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    Licarin A
    Information
    CAS No. 23518-30-1 Price $368 / 5mg
    Catalog No.CFN98244Purity>=98%
    Molecular Weight326.4 Type of CompoundLignans
    FormulaC20H22O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Licarin A and (-)-Licarin A are promising compounds that could be used for the development of schistosomicidal and trypanocidal agents; Licarin A presents effect against Leishmania (Leishmania) major associated with immunomodulation in vitro; (-)-Licarin A has antimycobacterial activity, represents a potentially active anti-tuberculosis agent to treat MDR M. tuberculosis and NTM strains.Licarin A significantly protects primary cultured neuronal cells against glutamate-induced oxidative stress, via antioxidative activities.
    Targets: DNA/RNA Synthesis | IL Receptor | Antifection
    In vitro:
    Br J Pharmacol. 2005 Nov;146(5):752-9.
    Meso-dihydroguaiaretic acid and licarin A of Machilus thunbergii protect against glutamate-induced toxicity in primary cultures of a rat cortical cells.[Pubmed: 16151440]
    We previously reported that four lignans isolated from the bark of Machilus thunbergii Sieb. et Zucc. (Lauraceae) protected primary cultures of rat cortical neurons from neurotoxicity induced by glutamate.
    METHODS AND RESULTS:
    2 Among the lignans, meso-dihydroguaiarectic acid (MDGA) and Licarin A significantly attenuated glutamate-induced neurotoxicity when added prior to or right after the excitotoxic glutamate challenge. 3 The neuroprotective activities of two lignans appeared to be more effective in protecting neurons against neurotoxicity induced by NMDA than that induced by kainic acid. 4 MDGA and Licarin A diminished the calcium influx that routinely accompanies with the glutamate-induced neurotoxicity, and inhibited the subsequent overproduction of cellular nitric oxide and peroxide to the level of control cells. They also preserved cellular activities of antioxidative enzymes such as superoxide dismutase, glutathione peroxidase and glutathione reductase reduced in the glutamate-injured neuronal cells.
    CONCLUSIONS:
    5 Thus, our results suggest that MDGA and Licarin A significantly protect primary cultured neuronal cells against glutamate-induced oxidative stress, via antioxidative activities.
    Exp Parasitol. 2013 Oct;135(2):307-13.
    Neolignan Licarin A presents effect against Leishmania (Leishmania) major associated with immunomodulation in vitro.[Pubmed: 23891943]
    Leishmaniasis' treatment is based mostly on pentavalent antimonials or amphotericin B long-term administration, expensive drugs associated with severe side effects. Considering these aforementioned, the search for alternative effective and safe leishmaniasis treatments is a necessity.
    METHODS AND RESULTS:
    This work evaluated a neolignan, Licarin A anti-leishmanial activity chemically synthesized by our study group. It was observed that Licarin A effectively inhibited Leishmania (Leishmania) major promastigotes (IC₅₀ of 9.59 ± 0.94 μg/mL) growth, by inducing in these parasites genomic DNA fragmentation in a typical death pattern by apoptosis. Additionally, the neolignan proved to be even more active against intracellular amastigotes of the parasite (EC₅₀ of 4.71 ± 0.29 μg/mL), and significantly more effective than meglumine antimoniate (EC₅₀ of 216.2 ± 76.7 μg/mL) used as reference drug. The antiamastigote activity is associated with an immunomodulatory activity, since treatment with Licarin A of the infected macrophages induced a decrease in the interleukin (IL)-6 and IL-10 production.
    CONCLUSIONS:
    This study demonstrates for the first time the antileishmanial activity of Licarin A and suggests that the compound may be a promising in the development of a new leishmanicidal agent.
    Phytochemistry. 2011 Aug;72(11-12):1424-30.
    Schistosomicidal and trypanocidal structure-activity relationships for (±)-licarin A and its (-)- and (+)-enantiomers.[Pubmed: 21570099]
    (±)-Licarin A (1) was obtained by oxidative coupling, and its enantiomers, (-)-Licarin A (2) and (+)-Licarin A (3), were resolved by chiral HPLC.
    METHODS AND RESULTS:
    Schistosomicidal and trypanocidal activities of these compounds were evaluated in vitro against Schistosoma mansoni adult worms and trypomastigote forms of Trypanosoma cruzi. The racemic mixture (1) displayed significant schistosomicidal activity with an LC₅₀ value of 53.57 μM and moderate trypanocidal activity with an IC₅₀ value of 127.17 μM. On the other hand, the (-)-enantiomer (2), displaying a LC₅₀ value of 91.71 μM, was more active against S. mansoni than the (+)-enantiomer (3), which did not show activity. For the trypanocidal assay, enantiomer 2 showed more significant activity (IC₅₀ of 23.46 μM) than enantiomer 3, which showed an IC₅₀ value of 87.73 μM.
    CONCLUSIONS:
    Therefore, these results suggest that (±)-Licarin A (1) and (-)-Licarin A (2) are promising compounds that could be used for the development of schistosomicidal and trypanocidal agents.
    Licarin A Description
    Source: The seeds of Myristica fragrans Houtt.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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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    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.0637 mL 15.3186 mL 30.6373 mL 61.2745 mL 76.5931 mL
    5 mM 0.6127 mL 3.0637 mL 6.1275 mL 12.2549 mL 15.3186 mL
    10 mM 0.3064 mL 1.5319 mL 3.0637 mL 6.1275 mL 7.6593 mL
    50 mM 0.0613 mL 0.3064 mL 0.6127 mL 1.2255 mL 1.5319 mL
    100 mM 0.0306 mL 0.1532 mL 0.3064 mL 0.6127 mL 0.7659 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
    Animal Research:
    Arch Med Res. 2013 Feb;44(2):99-104.
    Antitubercular activity and the subacute toxicity of (-)-Licarin A in BALB/c mice: a neolignan isolated from Aristolochia taliscana.[Pubmed: 23291382]
    (-)-Licarin A (LA) was isolated from diverse plants such as Aristolochia taliscana and possesses antimycobacterial, antiinflammatory, trypanocidal, and neuroprotective activities. The aim of the study was to determine the antitubercular and subacute toxicity of (-)-Licarin A isolated from A. taliscana in BALB/c mice.
    METHODS AND RESULTS:
    The antitubercular activity of (-)-Licarin A was tested in a TB murine model inducing disease with M. tuberculosis H37Rv or MDR. Mice were treated with (-)-Licarin A (5 mg/kg) for 30 and 60 days; post/treatment, lung bacilli loads and pneumonia percentage were determined. The subacute toxicity of (-)-Licarin A (21 days) was evaluated in healthy mice. After treatment, biochemical and hematological parameters were determined and main organs were analyzed histologically. In animals infected with drug-sensitive or MDR strains, (-)-Licarin A produced a significant decrease of pulmonary bacillary burdens at day 30 of treatment, and a significant pneumonia reduction at days 30 and 60 of treatment. Regarding subacute toxicity, (-)-Licarin A administration during 21 days showed no abnormalities in main-organ macro- and microarchitecture.
    CONCLUSIONS:
    (-)-Licarin A reduces pneumonia of mice infected with both mycobacterium strains. Also, subacute toxicity of (-)-Licarin A exhibits no major signs of damage. Biochemical and hematological parameters and histological analyses indicate that (-)-Licarin A caused no significant changes at the doses assayed.