Glaucocalyxin A

Glaucocalyxin A
Product Name Glaucocalyxin A
CAS No.: 79498-31-0
Catalog No.: CFN90207
Molecular Formula: C20H28O4
Molecular Weight: 332.43 g/mol
Purity: >=98%
Type of Compound: Diterpenoids
Physical Desc.: White powder
Targets: Akt | Caspase | Syk | JNK | p38MAPK | COX | IL Receptor | NF-kB | IkB | TNF-α | NO | IKK
Source: The herbs of Rabdosia rubescens.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Glaucocalyxin A could potentially be developed as an antiplatelet and antithrombotic agent, can inhibit platelet p-selectin secretion and integrin activation by convulxin, is a GPVI selective ligand. Glaucocalyxin A has regulation of microglia activity, can attenuate lipopolysaccharide -stimulated neuroinflammation through NF-κB and p38 MAPK signaling pathways.Glaucocalyxin A may become a potential anti-fibrotic agent in Idiopathic pulmonary fibrosis (IPF) management, it can effectively ameliorate pulmonary fibrosis through the antagonism of leukocyte infiltration and proinflammatory cytokine production.
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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.

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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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    Acta Biochim Biophys Sin (Shanghai). 2013 Nov;45(11):946-52.
    Glaucocalyxin A, a negative Akt regulator, specifically induces apoptosis in human brain glioblastoma U87MG cells.[Pubmed: 24041957]
    Akt is becoming an attractive target in the development of anti-tumor agents. In the present study, we aimed to discover novel negative Akt regulators against malignant glioma.
    METHODS AND RESULTS:
    An Akt regulator screening platform performed in an Akt-GFP overexpression cell line was developed, and natural product library was screened and evaluated using this platform. In addition, the cytotoxic effect of the regulator was detected by MTT assay. Cell apoptosis was assayed by Hoechst 33342 staining and flow cytometry analysis. Afterwards, the apoptotic signaling pathway was investigated by western blot analysis. Glaucocalyxin A, isolated from Rabdosia japonica, was identified as a potent negative regulator of Akt. In human-derived malignant glioma U87MG cells, Glaucocalyxin A inhibited Akt phosphorylation, suppressed proliferation, and promoted apoptosis in a dose-dependent manner, but not in normal glial cells. Furthermore, Glaucocalyxin A activated caspase-3, decreased BAD phosphorylation, and reduced the expression of X-linked inhibitor of apoptosis protein.
    CONCLUSIONS:
    Taken together, these results indicated that Glaucocalyxin A may become a promising candidate in the treatment of malignant glioma.
    Eur J Med Chem. 2014 Oct 30;86:235-41.
    Synthesis and biological evaluation of glaucocalyxin A derivatives as potential anticancer agents.[Pubmed: 25164762]
    A series of Mannich base type derivatives of Glaucocalyxin A (GLA) were designed and prepared.
    METHODS AND RESULTS:
    The cytotoxicity of these compounds was evaluated against six tumor cell lines (SMMC-7721, B16, SGC-7901, A549, KB, HL-60). Most compounds exhibited potent antiproliferative effects with low micromolar IC50 values. Compound 1 with para methyl benzyl amine moiety and compound 16 with cyclohexylamine moiety displayed the highest inhibition efficacy. Significantly, the cytotoxicity of compound 1 was much lower than GLA against the normal human liver cell (HL-7702). The in vitro stability assay revealed that transformation of GLA to Mannich base type derivatives improved the compound stability in rat plasma. Finally, decomposition product analysis supported that compound 1 could act as a prodrug and release GLA in the intracellular environment.
    PLoS One. 2013 Dec 30;8(12):e85120.
    Glaucocalyxin A inhibits platelet activation and thrombus formation preferentially via GPVI signaling pathway.[Pubmed: 24386454]
    A series of Mannich base type derivatives of Glaucocalyxin A (GLA) were designed and prepared.
    METHODS AND RESULTS:
    The cytotoxicity of these compounds was evaluated against six tumor cell lines (SMMC-7721, B16, SGC-7901, A549, KB, HL-60). Most compounds exhibited potent antiproliferative effects with low micromolar IC50 values. Compound 1 with para methyl benzyl amine moiety and compound 16 with cyclohexylamine moiety displayed the highest inhibition efficacy. Significantly, the cytotoxicity of compound 1 was much lower than GLA against the normal human liver cell (HL-7702).
    CONCLUSIONS:
    The in vitro stability assay revealed that transformation of GLA to Mannich base type derivatives improved the compound stability in rat plasma. Finally, decomposition product analysis supported that compound 1 could act as a prodrug and release GLA in the intracellular environment.
    Thromb Haemost. 1992 Apr 2;67(4):458-60.
    Inhibition by glaucocalyxin A of aggregation of rabbit platelets induced by ADP, arachidonic acid and platelet-activating factor, and inhibition of [3H]-PAF binding.[Pubmed: 1631795]
    Glaucocalyxin A is a new diterpenoid isolated from the ethereal extract of the leaves of Rabdosia japonica (Burm f) Hara var glaucocalyx (Maxim) Hara (Labiatae) collected in the northeastern China.
    METHODS AND RESULTS:
    When it was incubated with washed rabbit platelets, Glaucocalyxin A inhibited ADP- or arachidonic acid-induced platelet aggregation with IC50 values of 4.4 mumol/l, 14.1 mumol/l respectively. Glaucocalyxin A also inhibited PAF-induced aggregation of rabbit platelets which were refractory to ADP and arachidonic acid with an IC50 value of 13.7 mumol/l.
    CONCLUSIONS:
    Analysis of [3H]-PAF binding showed that Glaucocalyxin A prevented [3H]-PAF binding to intact washed rabbit platelets with an IC50 value of 8.16 mumol/l, which was consistent with its inhibition of PAF-induced platelet aggregation.
    Asian Pac J Cancer Prev. 2013;14(10):5805-10.
    Glaucocalyxin A activates FasL and induces apoptosis through activation of the JNK pathway in human breast cancer cells.[Pubmed: 24289581]
    This study was conducted to analyze the molecular mechanisms responsible for anti-proliferation effects of Glaucocalyxin A in cultured MCF-7 and Hs578T breast cancer cells. The concentration that reduced cell viability to 50% (IC50) after 72 h treatment was derived and potential molecular mechanisms of anti-proliferation using the IC50 were investigated as changes in cell cycle arrest and apoptosis.
    METHODS AND RESULTS:
    Gene and protein expression changes related to apoptosis were investigated by semi-quantitative RT-PCR and western blotting, respectively. Involvement of phosphorylated mitogen-activated protein kinases and JNK signaling in regulation of these molecules was characterized by western blotting. Cell viability decreased in a concentration-dependent manner and the IC50 was determined as 1 μM in MCF-7 and 4 μM in Hs578T cell. Subsequently, we demonstrated that the GLA-induced MCF-7 and Hst578T cell death was due to cell cycle arrest at the G2/M transition and was associated with activation of the c-jun N-terminal kinase (JNK) pathway.
    CONCLUSIONS:
    We conclude that GLA has the potential to inhibit the proliferation of human breast cancer cells through the JNK pathway and suggest its application forthe effective therapy for patients with breast cancer.
    PLoS One. 2013;8(2):e55792.
    Regulation of microglia activity by glaucocalyxin-A: attenuation of lipopolysaccharide-stimulated neuroinflammation through NF-κB and p38 MAPK signaling pathways.[Pubmed: 23393601 ]
    Microglial cells are the resident macrophages and intrinsic arm of the central nervous system innate immune defense. Microglial cells become activated in response to injury, infection, environmental toxins, and other stimuli that threaten neuronal survival. Therefore, regulating microglial activation may have therapeutic benefits that lead to alleviating the progression of inflammatory-mediated neurodegeneration. In the present study, we investigated the effect of Glaucocalyxin A (GLA) isolated from Rabdosia japonica on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated primary microglia and BV-2 cells. GLA significantly inhibited LPS-induced production of nitric oxide and reversed the morphological changes in primary microglia. Further, GLA suppressed expression of inducible nitric oxide synthase and cyclooxygenase-2 dose-dependently at the mRNA and protein levels. The production of proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1β (IL)-1β, and IL-6 were inhibited by suppressing their transcriptional activity. Furthermore, GLA suppressed nuclear factor-κB activation by blocking degradation of IκB-α and inhibited the induction of lipocalin-2 expression in LPS-stimulated BV-2 cells. Mechanistic study revealed that the inhibitory effects of GLA were accompanied by blocking the p38 mitogen activated protein kinase signaling pathway in activated microglia. In conclusion, given that microglial activation contributes to the pathogenesis of neurodegenerative diseases, GLA could be developed as a potential therapeutic agent for treating microglia-mediated neuroinflammatory diseases.
    Biochem Biophys Res Commun. 2017 Jan 1;482(1):147-153.
    Glaucocalyxin A improves survival in bleomycin-induced pulmonary fibrosis in mice.[Pubmed: 27816453 ]
    Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with unclear etiology and poor prognosis. Despite numerous studies on the pathogenesis of IPF, only scant treatment options are available for the management of IPF. Glaucocalyxin A (GLA), an ent-Kaurane diterpenoid, has been demonstrated to exert anti-inflammatory, anti-neoplastic and anti-platelet activities.
    METHODS AND RESULTS:
    In this study, we evaluated the role of GLA as an anti-fibrotic agent in bleomycin-induced pulmonary fibrosis in mice and investigated the underlying mechanisms by which GLA attenuates lung fibrosis. Intraperitoneal administration of GLA (10 mg/kg) significantly reduced collagen deposition and hydroxyproline content in mouse lungs treated with bleomycin. Importantly, GLA significantly improved survival in bleomycin treated mice. In addition, GLA reduced weight loss in mice that reflects cachexia due to pulmonary fibrosis. Mechanistically, GLA alleviated the infiltration of macrophages and neutrophils in lungs, attenuated the increases of proinflammatory cytokines in lung tissue and bronchoalveolar lavage fluid, and inhibited the activation of NF-κB in fibrotic lungs induced by bleomycin.
    CONCLUSIONS:
    These results provide evidence that GLA can effectively ameliorate pulmonary fibrosis through the antagonism of leukocyte infiltration and proinflammatory cytokine production, suggesting that it may become a potential anti-fibrotic agent in IPF management.
    J Pharm Pharmacol. 2014 Jul;66(7):927-34.
    Preparation, characteristic and pharmacological study on inclusion complex of sulfobutylether-β-cyclodextrin with glaucocalyxin A.[Pubmed: 24697809]
    The objective of this study was to improve the water solubility and solubility of Glaucocalyxin A (GLA) by producing its inclusion complex with sulfobutylether-β-cyclodextrin (SBE-β-CD).
    METHODS AND RESULTS:
    The formation of its 1:1 complex with SBE-β-CD in solution was confirmed by phase-solution and spectral-shift studies. The interaction of GLA and SBE-β-CD was examined by differential scanning calorimetry, powder X-ray diffraction, Fourier transform infrared spectroscopy, proton nuclear magnetic resonance spectroscopy and ultraviolet-visible spectroscopy to determine the formation of the GLA-SBE-β-CD inclusion complex. The solubilities of GLA and its complexes were 2.38 × 10(2) and 1.82 × 10(4)  μg/ml, respectively, and the values of the inclusion complexes were significantly improved by 76-fold compared with the solubility of free GLA. Moreover, a higher area under the curve0-∞ after inclusion technique was observed in the pharmacokinetics study.
    CONCLUSIONS:
    The aforementioned results indicate that GLA-SBE-β-CD could be useful with a better solubility and sustained function in drug delivery.
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