Product Name Obovatol
CAS No.: 83864-78-2
Catalog No.: CFN95054
Molecular Formula: C18H18O3
Molecular Weight: 282.3 g/mol
Purity: >=98%
Type of Compound: Lignans
Physical Desc.: Oil
Targets: Bcl-2/Bax | Caspase | JAK | STAT | EGFR | NF-kB | PARP | p38MAPK | COX | LOX | Calcium Channel | p21
Source: The herbs of Magnolia obovata
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $388/5mg
Obovatol has antioxidant, neuroprotective, antiinflammatory, antithrombotic and antitumour effects, it is a potent NF-κB inhibitors for Alzheimer's disease treatment. Obovatol shows inhibitory effect on the Salmonella type III secretion system, it could be useful for the prevention and supplementary treatment of bacterial infections. Obovatol inhibits receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL)-induced osteoclast differentiation in vitro and inflammatory bone loss in vivo, it may be a useful therapeutic agent for the treatment of pathological bone disorders characterized by excessive osteoclastic bone resorption.
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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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    Pharmacol Res. 2018 Mar;129:262-273.
    Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer's disease.[Pubmed: 29179999 ]
    Alzheimer's disease (AD) is the most prevalent form of dementia. The exact pathophysiology of this disease remains incompletely understood and safe and effective therapies are required.
    AD is highly correlated with neuroinflammation and oxidative stress in brain causing neuronal loss. Nuclear factor of activated B-cells (NF-κB) is involved in physiological inflammatory processes and thus representing a promising target for inflammation-based AD therapy. Phytochemicals are able to interfere with the NF-κB pathway. They inhibit the phosphorylation or the ubiquitination of signaling molecules, and thus, inhibit the degradation of IκB. The translocation of NF-κB to the nucleus and subsequent transcription of pro-inflammatory cytokines are inhibited by the actions of phytochemicals. Additionally, natural compounds preventing the interaction of NF-κB can block NF-κB's transcriptional activity by inhibiting its binding to target DNA. Many polyphenols including curcumin, resveratrol, pterostilbene, punicalagin, macranthoin G, salidroside, 4-O-methylhonokiol, lycopene, genistein, Obovatol and gallic acid were reported as potent NF-κB inhibitors for AD treatment. Several alkaloids such as galantamine, glaucocalyxin B, tetrandrine, berberine, oridonin, anatabine have been shown anti-inflammatory effects in AD models in vitro as well as in vivo. Besides, vitamins, tanshinone IIA, artemisinin, dihydroasparagusic acid, geniposide, xanthoceraside, l-theranine, 1,8-cineole and paeoniflorin were described as promising NF-κB inhibitors.
    In conclusion, natural products from plants represent interesting candidates for AD treatment. They may qualify as promising compounds for the development of derivatives providing enhanced pharmacological features.
    J Antibiot (Tokyo). 2017 Nov;70(11):1065-1069.
    Inhibitory effect of obovatol from Magnolia obovata on the Salmonella type III secretion system.[Pubmed: 28874849 ]
    In many pathogenic Gram-negative bacteria, such as Salmonella, Escherichia coli, Yersinia and Chlamydia spp., which cause diseases in humans, the type III secretion system (TTSS) is an important virulence factor that translocates effector proteins into the cytosol of host cells. Thus, the TTSS is a good target for antibacterial agents.
    Here we used a hemolysis assay to search for TTSS inhibitors and found that a compound from Magnolia obovata called Obovatol blocks the TTSS of Salmonella. Obovatol showed potent inhibitory activity (IC50=19.8 μM) against the TTSS-related hemolysis of Salmonella, which was not due to a reduction of bacterial growth. Instead, the compound inhibited bacterial motility, TTSS-related mRNA expression and effector protein secretion.
    These data demonstrate the inhibitory effect of Obovatol on the Salmonella TTSS and suggest that it could be useful for the prevention and supplementary treatment of bacterial infections.
    Eur J Pharmacol. 2014 Jan 15;723:473-80.
    Inhibitory effects of obovatol on osteoclast differentiation and bone resorption.[Pubmed: 24334279 ]
    Osteoclasts are polykaryons that have the unique capacity to degrade bone. Modulation of osteoclast formation and function is a promising strategy for the treatment of bone-destructive diseases.
    Here, we report that Obovatol, a natural compound isolated from Magnolia obovata, inhibits receptor activator of nuclear factor kappa B (NF-κB) ligand (RANKL)-induced osteoclast differentiation in vitro and inflammatory bone loss in vivo. We found that Obovatol strongly inhibited osteoclast formation from bone marrow-derived macrophages in a dose-dependent manner without cytotoxicity. Obovatol significantly suppressed RANKL-induced activation of NF-κB, c-Jun-N-terminal kinase, and extracellular signal-regulated kinase signaling pathways. Obovatol also inhibited RANKL-induced expression of the genes c-Fos and nuclear factor of activated T cells c1, which are transcription factors important for osteoclastogenesis. In addition to osteoclast differentiation, Obovatol blocked cytoskeletal organization and abrogated the bone resorbing activity of mature osteoclast. Obovatol also accelerated osteoclast apoptosis through the induction of caspase-3 activation. Consistent with its in vitro anti-resorptive effect, Obovatol prevented bone loss induced by lipopolysaccharide in vivo.
    Together, our data suggest that Obovatol may be a useful therapeutic agent for the treatment of pathological bone disorders characterized by excessive osteoclastic bone resorption.
    Arch Pharm Res. 2012 Dec;35(12):2191-8.
    Anti-platelet activity of diacetylated obovatol through regulating cyclooxygenase and lipoxygenase activities.[Pubmed: 23263814]
    Obovatol has been reported biological activities such as muscle relaxative, anti-gastric ulcer, anti-allergic and anti-bacterial activities.
    The present study was undertaken to investigate the effect of diacetylated Obovatol, an Obovatol derivative, on rabbit platelet aggregation, and their possible molecular mechanisms. Effects of diacetylated Obovatol on platelet activation including aggregation and serotonin secretion were examined. In addition, we investigated the effect of diacetylated Obovatol on archidonic acid and metabolites liberation and intracellular calcium mobilization. Diacetylated Obovatol concentration-dependently inhibited the washed rabbit platelet aggregation induced by collagen and arachidonic acid, suggesting that diacetylated Obovatol may selectively inhibits collagen- and arachidonic acid-mediated signal transduction. In accordance with these results, diacetylated Obovatol showed a concentration-dependent decrease in cytosolic Ca(2+) mobilization and serotonin secretion. However, diacetylated Obovatol did not inhibit arachidonic acid liberation; on the other hand, diacetylated Obovatol inhibited the formation of arachidonic acid metabolites such as thromboxane A(2), prostaglandin D(2) and 12-HETE through interfering with cyclooxygenase (COX)-1 and lipoxygenase (LOX) activities.
    The results demonstrated that diacetylated Obovatol has antiplatelet activities through inhibition of COX-1 and LOX activities.
    J Atheroscler Thromb. 2011;18(8):659-69.
    Antiplatelet activity of obovatol, a biphenolic component of Magnolia Obovata, in rat arterial thrombosis and rabbit platelet aggregation.[Pubmed: 21512279]
    Thrombosis occurs in the coronary arteries via the activation of platelets, and leads to acute myocardial infarction and sudden death. Obovatol, a major biphenolic component of Magnolia Obovata leaves, displays anti-inflammatory and acyl Co-A cholesterol acyltrasferase inhibitory effects. The purpose of this study was to determine the effects of Obovatol on thrombus formation in vivo and platelet activation in vitro and ex vivo.
    We investigated the antiplatelet and antithrombotic activities of Obovatol in rat carotid arterial thrombosis in vivo along with platelet aggregation in vitro and ex vivo. Its possible cellular mechanism of antiplatelet activity was investigated by testing PLC-γ2 activation, arachidonic acid cascade, calcium mobilization and granule secretion. Oral administration of Obovatol prevented carotid thrombosis, but also significantly inhibited collagen-induced platelet aggregation. Obovatol did not change coagulation times, such as activated partial thromboplastin time and prothrombin time, indicating that the antithrombotic effect of Obovatol might be due to antiplatelet activity rather than anticoagulation activity. Obovatol inhibited in vitro collagen- and arachidonic acid-induced rabbit platelet aggregation in a concentration-dependent manner (1-10 μM), with IC(50) values of 2.4 ± 0.8 and 4.8 ± 0.9 μM, respectively. Obovatol blocked collagen-mediated phospholipase C-γ2 phosphorylation, cytoplasmic calcium mobilization, arachidonic acid liberation and serotonin secretion.
    Obovatol has a potent antithrombotic effect, which may be due to antiplatelet activity. The antiplatelet activity of Obovatol is mediated by inhibition of PLC-γ2 phosphorylation. Thus, Obovatol may be a potential candidate to treat cardiovascular disease.
    Mol Med Rep. 2018 Aug;18(2):1651-1659.
    Obovatol inhibits the growth and aggressiveness of tongue squamous cell carcinoma through regulation of the EGF‑mediated JAK‑STAT signaling pathway.[Pubmed: 29845251]
    Migration and invasion are the most important characteristics of human malignancies which limit cancer drug therapies in the clinic. Tongue squamous cell carcinoma (TSCC) is one of the rarest types of cancer, although it is characterized by a higher incidence, rapid growth and greater potential for metastasis compared with other oral neoplasms worldwide. Studies have demonstrated that the phenolic compound Obovatol exhibits anti‑tumor effects. However, the potential mechanisms underlying Obovatol‑mediated signaling pathways have not been completely elucidated in TSCC.
    The present study investigated the anti‑tumor effects and potential molecular mechanisms mediated by Obovatol in TSCC cells and tissues. The results of the present study demonstrated that Obovatol exerted cytotoxicity in SCC9 TSCC cells, and inhibited their migration and invasion. In addition, Obovatol induced apoptosis in SCC9 TSCC cells by increasing caspase 9/3 and apoptotic protease enhancing factor 1 expression levels. Western blot analysis demonstrated that Obovatol inhibited the expression of pro‑epidermal growth factor (EGF), Janus kinase (JAK), and signal transducer and activator of transcription (STAT) in SCC9 TSCC cells. A study of the molecular mechanisms demonstrated that depletion of EGF reversed the Obovatol‑mediated inhibition of SCC9 TSCC cell growth and aggressiveness. Animal experiments indicated that Obovatol significantly inhibited TSCC tumor growth and increased the number of apoptotic cells in tumor tissues.
    In conclusion, the results of the present study provided scientific evidence that Obovatol inhibited TSCC cell growth and aggressiveness through the EGF‑mediated JAK‑STAT signaling pathway, suggesting that Obovatol may be a potential anti‑TSCC agent.
    Food Chem Toxicol. 2013 Jun;56:304-12.
    Neuroprotective effects of neolignans isolated from Magnoliae Cortex against glutamate-induced apoptotic stimuli in HT22 cells.[Pubmed: 23454146 ]
    In the course of screening for neuroprotective natural products, Magnoliae Cortex showed potent inhibition of hippocampal neuronal HT22 cell death.
    Obovatol, honokiol, and magnolol were isolated from the ethanolic extract of Magnoliae Cortex. Isolated compounds Obovatol, honokiol, and magnolol were protective against 5mM glutamate-induced cell death. When cells were stressed using glutamate, cell viability decreased to 16.98±4.58% over the control (100.00±10.15%). In contrast, 10 μM Obovatol, 10 μM honokiol, and 50 μM magnolol increased cell viability to 91.80±1.70%, 93.59±1.93%, and 85.36±7.40%, respectively. The neuroprotective effects of Obovatol and honokiol were attributable to the inhibition of intracellular reactive oxygen species production, followed by protection of the mitochondrial membrane potential (ΔΨm), recovery of Bcl-2 and Bid levels, inhibition of apoptosis-inducing factor expression, and phosphorylation of mitogen-activated protein kinases such as p38 kinases, extracellular signal-regulated kinases, and c-Jun N-terminal kinases. On the contrary, magnolol did not show any significant effect on the ΔΨm and apoptotic factors.
    Among three compounds, Obovatol most strongly scavenged 2,2-diphenyl-1-picrylhydrazyl radicals and inhibited the elevation of intracellular reactive oxygen species levels in glutamate-stressed HT22 cells. These data suggest that Obovatol and honokiol may have clinical applications for preventing neurodegenerative disorders.
    Phytother Res. 2016 Nov;30(11):1841-1847.
    Obovatol Induces Apoptosis in Non-small Cell Lung Cancer Cells via C/EBP Homologous Protein Activation.[Pubmed: 27489231 ]
    Although Obovatol, a phenolic compound from the bark of Magnolia obovata, was known to have antioxidant, neuroprotective, antiinflammatory, antithrombotic and antitumour effects, its underlying antitumour mechanism is poorly understood so far. Thus, in the present study, the antitumour molecular mechanism of Obovatol was investigated in non-small cell lung cancer cells (NSCLCs).
    Obovatol exerted cytotoxicity in A549 and H460 NSCLCs, but not in BEAS-2B cells. Also, Obovatol increased sub-G1 accumulation and early and late apoptotic portion in A549 and H460 NSCLCs. Consistently, Obovatol cleaved PARP, activated caspase 9/3 and Bax and attenuated the expression of cyclin D1 in A549 and H460 NSCLCs. Interestingly, Obovatol upregulated the expression of endoplasmic reticulum stress proteins such as C/EBP homologous protein (CHOP), IRE1α, ATF4 and p-elF2 in A549 and H460 NSCLCs. Conversely, depletion of CHOP blocked the apoptotic activity of Obovatol to increase sub-G1 accumulation in A549 and H460 NSCLCs.
    Overall, our findings support scientific evidences that Obovatol induces apoptosis via CHOP activation in A549 and H460 NSCLCs.
    Atherosclerosis. 2010 Jun;210(2):372-80.
    Obovatol from Magnolia obovata inhibits vascular smooth muscle cell proliferation and intimal hyperplasia by inducing p21Cip1.[Pubmed: 20022323]
    Obovatol is isolated from Magnolia obovata leaves and this active component has various pharmacological properties such as anti-oxidant, anti-platelet, anti-fungal and anti-inflammatory activities. In the present study, we investigated the inhibitory effects of Obovatol on in vitro vascular smooth muscle cell (VSMC) proliferation and in vivo neointimal formation in a rat carotid artery injury model.

    Obovatol (1-5 microM) exerted concentration-dependent inhibition on platelet-derived growth factor (PDGF)-BB-induced rat VSMC proliferation, without exhibiting any cellular toxicity or apoptosis, as determined by cell count, [3H]thymidine incorporation and Annexin-V-binding analyses. Treatment with Obovatol blocked the cell cycle in G1 phase by down-regulating the expression of cyclins and CDKs, and selectively up-regulating the expression of p21Cip1, a well-known CDK inhibitor. Effects of perivascular delivery of Obovatol were assessed 14 days after injury. The angiographic mean luminal diameters of the Obovatol-treated groups (100 microg and 1 mg: 0.78+/-0.06 and 0.77+/-0.07AU, respectively) were significantly larger than that of the control group (0.58+/-0.07AU). The Obovatol-treated groups (100 microg and 1mg: 0.14+/-0.04 and 0.09+/-0.03 mm2, respectively) showed significant reduction in neointimal formation versus the control group (0.17+/-0.02 mm2). Immunohistochemical staining demonstrated strong expression of p21Cip1 in the neointima of the Obovatol-treated groups.

    These data suggest that Obovatol inhibits VSMC proliferation by perturbing cell cycle progression, possibly due to activation of p21Cip1 pathway. These results also show that Obovatol may have potential as an anti-proliferative agent for the treatment of restenosis and atherosclerosis.

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