(R)-Shikonin
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| Category | Others |
| Catalog number | BBF-05805 |
| CAS | 517-89-5 |
| Molecular Weight | 288.30 |
| Molecular Formula | C16H16O5 |
| Purity | ≥98% |
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Description
(R)-Shikonin is a naphthoquinone extracted from Lithospermum erythrorhizon and Alkanna sp. It is a natural cardioprotective, antioxidative and anti-inflammatory agent.
Specification
| Synonyms | Shikonin; Isoarnebin 4; Tokyo Violet; Shikonin S; (R)-5,8-Dihydroxy-2-(1-hydroxy-4-methyl-3-pentenyl)-1,4-naphthalenedione; R-5,8-dihydroxy-2-[(1R)-1-hydroxy-4-methyl-3-pentenyl]-1,4-naphthalenedione; (+)-5,8-Dihydroxy-2-(1-hydroxy-4-methyl-3-pentenyl)-1,4-naphthoquinone; (+)-Shikonin; (R)-(+)-Shikonin; NSC 252844; Shikonine; Tokyo Violet |
| Storage | Store at 2-8°C under inert atmosphere |
| IUPAC Name | 5,8-dihydroxy-2-[(1R)-1-hydroxy-4-methylpent-3-enyl]naphthalene-1,4-dione |
| Canonical SMILES | CC(=CCC(C1=CC(=O)C2=C(C=CC(=C2C1=O)O)O)O)C |
| 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-/m1/s1 |
| InChI Key | NEZONWMXZKDMKF-SNVBAGLBSA-N |
Properties
| Appearance | Very Dark Red to Very Dark Brown Solid |
| Boiling Point | 567.4±50.0°C (Predicted) |
| Melting Point | 148°C |
| Flash Point | 311ºC |
| Density | 1.373±0.06 g/cm3 (Predicted) |
| Solubility | Soluble in Benzene (Very Slightly), Chloroform (Slightly), DMSO (Slightly), Methanol (Slightly) |
| LogP | 2.12040 |
Reference Reading
1.The anti-tumor effect of shikonin on osteosarcoma by inducing RIP1 and RIP3 dependent necroptosis.
Fu Z;Deng B;Liao Y;Shan L;Yin F;Wang Z;Zeng H;Zuo D;Hua Y;Cai Z BMC Cancer. 2013 Dec 6;13:580. doi: 10.1186/1471-2407-13-580.
BACKGROUND: ;Osteosarcoma is the most frequent primary malignant bone tumor, notorious for its lung metastasis. Shikonin, an effective constituent extracted from Chinese medicinal herb, was demonstrated to induce necroptosis in some cancers.;METHODS: ;MTT assay was performed to detect cell survival rate in vitro. Flow cytometry was used to analyze cell cycle and cell death. Western blot was performed to determine the expression levels of RIP1, RIP3, caspase-3, caspase-6 and PARP. The tibial primary and lung metastatic osteosarcoma models were used to evaluate the anti-tumor effect of shikonin in vivo.;RESULTS: ;The cell survival rate was decreased in a dose and time dependent manner when treated with shikonin. No major change in cell cycle was observed after shikonin treatment. The cell death induced by shikonin could be mostly rescued by specific necroptosis inhibitor necrostatin-1, but not by general caspase inhibitor Z-VAD-FMK. The number of necrotic cells caused by shikonin was decreased after being pretreated with Nec-1 detected by flow cytometry in K7 cells. After 8-hour treatment of shikonin, the expression levels of RIP1 and RIP3 were increased while caspase-3, caspase-6 and PARP were not activated in K7 and U2OS cells determined by Western blot.
2.Shikonin inhibits TNF-α production through suppressing PKC-NF-κB-dependent decrease of IL-10 in rheumatoid arthritis-like cell model.
Sun WX;Liu Y;Zhou W;Li HW;Yang J;Chen ZB J Nat Med. 2017 Apr;71(2):349-356. doi: 10.1007/s11418-016-1064-3. Epub 2016 Dec 9.
Shikonin, a major effective component in the Chinese herbal medicine Lithospermum erythrorhizon Sieb., exhibits an anti-inflammatory property towards rheumatoid arthritis (RA), but the potential mechanism is unclear. Our aim was to investigate the mechanism of shikonin on the lipopolysaccharide (LPS)-induced fibroblast-like synoviocyte (LiFLS) inflammation model. Fibroblast-like synoviocytes (FLSs) were treated with 200 μg/ml of LPS for 24 h to establish the RA-like model, LiFLS. FLSs were pretreated with shikonin (0.1-1 μM) for 30 min in the treatment groups. Quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assays were used to detect mRNA and protein levels of interleukin (IL)-10 and tumor necrosis factor (TNF)-α. Signal proteins involved in IL-10 production were analyzed by Western blotting. Shikonin significantly reversed the inhibitory effects of LPS on IL-10 expression in FLSs by inactivating the PKC-NF-κB pathway. In addition, shikonin inhibited LPS-induced TNF-α expression in FLSs, and this effect was markedly diminished by IL-10-neutralizing antibody. The IL-10-mediated suppression of TNF-α transcription was demonstrated by no response to the protein synthesis inhibitor cyclohexamide and no mRNA decay.
3.Pyruvate kinase isozyme M2 and glutaminase might be promising molecular targets for the treatment of gastric cancer.
Kitayama K;Yashiro M;Morisaki T;Miki Y;Okuno T;Kinoshita H;Fukuoka T;Kasashima H;Masuda G;Hasegawa T;Sakurai K;Kubo N;Hirakawa K;Ohira M Cancer Sci. 2017 Dec;108(12):2462-2469. doi: 10.1111/cas.13421. Epub 2017 Nov 27.
The aim of this study was to analyze the significance of glucose metabolism-related enzymes in the proliferation of gastric cancer under hypoxia. Four hypoxia-resistant gastric cancer cell lines and four parent cell lines were used. Reverse transcription-PCR was used to evaluate the mRNA expression levels of the following metabolism-related enzymes: pyruvate kinase isozyme M2 (PKM2), glutaminase (GLS), enolase 1 (ENO1), glucose-6-phosphate dehydrogenase (G6PDH), and PKM1. The effects of these enzymes on the proliferation of gastric cancer cells were examined using siRNAs, shikonin as a PKM2 inhibitor, or BPTES as a GLS inhibitor, in vitro and in vivo. Levels of both PKM2 and GLS mRNA were significantly high in all hypoxia-resistant cell lines, compared with those of their parent cells. Knockdown of PKM2 and GLS significantly decreased the proliferation of all hypoxia-resistant cells. The combination of siPKM2 and siGLS significantly decreased proliferation compared with treatment by siPKM2 or siGLS alone. The knockdown of ENO1, G6PDH, or PKM1 did not decrease the proliferation of all hypoxia-resistant cells. Combination treatment using shikonin and BPTES inhibited the proliferation of all hypoxia-resistant cancer cells more than that by either agent alone.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
