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Home >> Research Area >>Nature Products >> 16-Hydroxy-2-oxocleroda-3,13-dien-15,16-olide


Catalog No. BCN1536
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20mg $298 In stock
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Chemical Properties of 16-Hydroxy-2-oxocleroda-3,13-dien-15,16-olide

Cas No. 165459-53-0 SDF Download SDF
Type of Compound Diterpenoids Appearance Powder
Formula C20H28O4 M.Wt 332.4
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 16-Hydroxy-2-oxocleroda-3,13-dien-15,16-olide

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.0084 mL 15.0421 mL 30.0842 mL 60.1685 mL 75.2106 mL
5 mM 0.6017 mL 3.0084 mL 6.0168 mL 12.0337 mL 15.0421 mL
10 mM 0.3008 mL 1.5042 mL 3.0084 mL 6.0168 mL 7.5211 mL
50 mM 0.0602 mL 0.3008 mL 0.6017 mL 1.2034 mL 1.5042 mL
100 mM 0.0301 mL 0.1504 mL 0.3008 mL 0.6017 mL 0.7521 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.

Preparation of 16-Hydroxy-2-oxocleroda-3,13-dien-15,16-olide

This product is isolated and purified from the herbs of Polyalthia cheliensis

References on 16-Hydroxy-2-oxocleroda-3,13-dien-15,16-olide

16-hydroxycleroda-3,13-dien-15,16-olide regulates the expression of histone-modifying enzymes PRC2 complex and induces apoptosis in CML K562 cells.[Pubmed: 21983300]

Histone modifications play central epigenetic roles in regulating the entire genome of the cell and cell proliferation. Herein, we investigated the effects of the natural compound, 16-hydroxycleroda-3,13-dien-15,16-olide (PL3), on the expressions of histone-modifying enzymes, and examined how it induces apoptosis in leukemia K562 cells.

16-Hydroxycleroda-3,13-dien-15,16-olide deregulates PI3K and Aurora B activities that involve in cancer cell apoptosis.[Pubmed: 21530604]

The PI3K-AKT pathway and Aurora kinase play essential roles in such cellular processes as cell survival, angiogenesis, and differentiation, and are usually expressed at maximum levels during cancer cell proliferation. The present study investigated the effect of the natural compound, 16-hydroxycleroda-3,13-dien-15,16-olide (PL3), on regulating the PI3K-AKT pathway and Aurora B, which led to cancer cell apoptosis. PL3 acts as a PI3K inhibitor by influencing cell survival, signaling transduction, and cell cycle progression. It was observed that PL3 targeted and induced dephosphorylation of the PI3K pathway, degradation of Aurora B and mitotic-related gene expressions, and sequentially shut down the cell cycle. This eventually resulted in cell death. As Aurora B was downregulated, spindle dysfunction and destruction of the G₂/M phase checkpoint resulted in DNA-damaged cells undergoing apoptosis. Moreover, PL3 also resensitized T315I-mutated Bcr-ABL+ BA/F3 cells to improve the cytotoxicity of Imatinib in Imatinib-resistant cell line. Taken together, PL3 can perturb the PI3K-AKT pathway and Aurora B resulting in gene silencing and cell cycle disturbance. It was demonstrated that PL3 acted like a novel small-molecule PI3K modulator, thereby potentially contributing to cancer chemotherapy and combination medication.

6-Hydroxycleroda-3,13-dien-15,16-olide protects neuronal cells from lipopolysaccharide-induced neurotoxicity through the inhibition of microglia-mediated inflammation.[Pubmed: 19653144]

Polyalthia longifolia var. pendula is used as an antipyretic agent in indigenous systems of medicine. Microglia-mediated inflammation plays an important role in the pathway leading to neuronal cell death in a number of neurodegenerative diseases. The aim of this study was to investigate the effects of 6-hydroxycleroda-3,13-dien-15,16-olide (PL3) extracted from Polyalthia longifolia var. pendula on lipopolysaccharide(LPS)-induced inflammation in microglia-like HAPI cells and primary microglia cultures. In microglia-neuron co-cultures, LPS decreased the cell viability of neuroblastoma SH-SY5Y cells. LPS-induced cell death was attenuated by the NOS inhibitor, L-NAME, the COX-2 inhibitor, NS-398 or the NADPH oxidase inhibitor, DPI, respectively. In LPS-treated microglia cells, PL3 decreased the expression of iNOS, COX-2, gp91 (phox), and NF- kappaBp65, the degradation of I kappaB alpha, and the production of NO, PGE (2), iROS, and TNF- alpha. PL3 also enhanced the expression of HO-1, a cytoprotective and anti-inflammatory enzyme. Moreover, PL3 reduced LPS-activated microglia-induced cell death. The present results suggest that PL3 inhibits microglia-mediated inflammation and inflammation-related neuronal cell death. Therefore, PL3 has potential use for the treatment of inflammation-related neurodegenerative diseases.


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