Manassantin A

Manassantin A
Product Name Manassantin A
CAS No.: 88497-87-4
Catalog No.: CFN70465
Molecular Formula: C42H52O11
Molecular Weight: 732.9 g/mol
Purity: >=98%
Type of Compound: Lignans
Physical Desc.: Powder
Targets: HIF | COX | PGE | NF-κB | cAMP | TRP1 | MITF | p65 | TNF-α | STAT | ERK | JNK | PLA | LTC | MAPK
Source: The herbs of Saururus chinensis
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Manassantin A is a high potent HIF-1 inhibitor, it protects the gastric mucosa from ethanol-induced acute gastric injury, and suggest that these protective effects might be associated with COX/PGE2 stimulation, inhibition of iNOS production and NF-κB activation, and improvements in the antioxidant and anti-inflammatory status.Manassantin A represents a potential therapeutic approach for the treatment of airway allergic-inflammatory diseases. Manassantin A inhibits cAMP-induced melanin production by down-regulating the gene expressions of MITF and tyrosinase in melanocytes.
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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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    Korean Journal of Pharmacognosy, 2007, 38(2):176-180.
    Hepatoprotective constituents of Saururus chinensis roots against tacrine-induced cytotoxicity in human liver-derived Hep G2 cells.[Reference: WebLink]

    METHODS AND RESULTS:
    Five lignans, sauchinone (1), di-O-methyltetrahydrofuriguaiacin B (2), Manassantin A (3), manassantin B (4) and saucerneol B (5), have been isolated from the MeOH extract of Saurunis chinensis roots. The evaluation for protective effect of compounds 1-5 against tacrine-induced cytotoxicity in human liver-derived Hep G2 cells was conducted.
    CONCLUSIONS:
    Compounds 1, 2, and 5 showed significant protective effects with the EC 50 values of 74.2±0.9, 111.3±0.8, 64.3±0.8 μM, respectively. Silybin, one of the well-known hepatoprotective agents, used as a positive control, and also showed protective effect with an EC 50 value of 86.2±0.5 μM.
    Experimental dermatology, 2011, 20(9):761-763.
    Manassantin A inhibits cAMP-induced melanin production by down-regulating the gene expressions of MITF and tyrosinase in melanocytes.[Reference: WebLink]
    Microphthalmia-associated transcription factor (MITF) is inducible in response to cAMP through the cAMP-responsive element-binding protein (CREB) and plays a pivotal role in the melanocyte-specific expression of tyrosinase or tyrosinase-related proteins (TRPs) for melanin biosynthesis. Manassantin A from Saururus chinensis inhibits cAMP-induced melanin production in B16 melanoma cells.
    METHODS AND RESULTS:
    Here, we focused on molecular basis of the antimelanogenic activity. Manassantin A consistently inhibited the cAMP elevator 3-isobutyl-1-methylxanthine (IBMX)- or dibutyryl cAMP-induced melanin production in B16 cells or in melan-a melanocytes by down-regulating the expression of tyrosinase or TRP1 gene. Moreover, Manassantin A suppressed MITF induction through IBMX-activated CREB pathway, directly inhibiting the Ser-133 phosphorylation of CREB. However, Manassantin A did not affect IBMX-increased cAMP levels in these cells but also other cAMP-dependent melanogenic pathways through post-translational modifications of MITF.
    CONCLUSIONS:
    This putative molecular mechanism of Manassantin A in the inhibition of melanin production suggests its pharmacological potential in skin hyperpigmentation.
    Biochemical Pharmacology, 2003, 66(10):1925-1933.
    Suppression of RelA/p65 transactivation activity by a lignoid manassantin isolated from Saururus chinensis.[Reference: WebLink]
    In our search for NF-κB inhibitors from natural resources, we have previously identified two structurally related dilignans, Manassantin A and manassantin B as specific inhibitors of NF-κB activation from Saururus chinensis. However, their molecular mechanism of action remains unclear.
    METHODS AND RESULTS:
    We here demonstrate that Manassantin A and manassantin B are potent inhibitors of NF-κB activation by the suppression of transciptional activity of RelA/p65 subunit of NF-κB. These compounds significantly inhibited the induced expression of NF-κB reporter gene by LPS or TNF-α in a dose-dependent manner. However, these compounds did not prevent the DNA-binding activity of NF-κB assessed by electrophoretic mobility shift assay as well as the induced-degradation of IκB-α protein by LPS or TNF-α. Further analysis revealed that Manassantin A and manassantin B dose-dependently suppressed not only the induced NF-κB activation by overexpression of RelA/p65, but also transactivation activity of RelA/p65. Furthermore, treatment of cells with these compounds prevented the TNF-α-induced expression of anti-apoptotic NF-κB target genes Bfl-1/A1, a prosurvival Bcl-2 homologue, and resulted in sensitizing HT-1080 cells to TNF-α-induced cell death. Similarly, these compounds also suppressed the LPS-induced inducible nitric oxide synthase expression and nitric oxide production.
    CONCLUSIONS:
    Taken together, Manassantin A and manassantin B could be valuable candidate for the intervention of NF-κB-dependent pathological condition such as inflammation and cancer.
    Journal of Pharmacological Sciences, 2011, 115(1):84-88.
    Manassantin A and B from Saururus chinensis inhibit interleukin-6-induced signal transducer and activator of transcription 3 activation in Hep3B cells.[Reference: WebLink]
    Inhibition of interleukin-6 (IL-6) has been postulated to be an effective therapy in the pathogenesis of several inflammatory diseases. The current study was performed to examine potential effects of Manassantin A and manassantin B isolated from Saururus chinensis on the IL-6-induced response to human hepatoma cells.
    METHODS AND RESULTS:
    We found that Manassantin A and manassantin B inhibit signal transducer and activator of transcription 3 (Stat3) activity stimulated by IL-6. We also found that both compounds decreased IL-6-induced Stat3 phosphorylation and nuclear translocation. Both compounds blocked suppressor of cytokine signaling 3 (SOCS-3)-mRNA expression induced by IL-6. In addition, we found that Stat3 inhibitory effects of these compounds could be related to protein tyrosine phosphatase.
    CONCLUSIONS:
    These findings suggest that Manassantin A and manassantin B could be useful remedies for treatment of inflammatory diseases by inhibiting IL-6 action.
    Biological & Pharmaceutical Bulletin, 2011, 34(11):1769-1772.
    Manassantin A isolated from Saururus chinensis inhibits 5-lipoxygenase-dependent leukotriene C4 generation by blocking mitogen-activated protein kinase activation in mast cells.[Reference: WebLink]
    In this study, Manassantin A (Man A), an herbal medicine isolated from Saururus chinensis (S. chinensis), markedly inhibited 5-lipoxygenase (5-LO)-dependent leukotriene C(4) (LTC(4)) generation in bone marrow-derived mast cells (BMMCs) in a concentration-dependent manner.
    METHODS AND RESULTS:
    To investigate the molecular mechanisms underlying the inhibition of LTC(4) generation by Man A, we assessed the effects of Man A on phosphorylation of cytosolic phospholipase A(2) (cPLA(2)) and mitogen-activated protein kinases (MAPKs). Inhibition of LTC(4) generation by Man A was accompanied by a decrease in cPLA(2) phosphorylation, which occurred via the MAPKs including extracellular signal-regulated protein kinase-1/2 (ERK1/2) as well as p38 and c-Jun N-terminal kinase (JNK) pathways.
    CONCLUSIONS:
    Taken together, the present study suggests the Man A represents a potential therapeutic approach for the treatment of airway allergic-inflammatory diseases.
    Acta Pharmaceutica Sinica, 2014, 49(5):622-626.
    A novel HIF-1 inhibitor--manassantin A derivative LXY6099 inhibits tumor growth.[Reference: WebLink]
    Hypoxia-inducible factor-1 (HIF-1) is a key transcription factor on hypoxia responses in mammalian tissues. HIF-1 plays as a positive factor in solid tumor and leads to hypoxia-driven responses that enhance its downstream gene expression for tumor growth and survival. LXY6099 was obtained by the structural modification and optimization of Manassantin A (MA) as a high potent HIF-1 inhibitor.
    METHODS AND RESULTS:
    Antitumor activity of LXY6099 was observed in this study. LXY6099 with an IC50 value of 2.46 x 10(-10) mol x L(-1) showed more sensitive inhibition activity to HIF-1 than that of MA detected by reporter gene assay (> 100 folds). It showed strong inhibition on the growth of human solid tumor cell lines. Furthermore, LXY6099 exhibited significant antitumor activity against established human tumor xenografts in nu/nu mice with treatment of MX-1 breast cancer.
    CONCLUSIONS:
    Thus, LXY6099 as a novel HIF-1 inhibitor could be further developed into anti-cancer agents.
    Biological & Pharmaceutical Bulletin, 2016, 39(2):221-229.
    Protective Effects of Manassantin A against Ethanol-Induced Gastric Injury in Rats.[Reference: WebLink]
    Manassantin A, a neolignan isolated from Saururus chinensis, is a major phytochemical compound that has various biological activities, including anti-inflammatory, neuroleptic, and human acyl-CoA : cholesterol acyltransferase (ACAT) inhibitory activities.
    METHODS AND RESULTS:
    In this study, we investigated the protective effects of Manassantin A against ethanol-induced acute gastric injury in rats. Gastric injury was induced by intragastric administration of 5 mL/kg body weight of absolute ethanol to each rat. The positive control group and the Manassantin A group were given oral doses of omeprazole (20 mg/kg) or Manassantin A (15 mg/kg), respectively, 1 h prior to the administration of absolute ethanol. Our examinations revealed that Manassantin A pretreatment reduced ethanol-induced hemorrhage, hyperemia, and epithelial cell loss in the gastric mucosa. Manassantin A pretreatment also attenuated the increased lipid peroxidation associated with ethanol-induced acute gastric lesions, increased the mucosal glutathione (GSH) content, and enhanced the activities of antioxidant enzymes. The levels of pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β were clearly decreased in the Manassantin A-pretreated group. In addition, Manassantin A pretreatment enhanced the levels of cyclooxygenase (COX)-1, COX-2, and prostaglandin E2 (PGE2) and reduced the inducible nitric oxide synthase (iNOS) overproduction and nuclear factor kappa B (NF-κB) phosphorylation.
    CONCLUSIONS:
    Collectively, these results indicate that Manassantin A protects the gastric mucosa from ethanol-induced acute gastric injury, and suggest that these protective effects might be associated with COX/PGE2 stimulation, inhibition of iNOS production and NF-κB activation, and improvements in the antioxidant and anti-inflammatory status.
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