Product Name Dimethylacrylshikonin
CAS No.: 24502-79-2
Catalog No.: CFN90164
Molecular Formula: C21H22O6
Molecular Weight: 370.39 g/mol
Purity: >=98%
Type of Compound: Quinones
Physical Desc.: Powder
Targets: ROS | ERK | NF-kB | Bcl-2/Bax | Caspase | PARP | MEK | p38MAPK | Calcium Channel
Source: The roots of Lithosperraum erythrorhizon Sieb. et Zucc.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $158/20mg
Dimethylacrylshikonin is a promising agent for developing an improved strategy for radiotherapy against tumors, it inhibits the proliferation of MCF-7 cells in vitro by inducing apoptosis through the downregulation of Bcl-2, upregulation of Bax and partial inactivation of the NF-κB pathway. Dimethylacrylshikonin inhibits agonist-induced relaxation at lower concentrations and induces vasocontraction at higher concentrations.
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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.

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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.
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    Oncol Lett. 2014 Jun;7(6):1812-1818.
    β,β-Dimethylacrylshikonin sensitizes human colon cancer cells to ionizing radiation through the upregulation of reactive oxygen species.[Pubmed: 24932238]
    Shikonin, a naphthoquinone derivative, has been shown to possess antitumor activity.
    In the present study, the effects of shikonin and its analog, β,β-Dimethylacrylshikonin, were investigated as radiosensitizers on the human colon cancer cell line, HCT-116. Shikonin and, to a greater extent, its analog-induced apoptosis of HCT-116 cells further synergistically potentiated the induction of apoptosis when combined with ionizing radiation (IR) treatment. Shikonins also stimulated an increase in reactive oxygen species (ROS) production and IR-induced DNA damage. Pre-treatment with the ROS scavenger, N-acetylcysteine, suppressed the enhancement of IR-induced DNA damage and apoptosis stimulated by shikonins, indicating that shikonins exert their radiosensitizing effects through ROS upregulation. The radiosensitizing effect of shikonins was also examined in vivo using the xenograft mouse model. Consistent with the in vitro results, injection of β,β-Dimethylacrylshikonin combined with IR treatment significantly suppressed tumor growth of the HCT-116 xenograft.
    Taken together, the results show that β,β-Dimethylacrylshikonin is a promising agent for developing an improved strategy for radiotherapy against tumors.
    Phytother Res. 2012 May;26(5):764-71.
    Inhibitory effects of β,β-dimethylacrylshikonin on hepatocellular carcinoma in vitro and in vivo.[Pubmed: 22109831]
    Dimethylacrylshikonin is one of the most abundant naphthoquinones in the root extracts of Lithospermum erythrorhizon Sieb. et Zucc. (Boraginaceae), which have been reported to have antitumor effects.
    This study evaluated the antiproliferative activity of Dimethylacrylshikonin on human hepatocellular carcinoma (HCC) cells both in vitro and in vivo. In vitro, the MTT assay showed that Dimethylacrylshikonin inhibited the proliferation of SMMC-7721 cells in both dose- and time-dependent manners with its 50% inhibitory concentration (IC(50) ) at 48 h being 15.01 ± 0.76 µg/mL. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) and Hoechst staining detected the characteristics of cell apoptosis in Dimethylacrylshikonin-treated cells and the apoptotic rates of treated groups were increased in a dose-dependent manner. Flow cytometric analysis revealed that Dimethylacrylshikonin could block the cell cycle arrest at G2 phase. Furthermore, Dimethylacrylshikonin down-regulated the mRNA and protein expression of Bcl-2 but up-regulated that of Bax. The cleaved caspase-3 protein was also detected in treated cells. The experiment in vivo showed that Dimethylacrylshikonin significantly suppressed the growth of H(22) transplantable hepatoma, and induced the activation of caspase-3 determined by immunohistochemistry.
    The results indicate that Dimethylacrylshikonin has significant antitumor effects on hepatocellular carcinoma both in vitro and in vivo.
    Planta Med. 2004 Jan;70(1):23-8.
    Impairment of vascular function of rat thoracic aorta in an endothelium-dependent manner by shikonin/alkannin and derivatives isolated from roots of Macrotomia euchroma.[Pubmed: 14765288 ]

    The effects of a naphthoquinone analogue, shikonin/alkannin (SA) and derivatives (acetylshikonin and beta,beta-Dimethylacrylshikonin), on vascular reactivity were studied with isolated rat aortic rings. At lower concentrations, SA and its derivatives concentration-dependently inhibit the agonist-induced (acetylcholine and histamine) relaxation in PE precontracted aorta in an endothelium-dependent manner with IC (50) values ranging from 0.2 to 1.5 microM. In addition to the effect on agonist-induced vasorelaxation, the Ca (2+) ionophore A23187-induced vasorelaxation was also inhibited or reversed by SA. However, SA had no effect on sodium nitroprusside-induced (guanylate cyclase activator) vasorelaxation. These data suggested that SA and its derivatives might be acting as inhibitors of nitric oxide synthesis in endothelium. At a concentration greater than 10 microM, SA induced contraction of intact but not denuded aorta which could be inhibited by prior treatment with indomethacin, a cyclooxygenase inhibitor.
    In summary, the results from this study showed that SA and its derivatives inhibited agonist-induced relaxation at lower concentrations and induced vasocontraction at higher concentrations. All the effects seen with SA were endothelium-dependent, however, through different mechanisms.
    Biochem Pharmacol. 2012 Aug 15;84(4):507-12.
    β,β-Dimethylacrylshikonin exerts antitumor activity via Notch-1 signaling pathway in vitro and in vivo.[Pubmed: 22634048]
    Dimethylacrylshikonin (DA) is a major component of Radix Lithospermum erythrorhizon and has various biological activities.We have investigated the inhibitory effect of Dimethylacrylshikonin on the growth of hepatocellular carcinoma in vitro and in vivo. Notch signaling plays a critical role in maintaining the balance between cell proliferation, differentiation and apoptosis. Hence, perturbed Notch signaling may contribute to tumorigenesis.
    In the present study, we evaluated whether Dimethylacrylshikonin could be an effective inhibitor on cell growth in human gastric cancer cell line, and also the molecular mechanisms. Using multiple cellular and molecular approaches such as MTT assay, colony formation assay, DAPI staining, flow cytometry, real-time PCR and Western blot analysis, we found that Dimethylacrylshikonin inhibited cell growth in a dose- and time-dependent manner. Biochemical analysis revealed the involvement of cell cycle regulated proteins in DA-mediated of G₀-G₁ arrest of SGC-7901 cells. Furthermore, Dimethylacrylshikonin treatment led to reduced Notch-1 activation, expression of Jagged-1 and its downstream target Hes-1 in vitro and in vivo.
    Our data demonstrated that Dimethylacrylshikonin is a potent inhibitor of progression of gastric cancer cells, which could be due to attenuation of Notch-1. We also suggest that Dimethylacrylshikonin could be further developed as a potential therapeutic agent for the treatment of gastric cancer.
    PLoS One. 2012;7(7):e41773.
    β,β-Dimethylacrylshikonin induces mitochondria dependent apoptosis through ERK pathway in human gastric cancer SGC-7901 cells.[Pubmed: 22848597 ]
    Dimethylacrylshikonin, one of the active components in the root extracts of Lithospermum erythrorhizon, posses antitumor activity.
    In this study, we discussed the molecular mechanisms of Dimethylacrylshikonin in the apoptosis of SGC-7901 cells. Dimethylacrylshikonin reduced the cell viability of SGC-7901 cells in a dose- and time-dependent manner and induced cell apoptosis. Dimethylacrylshikonin treatment in SGC-7901 cells down-regulated the expression of XIAP, cIAP-2, and Bcl-2 and up-regulated the expression of Bak and Bax and caused the loss of mitochondrial membrane potential and release of cytochrome c. Additionally, Dimethylacrylshikonin treatment led to activation of caspases-9, 8 and 3, and cleavage of poly (ADP-ribose) polymerase (PARP), which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. β,β-Dimethylacrylshikonin induced phosphorylation of extracellular signal-regulated kinase (ERK) in SGC-7901 cells. U0126, a specific MEK inhibitor, blocked the ERK activation by Dimethylacrylshikonin and abrogated Dimethylacrylshikonin -induced apoptosis.
    Our results demonstrated that Dimethylacrylshikonin inhibited growth of gastric cancer SGC-7901 cells by inducing ERK signaling pathway, and provided a clue for preclinical and clinical evaluation of Dimethylacrylshikonin for gastric cancer therapy.
    Acta Pharmacol Sin. 2015 Jan;36(1):131-8.
    β, β-Dimethylacrylshikonin induces mitochondria-dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation.[Pubmed: 25434989]
    Dimethylacrylshikonin (DMAS) is an anticancer compound extracted from the roots of Lithospermum erythrorhizon. In the present study, we investigated the effects of Dimethylacrylshikonin on human lung adenocarcinoma cells in vitro and explored the mechanisms of its anti-cancer action.
    Human lung adenocarcinoma A549 cells were tested. Cell viability was assessed using an MTT assay, and cell apoptosis was evaluated with flow cytometry and DAPI staining. The expression of the related proteins was detected using Western blotting. The mitochondrial membrane potential was measured using a JC-1 kit, and subcellular distribution of cytochrome c was analyzed using immunofluorescence staining. Treatment of A549 cells with Dimethylacrylshikonin suppressed the cell viability in dose- and time-dependent manners (the IC50 value was 14.22 and 10.61 μmol/L, respectively, at 24 and 48 h). Dimethylacrylshikonin (7.5, 10, and 15 μmol/L) dose-dependently induced apoptosis, down-regulated cIAP-2 and XIAP expression, and up-regulated Bax and Bak expression in the cells. Furthermore, Dimethylacrylshikonin resulted in loss of mitochondrial membrane potential and release of cytochrome c in the cells, and activated caspase-9, caspase-8, and caspase-3, and subsequently cleaved PARP, which was abolished by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. Dimethylacrylshikonin induced sustained p38 phosphorylation in the cells, while pretreatment with SB203580, a specific p38 inhibitor, blocked Dimethylacrylshikonin -induced p38 activation and apoptosis.
    Dimethylacrylshikonin inhibits the growth of human lung adenocarcinoma A549 cells in vitro via activation of p38 signaling pathway.

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