Genistein

Genistein
Product Name Genistein
CAS No.: 446-72-0
Catalog No.: CFN98681
Molecular Formula: C15H10O5
Molecular Weight: 270.2 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Yellow powder
Targets: TGF-β/Smad | NF-kB | p38MAPK | ERK | Bcl-2/Bax | NOS | COX | NO | PGE | IkB | cAMP | p65 | Beta Amyloid | Estrogen receptor | IL Receptor | IKK | Progestogen receptor
Source: The herbs of Trifolium pratense L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $30/20mg
Genistein, a phytoestrogen found in soy products, is a highly specific inhibitor of protein tyrosine kinase (PTK) which blocks the mitogenic effect mediated by EGF on NIH-3T3 cells with IC50 of 12μM or by insulin with IC50 of 19 μM. Genistein has neuroprotective, antitumor effects, it modulates the expression of NF-κB and MAPK (p-38 and ERK1/2), thereby attenuating d-Galactosamine induced fulminant hepatic failure in Wistar rats.
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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

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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    Mol Carcinog. 2015 Apr;54(4):301-11.
    Genistein inhibits hepatocellular carcinoma cell migration by reversing the epithelial-mesenchymal transition: partial mediation by the transcription factor NFAT1.[Pubmed: 24243709]
    To investigate the effects and mechanism of Genistein on hepatocellular carcinoma.
    METHODS AND RESULTS:
    Cell counting kit-8 assays showed that Genistein at 3, 6, and 9 µM had no significant cytotoxic effects on HepG2, SMMC-7721, and Bel-7402 cells. Cell scratch and Transwell assays identified that Genistein inhibited migration of three cell lines. In three cell lines, Genistein enhanced E-cadherin and α-catenin, but reduced N-cadherin and Vimentin at both mRNA and protein levels in a dose-dependent manner. Simultaneously, treatment with Genistein suppressed epithelial-mesenchymal transition (EMT) induced by TGF-β. In HepG2 cells, Genistein reduced mRNA, and protein expressions of nuclear factor of activated T cells 1 (NFAT1), Abca3, Autotaxin, CD154, and Cox-2. Phorbol 12-myristate 13-acetate (PMA) and ionomycin enhanced activity of NFAT1, reduced E-cadherin and α-catenin protein levels, and increased protein levels of N-cadherin and Vimentin. Transwell demonstrated that PMA and ionomycin reversed the migration inhibitory effects of Genistein on HepG2 cells. In vivo, Genistein inhibited the intrahepatic metastasis by reversing the EMT, which was correlated with reduced NFAT1 . Genistein inhibited hepatocellular carcinoma cell migration by reversing the EMT, which was partly mediated by NFAT1.
    CONCLUSIONS:
    The fact that EMT can be reversed by Genistein may shed light on the possible mechanisms for its role in liver cancer therapy.
    Virus Res. 2014 Nov 4;192:114-20.
    Genistein inhibits the replication of avian leucosis virus subgroup J in DF-1 cells.[Pubmed: 25197039]
    To investigate the antiviral effects of Genistein on the replication of avian leukosis virus subgroup J (ALV-J) in DF-1 cells, the cells were treated with Genistein at different time points and the antiviral effects were examined by using a variety of assays.
    METHODS AND RESULTS:
    We determined that Genistein strongly inhibited viral gene expression and decreased the viral protein level in the cell supernatant and the cytoplasm without alerting virus receptor expression and viral attachment. We also observed that Genistein was not found to interfere with virus entry, but significantly inhibited both viral gene transcriptions at 24h post infection and virus release, which indicate that Genistein exerts its inhibitory effects on the late phase of ALV-J replicative cycle.
    CONCLUSIONS:
    These results demonstrate that Genistein effectively block ALV-J replication by inhibiting virus transcription and release in DF-1 cells, which may be useful for therapeutic drug design.
    Anticancer Res. 2014 Sep;34(9):4685-92.
    Genistein potentiates the antitumor effect of 5-Fluorouracil by inducing apoptosis and autophagy in human pancreatic cancer cells.[Pubmed: 25202045]
    Although 5-fluorouracil (5-FU)-based combination chemotherapy (i.e. FOLFIRINOX) has demonstrated effectiveness against pancreatic cancer, novel therapeutic strategies must be developed to increase the therapeutic window of these cytotoxic agents. Genistein is a soy-derived isoflavone with pleiotropic biological effects that can enhance the antitumor effect of chemotherapeutic agents.
    METHODS AND RESULTS:
    To understand how Genistein potentiates the antitumor effects of 5-FU, we examined apoptosis and autophagy in MIA PaCa-2 human pancreatic cancer cells and their derived xenografts. Apoptosis was evaluated using DNA fragmentation assays, and western blots of poly(ADP ribose)polymerase and caspase-3. Meanwhile, autophagy was evaluated using western blots of microtubule-associated protein light chain 3 (LC3)-I/II, fluorescent microscopy observation of green fluorescent protein-LC3B puncta formation, and acidic vesicular organelle formation using acridine orange staining. Tumors from animal treatment studies were examined for apoptosis and autophagy using the TdT-mediated dUTP nick-end labeling assay and immunohistochemical staining of LC3B, respectively. We observed that Genistein increased 5-FU-induced cell death through increased apoptosis, as well as autophagy. The increased autophagy was accompanied by decreased B-cell lymphoma 2 (Bcl2) and increased beclin-1 protein levels. Animal treatment studies supported these observations. The combination of 5-FU and Genistein significantly reduced final xenograft tumor volume when compared to 5-FU-alone by inducing apoptosis as well as autophagy.
    CONCLUSIONS:
    Genistein can potentiate the antitumor effect of 5-FU by inducing apoptotic as well as autophagic cell death. These results demonstrate the potential of Genistein as an adjuvant therapeutic agent against pancreatic cancer.
    Neurobiol Dis. 2004 Jun;16(1):21-8.
    Neuroprotective effect of genistein against beta amyloid-induced neurotoxicity.[Pubmed: 15207258 ]
    Estrogen is beneficial to patients with Alzheimer's disease (AD) but has a limited clinical use due to its proliferative and oncogenic effects on non-neuronal cells responsive to estrogen.
    METHODS AND RESULTS:
    In an attempt to find an estrogen substitute that retains the beneficial effects of estrogen with minimal side effects, we compared the neuroprotective and proliferative effects of Genistein, a selective estrogen receptor (ER) beta-agonist, with those of estrogen. Genistein and 17beta-estradiol showed comparable levels of protection against Abeta-induced deaths of cultured SH-SY5Y human neuroblastoma cells, which were blocked by an estrogen receptor antagonist, ICI 182,780. On the other hand, 17beta-estradiol, but not Genistein, induced proliferation of uterine endometrial cells.
    CONCLUSIONS:
    Our results suggest that Genistein is a potential alternative to estrogen in the treatment of Alzheimer's disease.
    Mutat Res. 2014 Oct;768:74-83.
    Genistein inhibits phorbol ester-induced NF-κB transcriptional activity and COX-2 expression by blocking the phosphorylation of p65/RelA in human mammary epithelial cells.[Pubmed: 24742714]
    Genistein, an isoflavone present in soy products, has chemopreventive effects on mammary carcinogenesis.
    METHODS AND RESULTS:
    In the present study, we have investigated the effects of Genistein on phorbol ester-induced expression of cyclooxygenase-2 (COX-2) that plays an important role in the pathophysiology of inflammation-associated carcinogenesis. Pretreatment of cultured human breast epithelial (MCF10A) cells with Genistein reduced COX-2 expression induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). There are multiple lines of evidence supporting that the induction of COX-2 is regulated by the eukaryotic transcription factor NF-κB. Genistein failed to inhibit TPA-induced nuclear translocation and DNA binding of NF-κB as well as degradation of IκB. However, Genistein abrogated the TPA-induced transcriptional activity of NF-κB as determined by the luciferase reporter gene assay. Genistein inhibited phosphorylation of the p65 subunit of NF-κB and its interaction with cAMP regulatory element-binding protein-binding protein (CBP)/p300 and TATA-binding protein (TBP). TPA-induced NF-κB phosphorylation was abolished by pharmacological inhibition of extracellular signal-regulated kinase (ERK). Likewise, pharmacologic inhibition or dominant negative mutation of ERK suppressed phosphorylation of p65.
    CONCLUSIONS:
    The above findings, taken together, suggest that Genistein inhibits TPA-induced COX-2 expression in MCF10A cells by blocking ERK-mediated phosphorylation of p65 and its subsequent interaction with CBP and TBP.
    Carcinogenesis. 1996 Feb;17(2):271-5.
    Molecular effects of genistein on estrogen receptor mediated pathways.[Pubmed: 8625449]
    Genistein, a component of soy products, may play a role in the prevention of breast and prostate cancer. However, little is known about the molecular mechanisms involved.
    METHODS AND RESULTS:
    In the present study, we examined the effects of Genistein on the estrogen receptor positive human breast cancer cell line MCF-7. We observed that Genistein stimulated estrogen-responsive pS2 mRNA expression at concentrations as low as 10(-8) M and these effects can be inhibited by tamoxifen. We also showed that Genistein competed with [3H]estradiol binding to the estrogen receptor with 50% inhibition at 5 x 10(-7) M. Thus, the estrogenic effect of Genistein would appear to be a result of an interaction with the estrogen receptor. The effect of Genistein on growth of MCF-7 cells was also examined. Genistein produced a concentration-dependent effect on the growth of MCF-7 cells. At lower concentrations (10(-8)-10(-6) M) Genistein stimulated growth, but at higher concentrations (> 10(-5) M) Genistein inhibited growth.
    CONCLUSIONS:
    The effects of Genistein on growth at lower concentrations appeared to be via the estrogen receptor pathway, while the effects at higher concentrations were independent of the estrogen receptor. We also found that Genistein, though estrogenic, can interfere with the effects of estradiol. In addition, prolonged exposure to Genistein resulted in a decrease in estrogen receptor mRNA level as well as a decreased response to stimulation by estradiol.
    Toxicol Appl Pharmacol. 2015 Mar 1;283(2):139-46.
    Genistein modulates the expression of NF-κB and MAPK (p-38 and ERK1/2), thereby attenuating d-Galactosamine induced fulminant hepatic failure in Wistar rats.[Pubmed: 25620059]
    Genistein is an isoflavanoid abundantly found in soy. It has been found to play an important role in the prevention of various chronic diseases including cancer. In this study, we evaluated potential therapeutic properties of Genistein against d-Galactosamine (d-GalN) induced inflammation and hepatotoxicity in male Wistar rats.
    METHODS AND RESULTS:
    Fulminant hepatic failure (FHF) was induced in rats by intraperitoneal injection of d-GalN (700mg/kgBW). Genistein (5mg/kgBW/day) was given as pre-treatment for 30days via intra-gastric route followed by d-GalN (700mg/kgBW) injection. The hepatoprotective and curative effects of Genistein were evident from a significant decrease in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels as well as prevention of histological damage by pre-treatment of Genistein. Genistein pre-treatment significantly inhibited the increased protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing nitric oxide (NO) and prostaglandin-E2 (PGE) levels, respectively. In addition Genistein significantly suppressed the production of d-GalN-induced proinflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β. These inhibitory effects were associated with the suppression of nuclear factor-kappa B (NF-ĸB) activation, IKKα/β and Mitogen activated protein kinase (MAPK) phosphorylation by Genistein in d-GalN-treated animals.
    CONCLUSIONS:
    In conclusion, our results suggest that Genistein may serve as a potential supplement in the prevention of hepatic and inflammatory diseases. Furthermore Genistein is able to maintain the redox potential and strengthens the antioxidant defense system of a cell.
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