Jolkinolide BCAS# 37905-08-1 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 37905-08-1 | SDF | Download SDF |
| PubChem ID | 161954 | Appearance | Powder |
| Formula | C20H26O4 | M.Wt | 330.42 |
| Type of Compound | Diterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| SMILES | CC1=C2C3C4(O3)CCC5C(CCCC5(C4C6C2(O6)OC1=O)C)(C)C | ||
| Standard InChIKey | SOVOCMGDFRGRKF-MCDHERAVSA-N | ||
| Standard InChI | InChI=1S/C20H26O4/c1-10-12-14-19(22-14)9-6-11-17(2,3)7-5-8-18(11,4)13(19)15-20(12,23-15)24-16(10)21/h11,13-15H,5-9H2,1-4H3/t11-,13+,14-,15-,18-,19+,20-/m1/s1 | ||
| 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. Jolkinolide B can induce neuroendocrine differentiation of human prostate LNCaP cancer cell line. 2. Jolkinolide B can induce apoptosis in MDA-MB-231 cells through inhibition of the PI3K/Akt signaling pathway. 3. Jolkinolide B has potent anti-inflammatory activities, the mechanism may be attributed to its suppression of NF-κB and activation. 4. Jolkinolide B exhibits significant antitumor activity, it is able to enhance apoptosis of human leukemic HL-60 and THP-1 cells, at least in part, through downregulation of JAK2/STAT3 and bcl-2, and upregulation of Bax and cytosolic cytochrome c. |
| Targets | JAK | STAT | Bcl-2/Bax | Caspase | TNF-α | NF-kB | IL Receptor | p38MAPK | JNK | ERK | mTOR | Akt | PI3K |
Jolkinolide B Dilution Calculator
Jolkinolide B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.0265 mL | 15.1323 mL | 30.2645 mL | 60.529 mL | 75.6613 mL |
| 5 mM | 0.6053 mL | 3.0265 mL | 6.0529 mL | 12.1058 mL | 15.1323 mL |
| 10 mM | 0.3026 mL | 1.5132 mL | 3.0265 mL | 6.0529 mL | 7.5661 mL |
| 50 mM | 0.0605 mL | 0.3026 mL | 0.6053 mL | 1.2106 mL | 1.5132 mL |
| 100 mM | 0.0303 mL | 0.1513 mL | 0.3026 mL | 0.6053 mL | 0.7566 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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Jolkinolide B inhibits RANKL-induced osteoclastogenesis by suppressing the activation NF-kappaB and MAPK signaling pathways.[Pubmed:24491533]
Biochem Biophys Res Commun. 2014 Mar 7;445(2):282-8.
Osteoclasts together with osteoblasts play pivotal roles in bone remodeling. The unique function and ability of osteoclasts to resorb bone makes them critical in both normal bone homeostasis and pathologic bone diseases such as osteoporosis and rheumatoid arthritis. Thus, new compounds that may inhibit osteoclastogenesis and osteoclast function may be of great value in the treatment of osteoclast-related diseases. In the present study, we examined the effect of Jolkinolide B (JB), isolated from the root of Euphorbia fischeriana Steud on receptor activator of NF-kappaB ligand (RANKL)-induced osteoclast formation. We found that JB inhibited RANKL-induced osteoclast differentiation from bone marrow macrophages (BMMs) without cytotoxicity. Furthermore, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CtsK), and calcitonin receptor (CTR), was significantly inhibited. JB inhibited RANKL-induced activation of NF-kappaB by suppressing RANKL-mediated IkappaBalpha degradation. Moreover, JB inhibited RANKL-induced phosphorylation of mitogen-activated protein kinases (p38, JNK, and ERK). This study thus identifies JB as an inhibitor of osteoclast formation and provides evidence that JB might be an alternative medicine for preventing and treating osteolysis.
Jolkinolide B induces apoptosis in MCF-7 cells through inhibition of the PI3K/Akt/mTOR signaling pathway.[Pubmed:23129237]
Oncol Rep. 2013 Jan;29(1):212-8.
The aim of this study was to explore the molecular mechanisms of Jolkinolide B (JB), which is extracted from the root of Euphorbia fischeriana Steud. In this study, we found that JB, a diterpenoid from the traditional Chinese medicinal herb, strongly inhibited the PI3K/Akt/mTOR signaling pathway. Furthermore, we evaluated the effects of JB on the proliferation and apoptosis of MCF-7 human breast cancer cells. Our results showed significant induction of apoptosis in MCF-7 cells incubated with JB. The viability of the MCF-7 cells was assessed by MTT assay. Flow cytometry was used to detect apoptosis and cell cycle analysis. Transmission electron microscopy (TEM) analysis was used to observe cell morphology. MCF-7 cells were subcutaneously inoculated into nude mice to study the in vivo antitumor effects of JB. The growth of MCF-7 cells was inhibited and arrested in the S phase by JB. The data showed significantly decreased tumor volume and weight in nude mice inoculated with MCF-7 cells. In addition, treatment with JB was able to induce downregulation of cyclinD1, cyclinE, mTOR, p-PI3K and p-Akt, and upregulation of PTEN and p-eIF4E. Collectively, JB-induced apoptosis of MCF-7 cells occurs through the PI3K/Akt/mTOR signaling pathway. Furthermore, the PI3K/Akt signaling cascade plays a role in the induction of apoptosis in JB-treated cells. These observations suggest that JB may have therapeutic applications in the treatment of cancer.
Protective effect of Jolkinolide B on LPS-induced mouse acute lung injury.[Pubmed:25819665]
Int Immunopharmacol. 2015 May;26(1):119-24.
Jolkinolide B (JB), an ent-abietane diterpenoid, isolated from the dried root of Euphorbia fischeriana, has been reported to have potent anti-tumor and anti-inflammatory activities. However, the effects of JB on acute lung injury (ALI) and underlying molecular mechanisms have not been investigated. The present study aimed to investigate the effect of JB on lipopolysaccharide (LPS)-induced ALI. Male C57BL/6 mice were pretreated with dexamethasone or JB 1h before intranasal instillation of LPS. The results showed that JB markedly attenuated LPS-induced histological alterations, lung edema, inflammatory cell infiltration, myeloperoxidase (MPO) activity as well as the production of TNF-alpha, IL-6 and IL-1beta. Furthermore, JB also significantly inhibited LPS-induced the degradation of IkappaBalpha and phosphorylation of NF-kappaB p65 and MAPK. Therefore, our study provides the first line of evidence that pretreatment of JB has a protective effect on LPS-induced ALI in mice. The anti-inflammatory mechanism of JB may be attributed to its suppression of NF-kappaB and MAPK activation.
Jolkinolide B from Euphorbia fischeriana Steud induces in human leukemic cells apoptosis via JAK2/STAT3 pathways.[Pubmed:23253949]
Int J Clin Pharmacol Ther. 2013 Mar;51(3):170-8.
Jolkinolide B from the roots of Euphorbia fischeriana Steud exhibits significant antitumor activities against several tumor lines. Previous study has shown that Jolkinolide B could induce apoptosis in human leukemia cells. However, the exact mechanism and signaling pathway involved in Jolkinolide B-induced apoptosis have not been fully elucidated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in dose- and time-dependent manner in human leukemic HL-60 and THP-1 cells. The induction of apoptosis was accompanied by the downregulation of JAK2/STAT3. Our results also suggest that expression of Bcl-2 and mitochondrial cytochrome c was dosedependently reduced following Jolkinolide B-treated THP-1 and HL-60 cells, whereas Jolkinolide B up-regulated the expression of Bax and cytosolic cytochrome c. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3, -8, and -9. JSI-124, a STAT-3 inhibitor, was able to block the negative effect of Jolkinolide B on cell apoptosis. Taken together, our study for the first time suggests that Jolkinolide B is able to enhance apoptosis of human leukemic HL-60 and THP-1 cells, at least in part, through downregulation of JAK2/STAT3 and bcl-2, and upregulation of Bax and cytosolic cytochrome c. Moreover, the triggering of caspase-3, -8, and -9 activation mediated apoptotic induction.
Jolkinolide B from Euphorbia fischeriana Steud induces apoptosis in human leukemic U937 cells through PI3K/Akt and XIAP pathways.[Pubmed:22083305]
Mol Cells. 2011 Nov;32(5):451-7.
Jolkinolide B, a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud, is known to induce apoptosis in cancer cells. However, the molecular mechanism of its anti-cancer activity has not been fully elucidated. In the present study, we found that Jolkinolide B reduced cell viability and induced apoptosis in a dose- and time-dependent manner in human leukemic U937. The induction of apoptosis was also accompanied by the downregulation of PI3K/Akt and the inhibitor of apoptosis protein (IAP) family proteins. Moreover, we observed that Jolkinolide B treatment resulted in activation of caspase-3 and -9, which may partly explain the anti-cancer activity of Jolkinolide B. Taken together, our study for the first time suggest that Jolkinolide B is able to enhance apoptosis of U937 cells, at least in part, through downregulation of PI3K/Akt and IAP family proteins. Moreover, triggering of caspase-3 and -9 activation mediated apoptotic induction.
