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    Linarin
    Information
    CAS No. 480-36-4 Price $40 / 20mg
    Catalog No.CFN98738Purity>=98%
    Molecular Weight592.6 Type of CompoundFlavonoids
    FormulaC28H32O14Physical DescriptionYellow powder
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    Linarin

    Linarin
    Product Name Linarin
    CAS No.: 480-36-4
    Catalog No.: CFN98738
    Molecular Formula: C28H32O14
    Molecular Weight: 592.6 g/mol
    Purity: >=98%
    Type of Compound: Flavonoids
    Physical Desc.: Yellow powder
    Targets: LTR | Caspase | TNF-伪 | STAT | AChR | IL Receptor | PI3K | Akt | PKA | Beta Amyloid | GSK-3 | NF-kB | Bcl-2/Bax
    Source: The herbs of Uncaria sinensis (Oliv.) Havil.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Price: $40 / 20mg
    Inquire / Order: manager@chemfaces.com
    Technical Inquiries: service@chemfaces.com
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  • Process Biochemistry2019, 87:213-220
  • Biochem Biophys Res Commun.2020, 527(4):889-895.
  • Jour. of Stored Pro & Postharvest Res.2016, 7(3):32-36
  • Plants (Basel).2020, 9(11):1422.
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  • Arch Pharm Res.2015, 38(6):1080-9
  • Asian Journal of Chemistry2014, 26(22):7811-7816
  • Exp Parasitol.2018, 194:67-78
  • Int J Mol Sci.2018, 19(2)
  • Appl Microbiol Biotechnol.2018, 102(12):5105-5120
  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: Linarin possesses analgesic, antipyretic, anti-acetylcholinesterase, hepatoprotective ,anti-inflammatory and neuroprotective activities, it prevents Aβ(25-35)-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3β and up-regulates Bcl-2. Linarin can protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction and may exert anti-resorptive actions, at least in part, via the reduction of RANKL and oxidative damage; it also can treat postmenopausal osteoporosis,it induces the osteogenic differentiation and mineralization of MC3T3-E1 osteoblastic cells by activating the BMP-2/RUNX2 pathway through PKA signalingin vitroand protected against OVX-induced bone lossin vivo.
    Targets: LTR | Caspase | TNF-α | STAT | AChR | IL Receptor | PI3K | Akt | PKA | Beta Amyloid | GSK-3 | NF-kB | Bcl-2/Bax
    In vitro:
    Eur J Pharmacol. 2014 Sep 5;738:66-73.
    Protective effect of linarin against D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure.[Pubmed: 24877692]
    Linarin was isolated from Chrysanthemum indicum L. Fulminant hepatic failure is a serious clinical syndrome that results in massive inflammation and hepatocyte death. Apoptosis is an important cellular pathological process in d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury, and regulation of liver apoptosis might be an effective therapeutic method for fulminant hepatic failure.
    METHODS AND RESULTS:
    This study examined the cytoprotective mechanisms of Linarin against GalN/LPS-induced hepatic failure. Mice were given an oral administration of Linarin (12.5, 25 and 50mg/kg) 1h before receiving GalN (800 mg/kg)/LPS (40 μg/kg). Linarin treatment reversed the lethality induced by GalN/LPS. After 6h of GalN/LPS injection, the serum levels of alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor (TNF)-α, interleukin-6 and interferon-γ were significantly elevated. GalN/LPS increased toll-like receptor 4 and interleukin-1 receptor-associated kinase protein expression. These increases were attenuated by Linarin. Linarin attenuated the increased expression of Fas-associated death domain and caspase-8 induced by GalN/LPS, reduced the cytosolic release of cytochrome c and caspase-3 cleavage induced by GalN/LPS, and reduced the pro-apoptotic Bim phosphorylation induced by GalN/LPS. However, Linarin increased the level of anti-apoptotic Bcl-xL and phosphorylation of STAT3.
    CONCLUSIONS:
    Our results suggest that Linarin alleviates GalN/LPS-induced liver injury by suppressing TNF-α-mediated apoptotic pathways.
    Int J Mol Med. 2016 Apr;37(4):901-10.
    Linarin promotes osteogenic differentiation by activating the BMP-2/RUNX2 pathway via protein kinase A signaling.[Pubmed: 26935542 ]
    Linarin (LIN), a flavonoid which exerts both anti-inflammatory and antioxidative effects, has been found to promote osteogenic differentiation. However, the molecular mechanism of its effect on osteoblast differentiation was unclear.
    METHODS AND RESULTS:
    In the present study, LIN from Flos Chrysanthemi Indici (FCI) was isolated in order to investigate the underlying mechanisms of LIN on MC3T3-E1 cells (a mouse osteoblastic cell line) and the osteoprotective effect of LIN in mice which had undergone an ovariectomy (OVX). The results revealed that LIN enhanced osteoblast proliferation and differentiation in MC3T3-E1 cells dose‑dependently, with enhanced alkaline phosphatase (ALP) activity and mineralization of extracellular matrix. LIN upregulated osteogenesis-related gene expression, including that of ALP, runt‑related transcription factor 2 (RUNX2), osteocalcin (OCN), bone sialoprotein (BSP), and type I collagen (COL‑I). Pretreatment with noggin, a bone morphogenetic protein-2 (BMP-2) antagonist, meant that LIN-induced gene expression levels of COL-1, ALP, OCN, BSP and RUNX2 were significantly reduced, as shown by RT-qPCR. Western blot analysis showed that LIN dose‑dependently increased the protein levels of BMP-2 and RUNX2 and enhanced the phosphorylation of SMAD1/5. In addition, LIN dose‑dependently upregulated protein kinase A (PKA) expression. H-89 (a PKA inhibitor) partially blocked the LIN-induced protein increase in BMP-2, p-SMAD1/5 and RUNX2. We noted that LIN preserved the trabecular bone microarchitecture of ovariectomized mice in vivo. Moreover, pretreatment with LIN significantly lowered serum levels of ALP and OCN in ovariectomized mice.
    CONCLUSIONS:
    Our data indicated that LIN induced the osteogenic differentiation and mineralization of MC3T3-E1 osteoblastic cells by activating the BMP-2/RUNX2 pathway through PKA signaling in vitro and protected against OVX-induced bone loss in vivo. The results strongly suggest that LIN is a useful natural alternative for the management of postmenopausal osteoporosis.
    Cell Immunol. 2011;268(2):112-6.
    Linarin isolated from Buddleja officinalis prevents hydrogen peroxide-induced dysfunction in osteoblastic MC3T3-E1 cells.[Pubmed: 21420072]
    The flowers and leaves buds of Buddleja officinalis MAXIM (Buddlejaceae) are used to treat eye troubles, hernia, gonorrhea and liver troubles in Asia.
    METHODS AND RESULTS:
    To elucidate the protective effects of Linarin isolated from B. officinalis on the response of osteoblast to oxidative stress, osteoblastic MC3T3-E1 cells were pre-incubated with Linarin for 1h before treatment with 0.3mM H(2)O(2) for 48h, and markers of osteoblast function and oxidative damage were examined. Linarin significantly (P<0.05) increased cell survival, alkaline phosphatase (ALP) activity, collagen content, calcium deposition, and osteocalcin secretion and decreased the production of receptor activator of nuclear factor-kB ligand (RANKL), protein carbonyl (PCO), and malondialdehyde (MDA) of osteoblastic MC3T3-E1 cells in the presence of hydrogen peroxide.
    CONCLUSIONS:
    These results demonstrate that Linarin can protect osteoblasts against hydrogen peroxide-induced osteoblastic dysfunction and may exert anti-resorptive actions, at least in part, via the reduction of RANKL and oxidative damage.
    Linarin Description
    Source: The herbs of Uncaria sinensis (Oliv.) Havil.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, 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 1.6875 mL 8.4374 mL 16.8748 mL 33.7496 mL 42.187 mL
    5 mM 0.3375 mL 1.6875 mL 3.375 mL 6.7499 mL 8.4374 mL
    10 mM 0.1687 mL 0.8437 mL 1.6875 mL 3.375 mL 4.2187 mL
    50 mM 0.0337 mL 0.1687 mL 0.3375 mL 0.675 mL 0.8437 mL
    100 mM 0.0169 mL 0.0844 mL 0.1687 mL 0.3375 mL 0.4219 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.
    Protocol
    Kinase Assay:
    Iran J Pharm Res. 2015 Summer;14(3):949-54.
    Linarin Inhibits the Acetylcholinesterase Activity In-vitro and Ex-vivo.[Pubmed: 26330885 ]
    Linarin is a flavone glycoside in the plants Flos chrysanthemi indici, Buddleja officinalis, Cirsium setosum, Mentha arvensis and Buddleja davidii, and has been reported to possess analgesic, Linarin is a flavone glycoside in the plants Flos chrysanthemi indici, Buddleja officinalis, Cirsium setosum, Mentha arvensis and Buddleja davidii, and has been reported to possess analgesic, antipyretic, anti-inflammatory and neuroprotective activities.
    METHODS AND RESULTS:
    In this paper, Linarin was investigated for its AChE inhibitory potential both in-vitro and ex-vivo. Ellman's colorimetric method was used for the determination of AChE inhibitory activity in mouse brain. In-vitro assays revealed that Linarin inhibited AChE activity with an IC50 of 3.801 ± 1.149 μM. Ex-vivo study showed that the AChE activity was significantly reduced in both the cortex and hippocampus of mice treated intraperitoneally with various doses of Linarin (35, 70 and 140 mg/Kg). The inhibition effects produced by high dose of Linarin were the same as that obtained after huperzine A treatment (0.5 mg/Kg). Molecular docking study revealed that both 4'-methoxyl group and 7-O-sugar moiety of Linarin played important roles in ligand-receptor binding and thus they are mainly responsible for AChE inhibitory activity.
    CONCLUSIONS:
    In view of its potent AChE inhibitory activity, Linarin may be a promising therapeutic agent for the treatment of some diseases associated with AChE, such as glaucoma, myasthenia gravis, gastric motility and Alzheimer's disease.
    Cell Research:
    J Med Food. 2013 Dec;16(12):1086-94.
    Phytochemical linarin enriched in the flower of Chrysanthemum indicum inhibits proliferation of A549 human alveolar basal epithelial cells through suppression of the Akt-dependent signaling pathway.[Pubmed: 24117095]

    METHODS AND RESULTS:
    In this study, we report the anti-proliferative effect and molecular mechanism of Chrysanthemum indicum (C. indicum) on A549 human alveolar basal epithelial cells. We also analyzed the changes in C. indicum component profiles due to modifications of predrying process, flower size, and extraction method. Among the varieties of modifications tested, high-temperature heat dry (HTD) of small flower biotype followed by the methanolic extraction resulted in the strongest anti-proliferative activity of C. indicum extract in A549 cells. High-performance liquid chromatography of C. indicum revealed that the levels of acacetin 7-O-rutinoside (Linarin) are markedly increased by heat treatment, especially HTD. Finally, we showed that Linarin-mediated inhibition of cell proliferation is associated with suppression of Akt activation and induction of cyclin-dependent kinase inhibitor p27(Kip1) as evidenced by cell cycle analysis and treatment with LY294002, an inhibitor of phosphatidylinositol 3-kinase/Akt pathway.
    CONCLUSIONS:
    Taken together, these findings suggest the need for further development and evaluation of Linarin from C. indicum for the treatment and prevention of lung cancer.
    Bioorg Med Chem. 2011 Jul 1;19(13):4021-7.
    Neuroprotective effects of linarin through activation of the PI3K/Akt pathway in amyloid-β-induced neuronal cell death.[Pubmed: 21652214 ]
    Linarin, a natural occurring flavanol glycoside derived from Mentha arvensis and Buddleja davidii is known to have anti-acetylcholinesterase effects.
    METHODS AND RESULTS:
    The present study intended to explore the neuroprotective effects of Linarin against Aβ(25-35)-induced neurotoxicity with cultured rat pheochromocytoma cells (PC12 cells) and the possible mechanisms involved. For this purpose, PC12 cells were cultured and exposed to 30 μM Aβ(25-35) in the absence or presence of Linarin (0.1, 1.0 and 10 μM). In addition, the potential contribution of the PI3K/Akt neuroprotective pathway in Linarin-mediated protection against Aβ(25-35)-induced neurotoxicity was also investigated. The results showed that Linarin dose-dependently increased cell viability and reduced the number of apoptotic cells as measured by MTT assay, Annexin-V/PI staining, JC-1 staining and caspase-3 activity assay. Linarin could also inhibit acetylcholinesterase activity induced by Aβ(25-35) in PC12 cells. Further study revealed that Linarin induced the phosphorylation of Akt dose-dependently. Treatment of PC12 cells with the PI3K inhibitor LY294002 attenuated the protective effects of Linarin. Furthermore, Linarin also stimulated phosphorylation of glycogen synthase kinase-3β (GSK-3β), a downstream target of PI3K/Akt. Moreover, the expression of the anti-apoptotic protein Bcl-2 was also increased by Linarin treatment.
    CONCLUSIONS:
    These results suggest that Linarin prevents Aβ(25-35)-induced neurotoxicity through the activation of PI3K/Akt, which subsequently inhibits GSK-3β and up-regulates Bcl-2. These findings raise the possibility that Linarin may be a potent therapeutic compound against Alzheimer's disease acting through both acetylcholinesterase inhibition and neuroprotection.
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