ShikoninCAS# 517-88-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 517-88-4 | SDF | Download SDF |
| PubChem ID | 72521 | Appearance | Purple powder |
| Formula | C16H16O5 | M.Wt | 288.31 |
| Type of Compound | Quinones | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 5,8-dihydroxy-2-[(1S)-1-hydroxy-4-methylpent-3-enyl]naphthalene-1,4-dione | ||
| SMILES | CC(=CCC(C1=CC(=O)C2=C(C=CC(=C2C1=O)O)O)O)C | ||
| Standard InChIKey | NEZONWMXZKDMKF-JTQLQIEISA-N | ||
| Standard InChI | InChI=1S/C16H16O5/c1-8(2)3-4-10(17)9-7-13(20)14-11(18)5-6-12(19)15(14)16(9)21/h3,5-7,10,17-19H,4H2,1-2H3/t10-/m0/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 | Shikonin is a natural red naphthoquinone pigment, has antimicrobial, anti-tumor, and anti-inflammatory effects; a purified shikonin preparation is widely used for the production of medicinals, cosmetics, and some food products; shikonin also enters into the antiinflammatory ointment and cream compositions used for the treatment of burns. It can suppress the cell viability, adhesion, invasion and migratory ability of MGC-803 cells through TLR2- or NF-κB-mediated pathway. |
| Targets | PI3K | Akt | TLR | NF-kB | MMP(e.g.TIMP) | ROS | Bcl-2/Bax | Caspase | PARP | p53 | Antifection |
| In vitro | Shikonin inhibits the cell viability, adhesion, invasion and migration of the human gastric cancer cell line MGC-803 via the Toll-like receptor 2/nuclear factor-kappa B pathway.[Pubmed: 25880237]J Pharm Pharmacol. 2015 Apr 16.Shikonin is an active naphthoquinone pigment isolated from the root of Lithospermum erythrorhizon. This study was designed to explore the inhibition of Shikonin on cell viability, adhesion, migration and invasion ability of gastric cancer (GC) and its possible mechanism.
Antimicrobial Activity of Shikonin Preparations.[Reference: WebLink]Pharm.Chem. J., 2001, 35(8):435-6.Shikonin is a natural red naphthoquinone pigment synthesized in the roots of plants belonging to the Boraginaceae family.
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| Kinase Assay | Shikonin inhibits IgE-mediated histamine release by human basophils and Syk kinase activity.[Pubmed: 18830561 ]Inflamm Res. 2008 Oct;57(10):484-8.Shikonin, a component of the herbal medicine "Shikon", is known to suppress inflammatory reactions, but its molecular targets are not identified. This study examines the effect of Shikonin on human basophil degranulation response and aims to identify its targets.
Human basophils in isolated leukocytes from healthy volunteers' peripheral blood; recombinant human Syk and Lyn tyrosine kinases.
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| Cell Research | Cbl participates in shikonin-induced apoptosis by negatively regulating phosphoinositide 3-kinase/protein kinase B signaling.[Pubmed: 25815461]Shikonin selectively induces apoptosis in human prostate cancer cells through the endoplasmic reticulum stress and mitochondrial apoptotic pathway.[Pubmed: 25879420]J Biomed Sci. 2015 Apr 1;22(1):26.Despite the recent progress in screening and therapy, a majority of prostate cancer cases eventually attain hormone refractory and chemo-resistant attributes. Conventional chemotherapeutic strategies are effective at very high doses for only palliative management of these prostate cancers. Therefore chemo-sensitization of prostate cancer cells could be a promising strategy for increasing efficacy of the conventional chemotherapeutic agents in prostate cancer patients. Recent studies have indicated that the chemo-preventive natural agents restore the pro-apoptotic protein expression and induce endoplasmic reticulum stress (ER stress) leading to the inhibition of cellular proliferation and activation of the mitochondrial apoptosis in prostate cancer cells. Therefore reprogramming ER stress-mitochondrial dependent apoptosis could be a potential approach for management of hormone refractory chemoresistant prostate cancers. Mol Med Rep. 2015 Jul;12(1):1305-13.Shikonin, a naturally occurring naphthoquinone, exhibits anti-tumorigenic activity. However, its precise mechanisms of action have remained elusive.
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Shikonin Dilution Calculator
Shikonin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.4685 mL | 17.3424 mL | 34.6849 mL | 69.3698 mL | 86.7122 mL |
| 5 mM | 0.6937 mL | 3.4685 mL | 6.937 mL | 13.874 mL | 17.3424 mL |
| 10 mM | 0.3468 mL | 1.7342 mL | 3.4685 mL | 6.937 mL | 8.6712 mL |
| 50 mM | 0.0694 mL | 0.3468 mL | 0.6937 mL | 1.3874 mL | 1.7342 mL |
| 100 mM | 0.0347 mL | 0.1734 mL | 0.3468 mL | 0.6937 mL | 0.8671 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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Shikonin induces apoptosis in the human gastric cancer cells HGC-27 through mitochondria-mediated pathway.[Pubmed:25829762]
Pharmacogn Mag. 2015 Apr-Jun;11(42):250-6.
BACKGROUND: Gastric cancer (GC) is one of the most frequently occurring digestive tract cancers and fewer chemotherapeutic drugs for GC have shown promising results. In this study, we investigated the anti-tumor activity of Shikonin, a natural compound isolated from the Chinese plant Lithospermum erythrorhizon, against the human GC cell line HGC-27. MATERIALS AND METHODS: HGC-27 cells treated with Shikonin at a concentration of 30muM or above showed significant growth inhibition compared to control cells. Shikonin-treated cells also underwent apoptosis as detected by flow cytometric analysis and microscopic examination of cellular morphology. Further investigation into the underlying mechanism of apoptosis by western blot showed that the Shikonin promoted the activation of poly-(ADP-ribose)-polymerase, caspase-3 and caspase-9 following 24 h or 48 h of treatment time, as well as the activation of caspase-8, but only after 48 h of treatment time. Furthermore, the levels of mitochondrial membrane potential, B-cell lymphoma 2 (Bcl-2) and Bcl-extra large were reduced following Shikonin treatment while the level of Bax was increased. In addition, Shikonin also caused a significant reduction of the protein Survivin, while having little effect on the expression on X-linked inhibitor of apoptosis protein. CONCLUSION: Taken together, these results showed that the Shikonin exhibited its anti-tumor activity against HGC-27 cells through inhibiting cell growth and promoting apoptosis by targeting mitochondrial-related signaling pathway. Our finding may represent a positive step in finding a natural and effective compound that could be important implication for future development of chemotherapeutic and/or chemopreventive agent against GC.
Shikonin inhibits the cell viability, adhesion, invasion and migration of the human gastric cancer cell line MGC-803 via the Toll-like receptor 2/nuclear factor-kappa B pathway.[Pubmed:25880237]
J Pharm Pharmacol. 2015 Aug;67(8):1143-55.
OBJECTIVES: Shikonin is an active naphthoquinone pigment isolated from the root of Lithospermum erythrorhizon. This study was designed to explore the inhibition of Shikonin on cell viability, adhesion, migration and invasion ability of gastric cancer (GC) and its possible mechanism. METHODS: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed for cell viability and adhesion ability of MGC-803 cells. Cell scratch repair experiments were conducted for the determination of migration ability while transwell assay for cell invasion ability. Western blot analysis and real-time polymerase chain reaction assay were used for the detection of protein and mRNA expressions. KEY FINDINGS: Fifty per cent inhibitory concentration of Shikonin on MGC-803 cells was 1.854 mum. Shikonin (1 mum) inhibited significantly the adhesion, invasion and migratory ability of MGC-803 cells. Interestingly, Shikonin in the presence or absence of anti-Toll-like receptor 2 (TLR2) antibody (2 mug) and nuclear factor-kappa B (NF-kappaB) inhibitor MG-132 (10 mum) could decrease these ability of MGC-803 cells markedly, as well as the expression levels of matrix metalloproteinases (MMP)-2, MMP-7, TLR2 and p65 NF-kappaB. In addition, the co-incubation of Shikonin and anti-TLR2/MG-132 has a significant stronger activity than anti-TLR2 or MG-132 alone. CONCLUSIONS: The results indicated that Shikonin could suppress the cell viability, adhesion, invasion and migratory ability of MGC-803 cells through TLR2- or NF-kappaB-mediated pathway. Our findings provide novel information for the treatment of Shikonin on GC.
Shikonin inhibits IgE-mediated histamine release by human basophils and Syk kinase activity.[Pubmed:18830561]
Inflamm Res. 2008 Oct;57(10):484-8.
OBJECTIVE: Shikonin, a component of the herbal medicine "Shikon", is known to suppress inflammatory reactions, but its molecular targets are not identified. This study examines the effect of Shikonin on human basophil degranulation response and aims to identify its targets. MATERIALS: Human basophils in isolated leukocytes from healthy volunteers' peripheral blood; recombinant human Syk and Lyn tyrosine kinases. METHODS: Histamine release from basophils stimulated with anti-IgE antibody was analyzed fluorimetrically. Syk and Lyn kinase activities were tested in Vitro with recombinant proteins and analyzed by off-chip mobility shift assay. RESULTS: Shikonin dose-dependently inhibited the histamine release from basophils induced by anti-IgE antibody (IC50 = 2.6 +/- 1.0 microM; mean +/- SEM). A search for the target(s) of Shikonin in the signal cascade of IgE-mediated activation showed that it strongly inhibits Syk (IC50 = 7.8 microM, in the recombinant kinase assay), which plays a pivotal role in the degranulation response. A less significant inhibition was found for Lyn, which phosphorylates FcepsilonRI-betagamma subunits and also Syk. CONCLUSIONS: These results indicate that the inhibition of Syk-dependent phosphorylation events might underlie the blocked histamine release from human basophils, thus contributing to the anti-inflammatory effects of Shikonin.
Shikonin selectively induces apoptosis in human prostate cancer cells through the endoplasmic reticulum stress and mitochondrial apoptotic pathway.[Pubmed:25879420]
J Biomed Sci. 2015 Apr 1;22:26.
BACKGROUND: Despite the recent progress in screening and therapy, a majority of prostate cancer cases eventually attain hormone refractory and chemo-resistant attributes. Conventional chemotherapeutic strategies are effective at very high doses for only palliative management of these prostate cancers. Therefore chemo-sensitization of prostate cancer cells could be a promising strategy for increasing efficacy of the conventional chemotherapeutic agents in prostate cancer patients. Recent studies have indicated that the chemo-preventive natural agents restore the pro-apoptotic protein expression and induce endoplasmic reticulum stress (ER stress) leading to the inhibition of cellular proliferation and activation of the mitochondrial apoptosis in prostate cancer cells. Therefore reprogramming ER stress-mitochondrial dependent apoptosis could be a potential approach for management of hormone refractory chemoresistant prostate cancers. We aimed to study the effects of the natural naphthoquinone Shikonin in human prostate cancer cells. RESULTS: The results indicated that Shikonin induces apoptosis in prostate cancer cells through the dual induction of the endoplasmic reticulum stress and mitochondrial dysfunction. Shikonin induced ROS generation and activated ER stress and calpain activity. Moreover, addition of antioxidants attenuated these effects. Shikonin also induced the mitochondrial apoptotic pathway mediated through the enhanced expression of the pro-apoptotic Bax and inhibition of Bcl-2, disruption of the mitochondrial membrane potential (MMP) followed by the activation of caspase-9, caspase-3, and PARP cleavage. CONCLUSION: The results suggest that Shikonin could be useful in the therapeutic management of hormone refractory prostate cancers due to its modulation of the pro-apoptotic ER stress and mitochondrial apoptotic pathways.
Cbl participates in shikonin-induced apoptosis by negatively regulating phosphoinositide 3-kinase/protein kinase B signaling.[Pubmed:25815461]
Mol Med Rep. 2015 Jul;12(1):1305-13.
Shikonin, a naturally occurring naphthoquinone, exhibits anti-tumorigenic activity. However, its precise mechanisms of action have remained elusive. In the present study, the involvement in the action of Shikonin of the ubiquitin ligases Cbl-b and c-Cbl, which are negative regulators of phosphoinositide 3-kinase (PI3K) activation, was investigated. Shikonin was observed to reduce cell viability and induce apoptosis and G2/M phase arrest in lung cancer cells. In addition, Shikonin increased the protein levels of B-cell lymphoma 2 (Bcl-2)-associated X and p53 and reduced those of Bcl-2. Additionally, Shikonin inhibited PI3k/Akt activity and upregulated Cbl protein expression. In addition, a specific inhibitor of PI3K, LY294002, was observed to have a synergistic effect on the proliferation inhibition and apoptotic induction of A549 cells with Shikonin. In conclusion, the results of the present study suggested that Cbl proteins promote Shikonin-induced apoptosis by negatively regulating PI3K/Akt signaling in lung cancer cells.
