28-DeoxonimbolideCAS# 126005-94-5 |
2D Structure
Quality Control & MSDS
3D structure
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Number of papers citing our products
Cas No. | 126005-94-5 | SDF | Download SDF |
PubChem ID | 159573 | Appearance | Powder |
Formula | C27H32O6 | M.Wt | 452.55 |
Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
SMILES | CC1=C2C(CC1C3=COC=C3)OC4C2(C(C5(C6C4OCC6(C=CC5=O)C)C)CC(=O)OC)C | ||
Standard InChIKey | CWGBIWRWBCYASK-DVTNSOTCSA-N | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | 1. 28-Deoxonimbolide exhibits potent cytotoxic activity against HL60 leukemia cells. |
Targets | Caspase |
28-Deoxonimbolide Dilution Calculator
28-Deoxonimbolide Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.2097 mL | 11.0485 mL | 22.097 mL | 44.194 mL | 55.2425 mL |
5 mM | 0.4419 mL | 2.2097 mL | 4.4194 mL | 8.8388 mL | 11.0485 mL |
10 mM | 0.221 mL | 1.1049 mL | 2.2097 mL | 4.4194 mL | 5.5243 mL |
50 mM | 0.0442 mL | 0.221 mL | 0.4419 mL | 0.8839 mL | 1.1049 mL |
100 mM | 0.0221 mL | 0.1105 mL | 0.221 mL | 0.4419 mL | 0.5524 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Preclinical evaluation of the supercritical extract of azadirachta indica (neem) leaves in vitro and in vivo on inhibition of prostate cancer tumor growth.[Pubmed:24674886]
Mol Cancer Ther. 2014 May;13(5):1067-77.
Azadirachta indica, commonly known as neem, has gained worldwide prominence because of its medical properties, namely antitumor, antiviral, anti-inflammatory, antihyperglycemic, antifungal, and antibacterial activities. Despite these promising results, gaps remain in our understanding of the molecular mechanism of action of neem compounds and their potential for use in clinical trials. We investigated supercritical extract of neem leaves (SENL) for the following: molecular targets in vitro, in vivo efficacy to inhibit tumor growth, and bioactive compounds that exert antitumor activity. Treatment of LNCaP-luc2 prostate cancer cells with SENL suppressed dihydrotestosterone-induced androgen receptor and prostate-specific antigen levels. SENL inhibited integrin beta1, calreticulin, and focal adhesion kinase activation in LNCaP-luc2 and PC3 prostate cancer cells. Oral administration of SENL significantly reduced LNCaP-luc2 xenograft tumor growth in mice with the formation of hyalinized fibrous tumor tissue, reduction in the prostate-specific antigen, and increase in AKR1C2 levels. To identify the active anticancer compounds, we fractionated SENL by high-pressure liquid chromatography and evaluated 16 peaks for cytotoxic activity. Four of the 16 peaks exhibited significant cytotoxic activity against prostate cancer cells. Mass spectrometry of the isolated peaks suggested the compounds with cytotoxic activity were nimbandiol, nimbolide, 2',3'-dihydronimbolide, and 28-Deoxonimbolide. Analysis of tumor tissue and plasma samples from mice treated with SENL indicated 28-Deoxonimbolide and nimbolide as the bioactive compounds. Overall, our data revealed the bioactive compounds in SENL and suggested that the anticancer activity could be mediated through alteration in androgen receptor and calreticulin levels in prostate cancer.
Spectroscopic and biological investigation of nimbolide and 28-deoxonimbolide from Azadirachta indica.[Pubmed:2614419]
J Nat Prod. 1989 Nov-Dec;52(6):1246-51.
The reisolation of nimbolide [1] from Azadirachta indica of Tanzanian origin and the isolation and structure elucidation of a new limonoid, 28-Deoxonimbolide [2], from the same plant source are reported. For the first time, unambiguous 1H- and 13C-nmr assignments of compounds 1 and 2 are presented, as well as their in vitro cytotoxic activity against human tumor cell lines.
Cytotoxic and apoptosis-inducing activities of limonoids from the seeds of Azadirachta indica (neem).[Pubmed:21381696]
J Nat Prod. 2011 Apr 25;74(4):866-70.
Thirty-five limonoids, including 15 of the azadiradione type (1-15), five of the gedunin type (16-20), four of the azadirachtin type (21-24), nine of the nimbin type (25-33), and two degraded limonoids (34, 35), isolated from Azadirachta indica seed extracts, were evaluated for their cytotoxic activities against five human cancer cell lines. Seven compounds (3, 6, 7, 16, 18, 28, and 29) exhibited cytotoxic activity against one or more cell lines. Among these compounds, 7-deacetyl-7-benzoylepoxyazadiradione (7), 7-deacetyl-7-benzoylgeduin (18), and 28-Deoxonimbolide (28) exhibited potent cytotoxic activity against HL60 leukemia cells with IC(50) values in the range 2.7-3.1 muM. Compounds 7, 18, and 28 induced early apoptosis in HL60 cells, observed by flow cytometry. Western blot analysis showed that compounds 7, 18, and 28 activated caspases-3, -8, and -9 in HL60 cells. This suggested that compounds 7, 18, and 28 induced apoptotic cell death in HL60 cells via both the mitochondrial- and the death receptor-mediated pathways. Futhermore, compound 7 was shown to possess high selective cytotoxicity for leukemia cells since it exhibited only weak cytotoxicity against a normal lymphocyte cell line (RPMI 1788).