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    CAS No. 520-33-2 Price $40 / 20mg
    Catalog No.CFN98842Purity>=98%
    Molecular Weight302.3 Type of CompoundFlavonoids
    FormulaC16H14O6Physical DescriptionPowder
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    Product Name Hesperetin
    CAS No.: 520-33-2
    Catalog No.: CFN98842
    Molecular Formula: C16H14O6
    Molecular Weight: 302.3 g/mol
    Purity: >=98%
    Type of Compound: Flavonoids
    Physical Desc.: Powder
    Targets: Caspase | PARP | Bcl-2/Bax | ROS | JNK | Calcium Channel | ATPase | PI3K | Akt | ERK | p38MAPK | VEGFR | PPAR | TNF-伪 | p21
    Source: The peels of Citrus maxima.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $40 / 20mg
    Download: COA    MSDS    SDF    Manual
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  • Molecules.2019, 24(11):E2102
  • Antioxidants (Basel).2020, 9(2):E99
  • iScience.2020, 23(2):100849.
  • Phytomedicine.2022, 100:154085.
  • BMC Complement Altern Med.2019, 19(1):11
  • Processes2022, 10(10), 2008.
  • Appl Microbiol Biotechnol.2018, 102(12):5105-5120
  • J Pharm Biomed Anal.2021, 196:113931.
  • Biosci Rep.2018, 38(4)
  • Molecules.2020, 25(3):734
  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
    Related Libraries
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  • Biological Activity
    Description: Hesperetin has antioxidative and anti-inflammatory effects, it inhibits vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling. Hesperetin-mediated apoptosis of MCF-7 cells involves accumulation of ROS and activation of ASK1/JNK pathway, it induces apoptosis in triple negative breast cancer MDA-MB-231 cells via intrinsic pathway via activation of caspase -9 and -3 and increase in Bax:Bcl-2 ratio.
    Targets: Caspase | PARP | Bcl-2/Bax | ROS | JNK | Calcium Channel | ATPase | PI3K | Akt | ERK | p38MAPK | VEGFR | PPAR | TNF-α | p21
    In vitro:
    Tumour Biol. 2015 Jun 17.
    The pleiotropic effects of fisetin and hesperetin on human acute promyelocytic leukemia cells are mediated through apoptosis, cell cycle arrest, and alterations in signaling networks.[Pubmed: 26081618]
    Fisetin and Hesperetin, flavonoids from various plants, have several pharmaceutical activities including antioxidative, anti-inflammatory, and anticancer effects. However, studies elucidating the role and the mechanism(s) of action of fisetin and Hesperetin in acute promyelocytic leukemia are absent. In this study, we investigated the mechanism of the antiproliferative and apoptotic actions exerted by fisetin and Hesperetin on human HL60 acute promyelocytic leukemia cells.
    The viability of HL60 cells was evaluated using the MTT assay, apoptosis by annexin V/propidium iodide (PI) staining and cell cycle distribution using flow cytometry, and changes in caspase-3 enzyme activity and mitochondrial transmembrane potential. Moreover, we performed whole-genome microarray gene expression analysis to reveal genes affected by fisetin and Hesperetin that can be important for developing of future targeted therapy. Based on data obtained from microarray analysis, we also described biological networks modulated after fisetin and Hesperetin treatment by KEGG and IPA analysis. Fisetin and Hesperetin treatment showed a concentration- and time-dependent inhibition of proliferation and induced G2/M arrest for both agents and G0/G1 arrest for Hesperetin at only the highest concentrations. There was a disruption of mitochondrial membrane potential together with increased caspase-3 activity. Furthermore, fisetin- and Hesperetin-triggered apoptosis was confirmed by annexin V/PI analysis. The microarray gene profiling analysis revealed some important biological pathways including mitogen-activated protein kinases (MAPK) and inhibitor of DNA binding (ID) signaling pathways altered by fisetin and Hesperetin treatment as well as gave a list of genes modulated ≥2-fold involved in cell proliferation, cell division, and apoptosis.
    Altogether, data suggested that fisetin and Hesperetin have anticancer properties and deserve further investigation.
    J Cell Physiol. 2015 Aug;230(8):1729-39.
    Hesperetin Induces Apoptosis in Breast Carcinoma by Triggering Accumulation of ROS and Activation of ASK1/JNK Pathway.[Pubmed: 25204891]
    Hesperetin, a flavanone glycoside predominantly found in citrus fruits, exhibits a wide array of biological properties. In the present study Hesperetin exhibited a significant cytotoxic effect in human breast carcinoma MCF-7 cells in a concentration- and time-dependent manner without affecting normal (HMEC) as well as immortalized normal mammary epithelial cells (MCF-10A).
    The cytotoxic effect of Hesperetin was due to the induction of apoptosis as evident from the phosphatidyl-serine externalization, DNA fragmentation, caspase-7 activation, and PARP cleavage. Apoptosis was associated with caspase-9 activation, mitochondrial membrane potential loss, release of cytochrome c, and increase in Bax:Bcl-2 ratio. Pre-treatment with caspase-9 specific inhibitor (Z-LEHD-fmk) markedly attenuated apoptosis suggesting an involvement of intrinsic mitochondrial apoptotic cascade. Further, DCFDA flow-cytometric analysis revealed triggering of ROS in a time-dependent manner. Pre-treatment with ROS scavenger N-acetylcysteine (NAC) and glutathione markedly abrogated Hesperetin-mediated apoptosis whereas carbonyl cyanide m-chlorophenylhydrazone (CCCP) pretreatment along with DHR123-based flow-cytometry indicated the generation of cytosolic ROS. Profiling of MAPKs revealed activation of JNK upon Hesperetin treatment which was abrogated upon NAC pre-treatment. Additionally, inhibition of JNK by SP600125 significantly reversed Hesperetin-mediated apoptosis. The activation of JNK was associated with the activation of ASK1.
    Silencing of ASK1 resulted in significant attenuation of JNK activation as well as reversed the Hesperetin-mediated apoptosis suggesting that Hesperetin-mediated apoptosis of MCF-7 cells involves accumulation of ROS and activation of ASK1/JNK pathway. In addition, Hesperetin also induced apoptosis in triple negative breast cancer MDA-MB-231 cells via intrinsic pathway via activation of caspase -9 and -3 and increase in Bax:Bcl-2 ratio.
    J Biochem Mol Toxicol. 2015 Mar;29(3):99-108.
    Hesperetin inhibit adipocyte differentiation and enhance Bax- and p21-mediated adipolysis in human mesenchymal stem cell adipogenesis.[Pubmed: 25345581]
    We aimed to explore the antiadipogenic and adipolysis effect of Hesperetin in human mesenchymal stem cells (hMSCs)-induced adipogenesis.
    IC50 value of Hesperetin was higher for hMSCs such as 149.2 ± 13.2 μmol for 24 h and 89.4 ± 11.4 μmol in 48 h, whereas in preadipocytes was 87.6 ± 9.5 μmol and 72.4 ± 5.6 μmol in 24 h and 48 h, respectively. Hesperetin treatment (5, 10, and 20 μmol) to adipogenesis-induced hMSCs (Group 1) and preadipocytes (Group 2) resulted in a significantly (p < 0.05) increased lipolysis. The treatment with Hesperetin decreased the expression of resistin, adiponectin, aP2, LPL, PPAR-γ, and TNF-α in Groups 1 and 2, whereas a significant increase was observed in Bcl, Bax, and p21 expression in Group 2 compared to untreated preadipocytes. hMSCs cultured in adipogenic medium along with Hesperetin significantly inhibited adipocyte differentiation and increased the proapoptotic gene expression levels in preadipocyte.
    Our result indicates the antiadipogenic and adipolysis effects of Hesperetin.
    Mater Sci Eng C Mater Biol Appl . 2017 Feb 1;71:954-964.
    Bioflavonoid hesperetin overcome bicalutamide induced toxicity by co-delivery in novel SNEDDS formulations: Optimization, in vivo evaluation and uptake mechanism[Pubmed: 27987794]
    Abstract In the present study, we designed Bicalutamide (BCT) and Hesperetin (HSP) co-loaded self nano-emulsifying drug delivery system (SNEDDS) to encounter the problem of BCT induced toxicity, low solubility, and bioavailability. Optimized BCT-HSP SNEDDS would produce an emulsion of globule size 30.84±1.24nm with a high encapsulation efficiency of BCT (91.29%) and HSP (88.19%), and showed rapid drug release. DPPH assay confirmed the retention of antioxidant potential of HSP in SNEDDS. DCFH-DA confirmed intense green fluorescence in HSP treated groups due to the generation of reactive oxygen species. Thermogravimetric analysis showed the change in the polymorphic form of BCT. After 14days of sub-acute toxicity study, no significant increase (p>0.05) in the hepatotoxicity markers was observed but BCT-HSP SNEDDS significantly decreased (p<0.001) the levels of nephrotoxicity biochemical markers. Additionally, the histopathological study showed that pulmonary fibrosis and alteration in the bowman's by BCT treatment were conquered by co-administration of HSP. BCT-HSP SNEDDS revealed high AUC0-t of BCT (1.23 fold) and HSP (3.42 fold) than aqueous suspension in male Sprague-Dawley rats. The BCT-HSP SNEDDS were absorbed by clathrin-mediated endocytosis and lymphatic transport absorption pathway. Our results proposed that the co-delivery approach may be useful for in vivo management of prostate cancer. Keywords: Antioxidant; Bicalutamide; Hesperetin; Prostate cancer; Reactive oxygen species; Toxicity.
    Biol Pharm Bull . 2016;39(12):2052-2059.
    Inhibitory Effect of Hesperetin and Naringenin on Human UDP-Glucuronosyltransferase Enzymes: Implications for Herb-Drug Interactions[Pubmed: 27904048]
    Abstract Hesperetin (HET) and naringenin (NGR) are flavanones found in citrus (oranges and grapefruit) and Aurantii Fructus Immaturus. The present study aims to investigate the inhibition potential of HET and NGR derivatives towards one of the most important phase II drug-metabolizing enzymes-uridine diphosphate (UDP)-glucuronosyltransferases (UGTs). We used trifluoperazine as a probe substrate to test UGT1A4 activity, and recombinant UGT-catalyzed 4-methylumbelliferone glucuronidation was used as a probe reaction for other UGT isoforms. Data show that HET and NGR displayed broad-spectrum inhibition against human UGTs. Besides, HET exhibited strong inhibitory effects on UGT1A1, 1A3 and 1A9 (both IC50 and Ki values lower than 10 μM), and the inhibitory effects of NGR against three major UGTs, including UGT1A1, 1A3 and 2B7. In a combination of inhibition parameters (Ki) and in vivo concentration of HET and NGR, the potential in vivo inhibition magnitude was predicted. Based on the reported maximum plasma concentration of HET and NGR in vivo, these findings indicate the potential herb-drug interactions (HDI) between HET or NGR and the drugs mainly undergoing UGT1A3 or UGT2B7 catalyzed metabolic elimination. Considering the variety of citrus that contains HET and NGR, so caution should be applied when taking drugs that utilize UGTs for metabolism and clearance with citrus fruits.
    Nutr Cancer . 2020;72(3):538-545.
    Hesperetin Induces Apoptosis in Human Glioblastoma Cells via p38 MAPK Activation[Pubmed: 31295040]
    Abstract Glioblastoma (GBM) is the most common and aggressive form of malignant brain tumor, with poor prognosis and a lack of effective treatment. Hesperetin, a natural product found in citrus fruits, displayed bioactivities including antioxidant, anti-inflammatory, and anticancer, while its effects on GBM cells were largely unknown. Here, we explored the anticancer effect of Hesperetin on human GBM cells in vitro, as well as the underlying signaling mechanisms. By CCK-8 assay and live/dead assay, Hesperetin presented significant inhibitory effect on human GBM U-251 and U-87 cell viability. By DAPI staining and Annexin V-FITC/PI assay, apoptotic death was proved to contribute to the cell viability reduction, and it was verified by the increased Bax/Bcl-2 ratio in western blotting results. Furthermore, by cell cycle analysis and western blotting for cyclin B1, CDK1, and p21, Hesperetin was found to induce cell-cycle arrest at G2/M phase. For signaling mechanism, the western blotting results showed elevated p38 MAPK activation, and the reduced Bcl-2 and enhanced Bax upon Hesperetin treatment were partly reversed by p38 MAPK inhibitor SB203580. In summary, we have discovered Hesperetin as a natural product candidate for the treatment of GBM, and that it could induce GBM cell apoptosis via p38 MAPK activation. Keywords: Hesperetin; apoptosis; cell cycle; glioblastoma; p38 MAPK.
    In vivo:
    Br J Pharmacol . 2017 Jan;174(1):41-56.
    The protective effect of the natural compound hesperetin against fulminant hepatitis in vivo and in vitro[Pubmed: 27714757]
    Abstract Background and purpose: Liver diseases are mostly accompanied by inflammation and hepatocyte death. Therapeutic approaches targeting both hepatocyte injury and inflammation are not available. Natural compounds are considered as potential treatment for inflammatory liver diseases. Hesperetin, a flavonoid component of citrus fruits, has been reported to have anti-inflammatory properties. The aim of this study was to evaluate the cytoprotective and anti-inflammatory properties of Hesperetin both in vitro and in models of fulminant hepatitis. Experimental approach: Apoptotic cell death and inflammation were induced in primary cultures of rat hepatocytes by bile acids and cytokine mixture respectively. Apoptosis was quantified by caspase-3 activity and necrosis by LDH release. The concanavalin A (ConA) and D-galactosamine/LPS (D-GalN/LPS) were used as models of fulminant hepatitis. Liver injury was assessed by alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, liver histology and TUNEL assay and inflammation by inducible NOS (iNOS) expression. Key results: Hesperetin blocked bile acid-induced apoptosis and cytokine-induced inflammation in rat hepatocytes. Moreover, Hesperetin improved liver histology and protected against hepatocyte injury in ConA- and D-GalN/LPS-induced fulminant hepatitis, as assessed by TUNEL assay and serum AST and ALT levels. Hesperetin also reduced expression of the inflammatory marker iNOS and the expression and serum levels of TNFα and IFN-γ, the main mediators of cell toxicity in fulminant hepatitis. Conclusion and implications: Hesperetin has anti-inflammatory and cytoprotective actions in models of acute liver toxicity. Hesperetin therefore has therapeutic potential for the treatment of inflammatory liver diseases accompanied by extensive hepatocyte injury, such as fulminant hepatitis.
    Hesperetin Description
    Source: The peels of Citrus maxima.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to:

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.308 mL 16.5399 mL 33.0797 mL 66.1594 mL 82.6993 mL
    5 mM 0.6616 mL 3.308 mL 6.6159 mL 13.2319 mL 16.5399 mL
    10 mM 0.3308 mL 1.654 mL 3.308 mL 6.6159 mL 8.2699 mL
    50 mM 0.0662 mL 0.3308 mL 0.6616 mL 1.3232 mL 1.654 mL
    100 mM 0.0331 mL 0.1654 mL 0.3308 mL 0.6616 mL 0.827 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Cell Research:
    Med Oncol. 2015 Apr;32(4):101.
    Hesperetin induces the apoptosis of hepatocellular carcinoma cells via mitochondrial pathway mediated by the increased intracellular reactive oxygen species, ATP and calcium.[Pubmed: 25737432]
    Hesperetin, a flavonoid from citrus fruits, has been proved to possess biological activity on various types of human cancers. However, few related studies on hepatocellular carcinoma are available. In this study, we aimed to investigate the effect of Hesperetin on hepatocellular carcinoma cells in vitro and in vivo and clarify its potentially specific mechanism.
    Compared with the control group, the proliferations of hepatocellular carcinoma cells in Hesperetin groups were significantly inhibited (P < 0.05), and a dose- and time-dependent inhibition of cell viability was observed. When pretreated with H2O2 (1 mM) or N-acetyl-L-cysteine (5 mM), the inhibition of cell viability by Hesperetin was enhanced or reduced, respectively (P < 0.05). Similarly, the levels of intracellular ROS, ATP and Ca(2+) changed in different groups (P < 0.05). The results of Hoechst 33258 staining showed that the percentages of apoptotic cells in Hesperetin groups are remarkably higher than that in control group (P < 0.05). And the results of Western blot showed that Hesperetin caused an increase in the levels of cytosolic AIF, cytosolic Apaf-1, cytosolic Cyt C, caspase-3, caspase-9 and Bax and a decrease in that of Bcl-2, mitochondrial AIF, mitochondrial Apaf-1 and mitochondrial Cyt C (P < 0.05). Meanwhile, Hesperetin significantly inhibited the growth of xenograft tumors.
    Our study suggests that Hesperetin could inhibit the proliferation and induce the apoptosis of hepatocellular carcinoma via triggering the activation of the mitochondrial pathway by increasing the levels of intracellular ROS, ATP and Ca(2+).
    Prev Nutr Food Sci. 2014 Dec;19(4):299-306.
    Hesperetin Inhibits Vascular Formation by Suppressing of the PI3K/AKT, ERK, and p38 MAPK Signaling Pathways.[Pubmed: 25580394]
    Hesperetin has been shown to possess a potential anti-angiogenic effect, including vascular formation by endothelial cells. However, the mechanisms underlying the potential anti-angiogenic activity of Hesperetin are not fully understood. In the present study, we evaluated whether Hesperetin has anti-angiogenic effects in human umbilical vascular endothelial cells (HUVECs).
    HUVECs were treated with 50 ng/mL vascular endothelial growth factor (VEGF) to induce proliferation as well as vascular formation, followed by treatment with several doses of Hesperetin (25, 50, and 100 μM) for 24 h. Cell proliferation and vascular formation were analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and tube formation assay, respectively. In addition, cell signaling related to cell proliferation and vascular formation was analyzed by western blot. Furthermore, a mouse aorta ring assay was performed to confirm the effect of Hesperetin on vascular formation. Hesperetin treatment did not cause differences in HUVECs proliferation. However, Hesperetin significantly inhibited VEGF-induced cell migration and tube formation of HUVECs (P<0.05). Moreover, Hesperetin suppressed the expression of ERK, p38 MAPK, and PI3K/AKT in the VEGF-induced HUVECs. In an ex vivo model, Hesperetin also suppressed microvessel sprouting of mouse aortic rings.
    Taken together, the findings suggest that Hesperetin inhibited vascular formation by endothelial cells via the inhibition of the PI3K/AKT, ERK and p38 MAPK signaling.

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