C@@H](C[C@]1(O)C)O)C1=[C@]=C/C(C)=C/C=C/C(C)=C/C=C/C=C(C)/C=C/C=C(C)/C(C[C@]23[C@](O2)(C[C@H](CC3(C)C)O)C)=O
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Structure Classification
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Initial Source
Halocynthia roretzi
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선적
Shipping with dry ice.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
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Data Sheet (336 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Martin LJ, et al. Fucoxanthin and Its Metabolite Fucoxanthinol in Cancer Prevention and Treatment. Marine drugs. 2015 Jul 31;13(8):4784-98. [Content Brief]
[2]. Rokkaku T, et al. Anticancer effects of marine carotenoids, fucoxanthin and its deacetylated product, fucoxanthinol, on osteosarcoma. International journal of oncology. 2013 Oct;43(4):1176-86. [Content Brief]
[3]. Zeng J, et al. Protective effects of fucoxanthin and fucoxanthinol against tributyltin-induced oxidative stress in HepG2 cells. Environmental science and pollution research international. 2018 Feb;25(6):5582-5589. [Content Brief]
[4]. Yamamoto K, et al. Fucoxanthin and its deacetylated product, fucoxanthinol, induce apoptosis of primary effusion lymphomas. Cancer letters. 2011 Jan 28;300(2):225-34. [Content Brief]
[5]. Konishi I, et al. Halocynthiaxanthin and fucoxanthinol isolated from Halocynthia roretzi induce apoptosis in human leukemia, breast and colon cancer cells. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 2006;142(1-2):53-9. [Content Brief]
[6]. Ishikawa C, et al. Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. International journal of cancer. 2008 Dec 01;123(11):2702-12. [Content Brief]
[7]. Matsumoto M, et al. Suppressive effects of the marine carotenoids, fucoxanthin and fucoxanthinol on triglyceride absorption in lymph duct-cannulated rats. European journal of nutrition. 2010 Jun;49(4):243-9. [Content Brief]
[8]. Tafuku S, et al. Anti-neoplastic effects of fucoxanthin and its deacetylated product, fucoxanthinol, on Burkitt's and Hodgkin's lymphoma cells. Oncology reports. 2012 Oct;28(4):1512-8. [Content Brief]
[9]. Pruccoli L, et al. Antioxidant and Neuroprotective Effects of Fucoxanthin and Its Metabolite Fucoxanthinol: A Comparative In Vitro Study. Current issues in molecular biology. 2024 Jun 14;46(6):5984-5998. [Content Brief]
[10]. Maeda H, et al. Fucoxanthin and its metabolite, fucoxanthinol, suppress adipocyte differentiation in 3T3-L1 cells. Int J Mol Med. 2006 Jul;18(1):147-52. [Content Brief]
[11]. Asai A, et al. Biotransformation of fucoxanthinol into amarouciaxanthin A in mice and HepG2 cells: formation and cytotoxicity of fucoxanthin metabolites. Drug metabolism and disposition: the biological fate of chemicals. 2004 Feb;32(2):205-11. [Content Brief]
[12]. Sugawara T, et al. Antiangiogenic activity of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Journal of agricultural and food chemistry. 2006 Dec 27;54(26):9805-10. [Content Brief]
[13]. Maeda H, et al. Fucoxanthinol, Metabolite of Fucoxanthin, Improves Obesity-Induced Inflammation in Adipocyte Cells. Marine drugs. 2015 Aug 04;13(8):4799-813. [Content Brief]
[14]. Hashimoto T, et al. Pharmacokinetics of fucoxanthinol in human plasma after the oral administration of kombu extract. The British journal of nutrition. 2012 Jun;107(11):1566-9. [Content Brief]
[15]. Sugawara T, et al. Brown algae fucoxanthin is hydrolyzed to fucoxanthinol during absorption by Caco-2 human intestinal cells and mice. J Nutr. 2002 May;132(5):946-51. [Content Brief]
[16]. Takahashi K, et al. Anticancer effects of fucoxanthin and fucoxanthinol on colorectal cancer cell lines and colorectal cancer tissues. Oncology letters. 2015 Sep;10(3):1463-1467. [Content Brief]
[17]. Tsukui T, et al. Fucoxanthin and fucoxanthinol enhance the amount of docosahexaenoic acid in the liver of KKAy obese/diabetic mice. Journal of agricultural and food chemistry. 2007 Jun 27;55(13):5025-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Fucoxanthinol Related Classifications
HY-N11231 Related Classifications
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