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    CAS No. 480-19-3 Price $60 / 20mg
    Catalog No.CFN98735Purity>=98%
    Molecular Weight316.3 Type of CompoundFlavonoids
    FormulaC16H12O7Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Isorhamnetin, a natural flavonol aglycon, is a tyrosinase inhibitor and has anti-adipogenic, cardioprotective, anti-tumor, and antioxidant activities. it inhibits the H(2)O(2)-induced activation of the intrinsic apoptotic pathway via ROS scavenging and ERK inactivation, it inhibits NF-κB signaling. Isorhamnetin prevents angiotensin II (AngII)-induced endothelial dysfunction by inhibiting the overexpression of p47(phox) and the subsequent increases O2-production, resulting in increased nitric oxide bioavailability.
    Targets: NOS | COX | TNF-α | IL Receptor | NF-kB | p65 | IkB | P-gp | Nrf2 | HO-1 | ROS | ERK | PKC | AMPK | P450 (e.g. CYP17) | PPAR | GSK-3 | Wnt/β-catenin | c-Myc | Caspase | Bcl-2/Bax | IKK
    In vitro:
    J Periodontal Res. 2013 Dec;48(6):687-95.
    Isorhamnetin inhibits Prevotella intermedia lipopolysaccharide-induced production of interleukin-6 in murine macrophages via anti-inflammatory heme oxygenase-1 induction and inhibition of nuclear factor-κB and signal transducer and activator of transcrip[Pubmed: 23441850]
    Interleukin-6 (IL-6) is a key proinflammatory cytokine that has been considered to be important in the pathogenesis of periodontal disease. Therefore, host-modulatory agents directed at inhibiting IL-6 appear to be beneficial in terms of attenuating periodontal disease progression and potentially improving disease susceptibility. In the current study, we investigated the effect of the flavonoid Isorhamnetin on the production of IL-6 in murine macrophages stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action.
    Lipopolysaccharide from P. intermedia ATCC 25611 was isolated using the standard hot phenol-water method. Culture supernatants were collected and assayed for IL-6. We used real-time PCR to quantify IL-6 and heme oxygenase-1 (HO-1) mRNA expression. The expression of HO-1 protein and the levels of signaling proteins were monitored using immunoblot analyses. The DNA-binding activity of nuclear factor-κB (NF-κB) was analyzed using ELISA-based assay kits. Isorhamnetin significantly down-regulated P. intermedia LPS-induced production of IL-6 as well as its mRNA expression in RAW264.7 cells. Isorhamnetin up-regulated the expression of HO-1 at both gene transcription and translation levels in cells stimulated with P. intermedia LPS. In addition, inhibition of HO-1 activity by tin protoporphyrin IX blocked the inhibitory effect of Isorhamnetin on IL-6 production. Isorhamnetin failed to prevent LPS from activating either c-Jun N-terminal kinase or p38 pathways. Isorhamnetin did not inhibit NF-κB transcriptional activity at the level of inhibitory κB-α degradation. Isorhamnetin suppressed NF-κB signaling through inhibition of nuclear translocation and DNA binding activity of NF-κB p50 subunit and attenuated signal transducer and activator of transcription 1 signaling.
    Although further research is required to clarify the detailed mechanism of action, we propose that Isorhamnetin may contribute to blockade of the host-destructive processes mediated by IL-6 and could be a highly efficient modulator of the host response in the treatment of inflammatory periodontal disease. Further research in animal models of periodontitis is required to better evaluate, the potential of Isorhamnetin as a novel agent for treating periodontal disease.
    J Nutr. 2007 Apr;137(4):910-5.
    Quercetin and isorhamnetin prevent endothelial dysfunction, superoxide production, and overexpression of p47phox induced by angiotensin II in rat aorta.[Pubmed: 17374653]
    The dietary flavonoid quercetin reduces blood pressure and improves endothelial function in several rat models of hypertension.
    We analyzed the effects of quercetin and its methylated metabolite Isorhamnetin on the aortic endothelial dysfunction induced by incubation with angiotensin II (AngII) in vitro for 6 h. AngII diminished the relaxant responses to acetylcholine in phenylephrine-contracted aorta. Coincubation with quercetin or Isorhamnetin, or addition of superoxide (O(2)(-)) dismutase or apocynin to the assay medium, prevented these inhibitory effects. At 6 h, AngII induced a marked increase in O(2)(-) production as measured by dihydroethidium fluorescence, which was prevented by quercetin and Isorhamnetin. AngII also increased the expression of p47(phox), a regulatory subunit of the membrane NADPH oxidase. Immunohistochemical analysis revealed that overexpression of p47(phox) occurred mainly in the medial layer. p47(phox) overexpression was also prevented by quercetin and Isorhamnetin.
    Taken together, these results show for the first time, to our knowledge, that quercetin and Isorhamnetin prevent AngII-induced endothelial dysfunction by inhibiting the overexpression of p47(phox) and the subsequent increased O(2)(-) production, resulting in increased nitric oxide bioavailability.
    Life Sci. 2010 Mar 13;86(11-12):416-23.
    Isorhamnetin-induced anti-adipogenesis is mediated by stabilization of beta-catenin protein.[Pubmed: 20097210 ]
    Previous studies have shown that Isorhamnetin has anti-adipogenic effects in mouse 3T3-L1 cells. This study was conducted to elucidate the inhibitory mechanisms of Isorhamnetin during adipogenic differentiation of human adipose tissue-derived stem cells (hAMSCs).
    The effect of Isorhamnetin on adipogenic differentiation of hAMSCs was quantified by Oil Red O staining and a triglyceride assay. In addition, real-time PCR and Western blot were used to determine the expression of adipogenesis-related genes. Isorhamnetin inhibited the adipocyte differentiation of hAMSCs. Additionally, when the effects of Wnt antagonists that promote adipogenesis were evaluated, Isorhamnetin was found to down-regulate the mRNA levels of sFRP1 and Dkk1, but had no effect on the mRNA levels of sFRP2, sFRP3, sFRP4 and Dkk3. Isorhamnetin also inhibited the expression of Wnt receptor and co-receptor genes. Furthermore, Isorhamnetin increased the protein levels of beta-catenin, an effector molecule of Wnt signaling, but had no effect on the mRNA levels of beta-catenin. The phosphorylation level of GSK 3beta was also increased by Isorhamnetin. These results were confirmed by the fact that the expression of c-myc, cyclin D1 and PPARdelta, which are target genes of beta-catenin, was upregulated by Isorhamnetin. Moreover, Isorhamnetin reduced the mRNA expression levels of C/EBPalpha and PPARgamma, which are known to be inhibited by c-myc or by cyclin D1 and PPARdelta, respectively.
    Our results indicate that Isorhamnetin inhibits the adipogenic differentiation of hAMSCs and that its mechanisms are mediated by the stabilization of beta-catenin.
    Isorhamnetin Description
    Source: The herbs of Typha orientalis Presl.
    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: service@chemfaces.com

    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 3.1616 mL 15.8078 mL 31.6156 mL 63.2311 mL 79.0389 mL
    5 mM 0.6323 mL 3.1616 mL 6.3231 mL 12.6462 mL 15.8078 mL
    10 mM 0.3162 mL 1.5808 mL 3.1616 mL 6.3231 mL 7.9039 mL
    50 mM 0.0632 mL 0.3162 mL 0.6323 mL 1.2646 mL 1.5808 mL
    100 mM 0.0316 mL 0.1581 mL 0.3162 mL 0.6323 mL 0.7904 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.
    Kinase Assay:
    Food Chem Toxicol. 2014 Apr;66:313-20.
    Transport characteristics of isorhamnetin across intestinal Caco-2 cell monolayers and the effects of transporters on it.[Pubmed: 24525098]
    Flavonoid Isorhamnetin occurs in various plants and herbs, and demonstrates various biological effects in humans. This work will clarify the Isorhamnetin absorption mechanism using the Caco-2 monolayer cell model.
    The Isorhamnetin transport characteristics at different concentrations, pHs, temperatures, tight junctions and potential transporters were systemically investigated. Isorhamnetin was poorly absorbed by both passive diffusion and active transport mechanisms. Both trans- and paracellular pathways were involved during Isorhamnetin transport. Active transport under an ATP-dependent transport mechanism was mediated by the organic anion transporting peptide (OATP); Isorhamnetin's permeability from the apical to the basolateral side significantly decreased after estrone-3-sulfate was added (p<0.01). Efflux transporters, P-glycoproteins (P-gp), breast cancer resistance proteins (BCRP) and multidrug resistance proteins (MRPs) participated in the Isorhamnetin transport process. Among them, the MRPs (especially MRP2) were the main efflux transporters for Isorhamnetin; transport from the apical to the basolateral side increased 10.8-fold after adding an MRP inhibitor (MK571).
    This study details Isorhamnetin's cellular transport and elaborates Isorhamnetin's absorption mechanisms to provide a foundation for further studies.
    Toxicol Appl Pharmacol. 2014 Jan 15;274(2):293-301.
    Isorhamnetin protects against oxidative stress by activating Nrf2 and inducing the expression of its target genes.[Pubmed: 24211276]
    Isorhamentin is a 3'-O-methylated metabolite of quercetin, and has been reported to have anti-inflammatory and anti-proliferative effects. However, the effects of Isorhamnetin on Nrf2 activation and on the expressions of its downstream genes in hepatocytes have not been elucidated.
    Here, we investigated whether Isorhamnetin has the ability to activate Nrf2 and induce phase II antioxidant enzyme expression, and to determine the protective role of Isorhamnetin on oxidative injury in hepatocytes. In HepG2 cells, Isorhamnetin increased the nuclear translocation of Nrf2 in a dose- and time-dependent manner, and consistently, increased antioxidant response element (ARE) reporter gene activity and the protein levels of hemeoxygenase (HO-1) and of glutamate cysteine ligase (GCL), which resulted in intracellular GSH level increases. The specific role of Nrf2 in Isorhamnetin-induced Nrf2 target gene expression was verified using an ARE-deletion mutant plasmid and Nrf2-knockout MEF cells. Deletion of the ARE in the promoter region of the sestrin2 gene, which is recently identified as the Nrf2 target gene by us, abolished the ability of Isorhamnetin to increase luciferase activity. In addition, Nrf2 deficiency completely blocked the ability of Isorhamnetin to induce HO-1 and GCL. Furthermore, Isorhamnetin pretreatment blocked t-BHP-induced ROS production and reversed GSH depletion by t-BHP and consequently, due to reduced ROS levels, decreased t-BHP-induced cell death. In addition Isorhamnetin increased ERK1/2, PKCδ and AMPK phosphorylation. Finally, we showed that Nrf2 deficiency blocked the ability of Isorhamnetin to protect cells from injury induced by t-BHP.
    Taken together, our results demonstrate that Isorhamnetin is efficacious in protecting hepatocytes against oxidative stress by Nrf2 activation and in inducing the expressions of its downstream genes.
    Toxicol Appl Pharmacol. 2006 May 15;213(1):18-26.
    Effect of Ginkgo biloba extract on procarcinogen-bioactivating human CYP1 enzymes: identification of isorhamnetin, kaempferol, and quercetin as potent inhibitors of CYP1B1.[Pubmed: 16226778 ]

    In the present study, we investigated the effect of Ginkgo biloba extracts and some of its individual constituents on the catalytic activity of human cytochrome P450 enzymes CYP1B1, CYP1A1, and CYP1A2. G. biloba extract of known abundance of terpene trilactones and flavonol glycosides inhibited 7-ethoxyresorufin O-dealkylation catalyzed by human recombinant CYP1B1, CYP1A1, and CYP1A2, and human liver microsomes, with apparent Ki values of 2 +/- 0.3, 5 +/- 0.5, 16 +/- 1.4, and 39 +/- 1.2 microg/ml (mean +/- SE), respectively. In each case, the mode of inhibition was of the mixed type. Bilobalide, ginkgolides A, B, C, and J, quercetin 3-O-rutinoside, kaempferol 3-O-rutinoside, and isorhamentin 3-O-rutinoside were not responsible for the inhibition of CYP1 enzymes by G. biloba extract, as determined by experiments with these individual chemicals at the levels present in the extract. In contrast, the aglycones of quercetin, kaempferol, and isorhamentin inhibited CYP1B1, CYP1A1, and CYP1A2. Among the three flavonol aglycones, isorhamentin was the most potent in inhibiting CYP1B1 (apparent Ki = 3 +/- 0.1 nM), whereas quercetin was the least potent in inhibiting CYP1A2 (apparent Ki = 418 +/- 50 nM). The mode of inhibition was competitive, noncompetitive, or mixed, depending on the enzyme and the flavonol. G. biloba extract also reduced benzo[a]pyrene hydroxylation, and the effect was greater with CYP1B1 than with CYP1A1 as the catalyst.
    Overall, our novel findings indicate that G. biloba extract and the flavonol aglycones Isorhamnetin, kaempferol, and quercetin preferentially inhibit the in vitro catalytic activity of human CYP1B1.
    Cell Research:
    J Cell Biochem. 2012 Feb;113(2):473-85.
    Isorhamnetin inhibits H₂O₂-induced activation of the intrinsic apoptotic pathway in H9c2 cardiomyocytes through scavenging reactive oxygen species and ERK inactivation.[Pubmed: 21948481 ]
    As a traditional Chinese medicine, the sea buckthorn (Hippophae rhamnoides L.) has a long history in the treatment of ischemic heart disease and circulatory disorders. However, the active compounds responsible for and the underlying mechanisms of these effects are not fully understood.
    In this article, Isorhamnetin pretreatment counteracted H(2)O(2)-induced apoptotic damage in H9c2 cardiomyocytes. Isorhamnetin did not inhibit the death receptor-dependent or extrinsic apoptotic pathways, as characterized by its absence in both caspase-8 inactivation and tBid downregulation along with unchanged Fas and TNFR1 mRNA levels. Instead, Isorhamnetin specifically suppressed the mitochondria-dependent or intrinsic apoptotic pathways, as characterized by inactivation of caspase-9 and -3, maintenance of the mitochondrial membrane potential (ΔΨm), and regulation of a series of Bcl-2 family genes upstream of ΔΨm. The anti-apoptotic effects of Isorhamnetin were linked to decreased ROS generation. H(2)O(2) activated ERK and p53, whereas Isorhamnetin inhibited their activation. ERK overexpression overrode the Isorhamnetin-induced inhibition of the intrinsic apoptotic pathway in H9c2 cardiomyocytes, which indicated that an ERK-dependent pathway was involved. Furthermore, N-acetyl cysteine (a potent ROS scavenger) could attenuate the H(2)O(2)-induced apoptosis. However, PD98059 (an ERK-specific inhibitor) could not effectively antagonize ROS generation, which indicates that ROS may be an upstream inducer of ERK.
    In conclusion, Isorhamnetin inhibits the H(2)O(2)-induced activation of the intrinsic apoptotic pathway via ROS scavenging and ERK inactivation. Therefore, Isorhamnetin is a promising reagent for the treatment of ROS-induced cardiomyopathy.
    Animal Research:
    J Nutr Biochem. 2014 Sep;25(9):923-33.
    Plant flavonol isorhamnetin attenuates chemically induced inflammatory bowel disease via a PXR-dependent pathway.[Pubmed: 24913217]
    Isorhamnetin is an O-methylated flavonol present in fruit and vegetables. We recently reported the identification of Isorhamnetin as an activator of the human pregnane X receptor (PXR), a known target for abrogating inflammation in inflammatory bowel disease (IBD). The current study investigated the role of Isorhamnetin as a putative mouse PXR activator in ameliorating chemically induced IBD.
    Using two different models (ulcerative colitis like and Crohn's disease like) of experimental IBD in mice, we demonstrated that Isorhamnetin abrogated inflammation through inhibiting the activity of myeloperoxidase, the levels of TNF-α and IL-6, the mRNA expression of proinflammatory mediators (iNOS, ICAM-1, COX2, TNF-α, IL-2 and IL-6) and the phosphorylation of IκBα and NF-κB p65. PXR gene overexpression inhibited NF-κB luciferase activity, and the inhibition was potentiated by Isorhamnetin treatment. PXR knockdown by siRNA demonstrated the necessity for PXR in Isorhamnetin-mediated up-regulation of xenobiotic metabolism genes. Ligand pocket-filling mutants (S247W/C284W and S247W/C284W/S208W) of human PXR weakened the effect of Isorhamnetin on PXR activation. Molecular docking studies and time-resolved fluorescence resonance energy transfer competitive binding assays confirmed the ligand (Isorhamnetin)-binding affinity.
    These results clearly demonstrated the ameliorating effect of Isorhamnetin on experimental IBD via PXR-mediated up-regulation of xenobiotic metabolism and down-regulation of NF-κB signaling. The novel findings may contribute to the effective utilization of Isorhamnetin or its derivatives as a PXR ligand in the treatment of human IBD.