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    CAS No. 58812-37-6 Price $100 / 20mg
    Catalog No.CFN99908Purity>=98%
    Molecular Weight574.62Type of CompoundTriterpenoids
    FormulaC30H38O11Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Our products had been exported to the following research institutions and universities, And still growing.
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    Featured Products
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    Biological Activity
    Description: Toosendanin (TSN) was used as a digestive tract-parasiticide and agricultural insecticide in ancient China;TSN is a selective presynaptic blocker, a L-type Ca 2+ channel agonist and an effective antibotulismic agent, by interfering with neurotransmitter release through an initial facilitation followed by a subsequent depression. TSN has effects on the growth, cell cycle arrest, induction of apoptosis and the involved signaling pathway in human promyelocytic leukemia HL-60 cells.
    Targets: Calcium Channel | JNK | Bcl-2/Bax | PARP | Caspase
    In vitro:
    Prog Neurobiol. 2007 May;82(1):1-10.
    Biological effects of toosendanin, a triterpenoid extracted from Chinese traditional medicine.[Pubmed: 17363132 ]
    Toosendanin (TSN) is a triterpenoid extracted from Melia toosendan Sieb et Zucc, which was used as a digestive tract-parasiticide and agricultural insecticide in ancient China. TSN was demonstrated to be a selective presynaptic blocker and an effective antibotulismic agent.
    By interfering with neurotransmitter release through an initial facilitation followed by a subsequent depression, TSN eventually blocks synaptic transmission at both the neuro-muscular junction and central synapses. Despite sharing some similar actions with botulinum neurotoxin (BoNT), TSN has a marked antibotulismic effect in vivo and in vitro. Studies suggest that the antibotulismic effect of TSN is achieved by preventing BoNT from approaching its enzymatic substrate, the SNARE protein. It is also found that TSN can induce differentiation and apoptosis in several cell lines, and suppress proliferation of various human cancer cells. TSN inhibits various K(+)-channels, selectively facilitates Ca(2+)-influx via L-type Ca(2+) channels and increases intracellular Ca(2+) concentration ([Ca(2+)](i)).
    The TSN-induced [Ca(2+)](i) increase and overload could be responsible for the TSN-induced biphasic effect on transmitter release, cell differentiation, apoptosis as well as the cytoxicity of TSN.
    J Med Entomol. 2013 Jan;50(1):112-21.
    Effects of the botanical insecticide, toosendanin, on blood digestion and egg production by female Aedes aegypti (Diptera: Culicidae): topical application and ingestion.[Pubmed: 23427659]
    Botanical insecticides offer novel chemistries and actions that may provide effective mosquito control.
    Toosendanin (TSN, 95% purity) is one such insecticide used to control crop pests in China, and in this study, it was evaluated for lethal and sublethal effects on larvae and females of the yellowfever mosquito, Aedes aegypti (L.). Toosendanin was very toxic to first instar larvae after a 24 h exposure (LC50 = 60.8 microg/ml) and to adult females up to 96 h after topical treatment (LD50 = 4.3 microg/female) or ingestion in a sugar bait (LC50 = 1.02 microg/microl). Treatment of first instars for 24 h with a range of sublethal doses (6.3-25 microg/ml) delayed development to pupae by 1 to 2 d. Egg production and larval hatching from eggs were dose dependently reduced (>45%) by Toosendanin doses (1.25-10.0 microg) topically applied to females 24 h before or 1 h after a bloodmeal. Ingestion of Toosendanin (0.031-0.25 microg/microl of sugar bait) by females 24 h before a bloodmeal also greatly reduced egg production and larval hatch; no eggs were oviposited by females ingesting the highest dose. Further studies revealed that topical or ingested Toosendanin dose-dependently disrupted yolk deposition in oocytes, blood ingestion and digestion, and ovary ecdysteroid production in blood-fed females.
    Overall, our results indicate that Toosendanin is an effective insecticide for Ae. aegypti larvae and adults, because of its overt toxicity at high doses and disruption of development and reproduction at sublethal doses.
    In vivo:
    J. Appl. Entomol., 1995, 119(1-5):367-70.
    Antifeedant and growth inhibitory effects of the limonoid toosendanin and Melia toosendan extracts on the variegated cutworm, Peridromasaucia (Lep., Noctuidae)[Reference: WebLink]
    Antifeedant and growth inhibitory effects of Toosendanin, a limonoid allelochemical from the bark of the trees Melia toosendan and M. azedarach, were determined for the variegated cutworm, Peridroma saucia, using different bioassays.
    Toosendanin significantly deterred feeding of 2nd and 4th instar larvae in diet choice and leaf disc choice bioassays, respectively. Refined bark extracts containing 60–75% Toosendanin were less deterrent than the pure compound in both bioassays. However, the 60% extract significantly inhibited growth of neonate larvae in a dose-dependent manner when incorporated into an artificial diet, with an EC50 (concentration reducing growth by 50% relative to controls) of 42.3 ppm at 7 days. Extracts containing 60% and 75% Toosendanin were more inhibitory than equivalent amounts of pure Toosendanin in this chronic growth bioassay, suggesting the presence of other minor constituents which must be significantly more inhibitory, though less deterrent to feeding, than Toosendanin itself.
    Nutritional analyses of 4th instar larvae following both oral and topical administration of Toosendanin or the 75% extract confirm that both materials possess a combination of antifeedant and growth inhibitory properties.
    Toosendanin Description
    Source: The barks of Melia toosendan Sieb. et Zucc.
    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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.7403 mL 8.7014 mL 17.4028 mL 34.8056 mL 43.507 mL
    5 mM 0.3481 mL 1.7403 mL 3.4806 mL 6.9611 mL 8.7014 mL
    10 mM 0.174 mL 0.8701 mL 1.7403 mL 3.4806 mL 4.3507 mL
    50 mM 0.0348 mL 0.174 mL 0.3481 mL 0.6961 mL 0.8701 mL
    100 mM 0.0174 mL 0.087 mL 0.174 mL 0.3481 mL 0.4351 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.
    Kinase Assay:
    Eur J Pharmacol. 2004 Oct 6;501(1-3):71-8.
    Toosendanin, a triterpenoid derivative, acts as a novel agonist of L-type Ca2+ channels in neonatal rat ventricular cells.[Pubmed: 15464064 ]
    Toosendanin, a triterpenoid derivative extracted from Melia toosendan Sieb et Zucc, was demonstrated to be potentially useful in medical and scientific researches.
    Here, we investigated the effects of Toosendanin on L-type voltage-dependent Ca(2+) channels in cultured neonatal rat ventricular cells, using whole-cell patch-clamp method. Toosendanin irreversibly increased L-type Ca(2+) current (I(Ca(L))) in a concentration-dependent manner and shifted the maximum of the current/voltage relationship from 8.3+/-3.7 to 1.7+/-3.7 mV, without modifying the threshold potential of the current. Toosendanin shifted the steady-state activation and inactivation curves to the left. The deactivation kinetics of the I(Ca(L)) was significantly slowed by Toosendanin while the activation kinetics was not affected. The cells pretreated with 100 nM 1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)phenyl]-3-pyridinecarboxylic acid methyl ester (S(-)-BayK8644) still respond to further addition of 87 microM Toosendanin, and vice versa.
    These results prove Toosendanin to be a novel L-type Ca(2+) channel agonist, which possesses a distinct binding site from BayK8644.
    Cell Research:
    Neurosci Res. 2003 Feb;45(2):225-31.
    Toosendanin induces outgrowth of neuronal processes and apoptosis in PC12 cells.[Pubmed: 12573469]

    In the present study, the effects of Toosendanin on cell differentiation and apoptosis were investigated in PC12 cells. The results showed that after 24-48 h of culture in a medium containing Toosendanin (approximately 1-10x10(-7) M), cell differentiation and outgrowth of neuronal processes were promoted. Combined treatment with Toosendanin and a calcium channel blocker, nifedipine or omega-conotoxin GVIA, resulted in a significant inhibition of the Toosendanin-induced effects. Pretreatment of PC12 cells with BAPTA-AM also inhibited the Toosendanin-induced effects; however, these effects were not inhibited by pertussis toxin and H-7 in the medium. Toosendanin also induced cell apoptosis. Based on the DNA content determined by flow cytometric analysis, the number of apoptotic cells significantly increased when the incubation time in the Toosendanin-containing medium was lasted up to 72 h.
    Toosendanin at a higher concentration (> or =1 x 10(-6) M) caused cell death while it had no effect on cell division at concentrations lower than 1 x 10(-7) M.
    Toxicol In Vitro. 2013 Feb;27(1):232-8.
    Toosendanin induces apoptosis through suppression of JNK signaling pathway in HL-60 cells.[Pubmed: 23111283]
    Toosendanin (TSN), a triterpenoid isolated from Melia toosendan Sieb. et Zucc., has been found to suppress proliferation and induce apoptosis in a variety of human cancer cells. However, the mechanism how TSN induces apoptosis remains poorly understood.
    In this study, we examined the effects of TSN on the growth, cell cycle arrest, induction of apoptosis and the involved signaling pathway in human promyelocytic leukemia HL-60 cells. Proliferation of HL-60 cells was inhibited in a dose-dependent manner with the IC(50 (48 h)) of 28 ng/mL. The growth inhibition was due primarily to the S phase arrest and cell apoptosis. Cell apoptosis induced by TSN was confirmed by Annexin V-FITC/propidium iodide staining. The increase of the pro-apoptotic protein Bax, cleaved PARP and caspase-3, and the decrease of anti-apoptotic protein Bcl-2 were observed. Western blot analysis indicated that TSN inhibits the CDC42/MEKK1/JNK pathway.
    Taken together, our study suggested, for the first time, that the pro-apoptotic effects of TSN on HL-60 cells were mediated through JNK signaling pathway.