|Description:||1. Dihydrocucurbitacin B is effective against cancer. |
2. Dihydrocucurbitacin B curbs DTH reactions by inhibiting NFAT, which in turn suppresses the proliferation of the most relevant cells involved in DTH reactions, namely the T cells.
3. Dihydrocucurbitacin B reduces cell proliferation due to a decrease in the expression of cyclins, mainly cyclin-B1 and disruption of the actin cytoskeleton, arresting B16F10 cells in G2/M phase.
4. Dihydrocucurbitacin B modifies the evolution of the clinical symptoms, reduces the swelling and bone and tissue damage along with the development of the disease, modifies the cell infiltration and the expression of both nitric oxide synthase-2 and cyclooxygenase-2.
|Targets:||IL Receptor | TNF-α | COX | NOS|
|Source:||The rhizomes of Hemsleya amabilis Diels.|
|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: email@example.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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.7835 mL||8.9174 mL||17.8348 mL||35.6697 mL||44.5871 mL|
|5 mM||0.3567 mL||1.7835 mL||3.567 mL||7.1339 mL||8.9174 mL|
|10 mM||0.1783 mL||0.8917 mL||1.7835 mL||3.567 mL||4.4587 mL|
|50 mM||0.0357 mL||0.1783 mL||0.3567 mL||0.7134 mL||0.8917 mL|
|100 mM||0.0178 mL||0.0892 mL||0.1783 mL||0.3567 mL||0.4459 mL|
Bioorg Med Chem. 2012 May 1;20(9):3016-30.
|Synthesis and cytotoxic activity evaluation of dihydrocucurbitacin B and cucurbitacin B derivatives.[Pubmed: 22472043]|
|Two cucurbitacins, Dihydrocucurbitacin B (1) and cucurbitacin B (2), which can be obtained in large amounts from the roots of Wilbrandia ebracteata and from the fruits of Luffa operculata, respectively, were used as starting materials for the preparation of a library of 29 semi-synthetic derivatives. The structural changes that were performed include the removal, modification or permutation of functional groups in rings A and B as well as in the side chain. All new semisynthetic compounds, as well as 1 and 2, were tested in vitro for their cytotoxic effects on non-small-cell lung cancer cells (A549 cells). Some of these compound displayed potent to moderate activity against A549 tumor cells, especially those cucurbitacin B derivatives which were modified at ring A.|
Cancer Chemother Pharmacol. 2009 Aug;64(3):529-38.
|Evaluation of the antitumoral effect of dihydrocucurbitacin-B in both in vitro and in vivo models.[Pubmed: 19184021]|
|AIMS: We evaluated both in vitro and in vivo antitumoral properties of an isolated compound from Wilbrandia ebracteata, Dihydrocucurbitacin B (DHCB), using B16F10 cells (murine melanoma). MATERIALS AND METHODS: We made use of MTT and (3)H-Thymidine assays to investigate the cell viability and cell proliferation, flow cytometry analysis to monitor cell cycle and apoptosis, western blot analysis to evaluate the expression of cell cycle proteins, imunofluorescence analysis and in vivo tumor growth and metastasis. RESULTS: Dihydrocucurbitacin B significantly reduced cell proliferation without important effects on cells viability. Dihydrocucurbitacin B lead cells to accumulate in G2/M phases accompanied by the appearance of polyploid cells, confirmed by fluorescence assays that demonstrated a remarkable alteration in the cell cytoskeleton and formation of binuclear cells. Annexin-V-FITC incorporation demonstrated that Dihydrocucurbitacin B did not induce apoptosis. About 10 microg/mL Dihydrocucurbitacin B was found to decrease cyclin-A, and especially in cyclin-B1. The in vivo experiments showed that Dihydrocucurbitacin B treatment (once a day up to 12 days; p.o.) was able to reduce the tumor growth and lung metastasis up to 83.5 and 50.3%, respectively. CONCLUSIONS: Dihydrocucurbitacin B reduces cell proliferation due to a decrease in the expression of cyclins, mainly cyclin-B1 and disruption of the actin cytoskeleton, arresting B16F10 cells in G2/M phase. Taken together, the in vitro and in vivo experiments suggest that Dihydrocucurbitacin B was effective against cancer, however, it remains to be proved if Dihydrocucurbitacin B will be a good candidate for drug development.|
Dihydrocucurbitacin B inhibits delayed type hypersensitivity reactions by suppressing lymphocyte proliferation.
|Dihydrocucurbitacin B inhibits delayed type hypersensitivity reactions by suppressing lymphocyte proliferation.[Pubmed: 17562851]|
|We have studied the effects of Dihydrocucurbitacin B, a triterpene isolated from Cayaponia tayuya roots, on different models of delayed type hypersensitivity (DTH) in mice, as well as on T-lymphocyte proliferation and the mediators involved. In experiments with mice, Dihydrocucurbitacin B inhibited the inflammatory reactions induced by oxazolone, dinitrofluorobenzene, and sheep red blood cells, reducing both the edema and cell infiltration. Moreover, the analysis of inflamed tissues showed that Dihydrocucurbitacin B reduced the presence of the most relevant cytokines implicated in these processes, including interleukin-1 beta, interleukin-4, and tumor necrosis factor-alpha. Dihydrocucurbitacin B was also found to inhibit the proliferation of phytohemagglutinin-stimulated human T lymphocytes (IC(50) = 1.48 microM), halting the cell cycle in the G(0) phase. In addition, the triterpene reduced the production of interleukin-2, interleukin-4, interleukin-10, and interferon-gamma in human T lymphocytes, and it hampered the induction of the principal cyclins involved in the cell cycle, including A(1), B(1), D(2), and E(1). Finally, Dihydrocucurbitacin B was found to exert a selective inhibition on the nuclear factor of activated T cells (NFAT) in human lymphocytes without affecting the calcium influx. Taken together, these results suggest that Dihydrocucurbitacin B curbs DTH reactions by inhibiting NFAT, which in turn suppresses the proliferation of the most relevant cells involved in DTH reactions, namely the T cells.|
Eur J Pharmacol. 2006 Feb 17;532(1-2):145-54.
|Dihydrocucurbitacin B, isolated from Cayaponia tayuya, reduces damage in adjuvant-induced arthritis.[Pubmed: 16443215]|
|23,24-Dihydrocucurbitacin B, from the anti-rheumatic plant Cayaponia tayuya, was tested on arthritis induced by adjuvant to corroborate the anti-inflammatory properties of this plant. Arthritis was induced in Lewis rats; the resulting arthritic rats were then treated with Dihydrocucurbitacin B (1 mg/kg orally, daily, 1 week). The effect of Dihydrocucurbitacin B on the synthesis, release, and activity of pro-inflammatory enzymes (elastase, cyclooxygenase-2, and nitric oxide synthase-2) as well as its effect on different mediators (tumor necrosis factor-alpha and interleukin-1beta) were determined. Dihydrocucurbitacin B modified the evolution of the clinical symptoms, reducing the swelling and bone and tissue damage along with the development of the disease, modifying the cell infiltration and the expression of both nitric oxide synthase-2 and cyclooxygenase-2. In addition, it decreased the tumor necrosis factor-alpha and interleukin-1beta production in lymphocytes, but did not modify it in macrophages.|