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    Dihydrotanshinone I
    CAS No. 87205-99-0 Price $80 / 20mg
    Catalog No.CFN97435Purity>=98%
    Molecular Weight278.3 Type of CompoundDiterpenoids
    FormulaC18H14O3Physical DescriptionRed powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Dihydrotanshinone I is a potent inhibitor of the HuR:RNA interaction, it exhibits strong inhibition towards human liver microsome (HLM)-catalyzed propofol glucuronidation, and UDP-glucuronosyltransferase (UGT) 1A7. Dihydrotanshinone I has antibacterial, anti-cancer, anti-angiogenic, and cytotoxic activities, it induces caspase and ROS dependent apoptosis and autophagy.
    Targets: TNF-α | NF-kB | p65 | COX | MMP(e.g.TIMP) | VEGFR | IL Receptor | ERK | p38MAPK | JNK | p21 | Caspase | ROS | Autophagy | Antifection | AChR
    In vitro:
    Biosci Biotechnol Biochem. 1999 Dec;63(12):2236-9.
    Antibacterial activities of cryptotanshinone and dihydrotanshinone I from a medicinal herb, Salvia miltiorrhiza Bunge.[Pubmed: 10664860 ]
    Cryptotanshinone and Dihydrotanshinone I, constituents of a medicinal plant, Salvia miltiorrhiza Bunge, had antibacterial activity against a broad range of Gram positive bacteria.
    These compounds generated superoxide radicals in Bacillus subtilis lysates. A recombination-deficient mutant strain of B. subtilis was 2- to 8-fold more sensitive than a wild strain, and this hypersensitivity was reduced in the presence of dithiothreitol as an antioxidant. DNA, RNA, and protein syntheses in B. subtilis were non-selectively inhibited by these compounds.
    These results suggest that superoxide radicals are important in the antibacterial actions of the agents.
    Acta Biochim Biophys Sin (Shanghai). 2008 Jan;40(1):1-6.
    Dihydrotanshinone I inhibits angiogenesis both in vitro and in vivo.[Pubmed: 18180848]
    Dihydrotanshinone I (DI), a naturally occurring compound extracted from Salvia miltiorrhiza Bunge, has been reported to have cytotoxicity to a variety of tumor cells. In this study, we investigated its anti-angiogenic capacity in human umbilical vein endothelial cells.
    DI induced a potent cytotoxicity to human umbilical vein endothelial cells, with an IC(50) value of approximately 1.28 microg/ml. At 0.25-1 microg/ml, DI dose-dependently suppressed human umbilical vein endothelial cell migration, invasion, and tube formation detected by wound healing, Transwell invasion and Matrigel tube formation assays, respectively. Moreover, DI showed significant in vivo anti-angiogenic activity in chick embryo chorioallantoic membrane assay. DI induced a 61.1% inhibitory rate of microvessel density at 0.2 microg/egg.
    Taken together, our results showed that DI could inhibit angiogenesis through suppressing endothelial cell proliferation, migration, invasion and tube formation, indicating that DI has a potential to be developed as a novel anti-angiogenic agent.
    Mol Cell Biochem. 2012 Apr;363(1-2):191-202.
    Combination treatment with dihydrotanshinone I and irradiation enhances apoptotic effects in human cervical cancer by HPV E6 down-regulation and caspases activation.[Pubmed: 22147199 ]
    The aim of this study was to investigate the effect of Dihydrotanshinone I (DI) in inhibiting the growth of human cervical cancer cells both in vitro and in vivo, and molecular targets in HeLa cells when treated by DI or irradiation with or without being combined. In this study, MTT, clonogenic assay, flow cytometry, and Western blotting were performed to assess the effect of treatment on cells.
    After treatment with IR, DI, and DI + IR, the apoptosis was 5.8, 13.3 and 22.5% (P < 0.05 vs. control), respectively. Clonogenic assay revealed that the survival of irradiated HeLa cell was significantly reduced by DI treatment. Combination treatment with IR and DI could down-regulate HPV E6 gene expression. Effect of DI on up-regulation of p21 expression and down-regulation of cyclin B1, p34(cdc2) expression in irradiated HeLa cell was concomitant with cell cycle arrest in G(2) phase. The significant increase in caspase-3 activity was also observed in the combination treatment. When HeLa cells were grown as xenografts in nude mice, combination treatment with DI and IR induced a significant decrease in tumor growth, and without signs of general or organ toxicity.
    These data suggest DI should be tested as the radiosensitizer in vitro and in vivo, which has potential in the treatment of human cervical cancer.
    In vivo:
    Phytomedicine. 2015 Nov 15;22(12):1079-87.
    Dihydrotanshinone I induced apoptosis and autophagy through caspase dependent pathway in colon cancer.[Pubmed: 26547530 ]
    Dihydrotanshinone I (DHTS) was previously reported to exhibit the most potent anti-cancer activity among several tanshinones in colon cancer cells. Its cytotoxic action was reactive oxygen species (ROS) dependent but p53 independent. To further study the anti-cancer activity of DHTS and its molecular mechanisms of action in colon cancer both in vitro and in vivo.
    Caspase activity was detected by fluorescence assay. Apoptosis was detected by flow cytometry and TUNEL assay. Protein levels were analyzed by western blotting. Knockdown of target gene was achieved by siRNA transfection. Formation of LC3B puncta and activation of caspase-3 were detected by confocal fluorescence microscope. In vivo anti-colon cancer activity of DHTS was observed in xenograft tumors in NOD/SCID mice. Anti-colon cancer activity of DHTS by inducing apoptosis and autophagy was observed both in vitro and in vivo. Mitochondria mediated caspase dependent pathway was essential in DHTS-induced cytotoxicity. The apoptosis induced by DHTS was suppressed by knockdown of apoptosis inducing factor (AIF), inhibition of caspase-3/9 but was increased after knockdown of caspase-2. Meantime, knockdown of caspase-2, pretreatment with Z-VAD-fmk or NAC (N-Acety-L-Cysteine) efficiently inhibited the autophagy induced by DHTS. A crosstalk between cytochrome c and AIF was also reported.
    DHTS-induced caspase and ROS dependent apoptosis and autophagy were mediated by mitochondria in colon cancer. DHTS could be a promising leading compound for the development of anti-tumor agent or be developed as an adjuvant drug for colon cancer therapy.
    Dihydrotanshinone I Description
    Source: The roots of Salvia miltiorrhiza Bge.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: 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.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: 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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.5932 mL 17.9662 mL 35.9324 mL 71.8649 mL 89.8311 mL
    5 mM 0.7186 mL 3.5932 mL 7.1865 mL 14.373 mL 17.9662 mL
    10 mM 0.3593 mL 1.7966 mL 3.5932 mL 7.1865 mL 8.9831 mL
    50 mM 0.0719 mL 0.3593 mL 0.7186 mL 1.4373 mL 1.7966 mL
    100 mM 0.0359 mL 0.1797 mL 0.3593 mL 0.7186 mL 0.8983 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Fitoterapia. 2013 Mar;85:109-13.
    Cryptotanshinone and dihydrotanshinone I exhibit strong inhibition towards human liver microsome (HLM)-catalyzed propofol glucuronidation.[Pubmed: 23333907]
    Danshen is one of the most famous herbs in the world, and more and more danshen-prescribed drugs interactions have been reported in recent years. Evaluation of inhibition potential of danshen's major ingredients towards UDP-glucuronosyltransferases (UGTs) will be helpful for understanding detailed mechanisms for danshen-drugs interaction. Therefore, the aim of the present study is to investigate the inhibitory situation of cryptotanshinone and Dihydrotanshinone I towards UGT enzyme-catalyzed propofol glucuronidation.
    In vitro the human liver microsome (HLM) incubation system was used, and the results showed that cryptotanshinone and Dihydrotanshinone I exhibited dose-dependent inhibition towards HLM-catalyzed propofol glucuronidation. Dixon plot and Lineweaver-Burk plot showed that the inhibition type was best fit to competitive inhibition type for both cryptotanshinone and Dihydrotanshinone I. The second plot using the slopes from the Lineweaver-Burk plot versus the concentrations of cryptotanshinone or Dihydrotanshinone I was employed to calculate the inhibition parameters (Ki) to be 0.4 and 1.7μM, respectively. Using the reported maximum plasma concentration (Cmax), the altered in vivo exposure of propofol increased by 10% and 8.2% for the co-administration of Dihydrotanshinone I and cryptotanshinone, respectively.
    All these results indicated the possible danshen-propofol interaction due to the inhibition of Dihydrotanshinone I and cryptotanshinone towards the glucuronidation reaction of propofol.
    J Mol Neurosci. 2014 Jul;53(3):506-10.
    Acetylcholinesterase complexes with the natural product inhibitors dihydrotanshinone I and territrem B: binding site assignment from inhibitor competition and validation through crystal structure determination.[Pubmed: 24573600]
    Acetylcholinesterase (AChE) is a critical enzyme that regulates neurotransmission by degrading the neurotransmitter acetylcholine in synapses of the nervous system. It is an important target for both therapeutic drugs that treat Alzheimer's disease and organophosphate (OP) chemical warfare agents that cripple the nervous system and cause death through paralysis.
    We are exploring a strategy to design compounds that bind tightly at or near a peripheral or P-site near the mouth of the AChE active site gorge and exclude OPs from the active site while interfering minimally with the passage of acetylcholine. However, to target the AChE P-site, much more information must be gathered about the structure-activity relationships of ligands that bind specifically to the P-site. Here, we review our recent reports on two uncharged, natural product inhibitors of AChE, Dihydrotanshinone I and territrem B, that have relatively high affinities for the enzyme. We describe an inhibitor competition assay and comment on the structures of these inhibitors in complex with recombinant human acetylcholinesterase as determined by X-ray crystallography.
    Our results reveal that Dihydrotanshinone I binding is specific to only the P-site, while territrem B binding spans the P-site and extends into the acylation or A-site at the base of the gorge.
    Int Immunopharmacol. 2015 Sep;28(1):764-72.
    Blockade of TNF-α-induced NF-κB signaling pathway and anti-cancer therapeutic response of dihydrotanshinone I.[Pubmed: 26283590]
    The nuclear factor-κB (NF-κB) transcription factors control many physiological processes including inflammation, immunity, apoptosis, and angiogenesis. We identified Dihydrotanshinone I as an inhibitor of NF-κB activation through our research on Salvia miltiorrhiza Bunge.
    In this study, we found that Dihydrotanshinone I significantly inhibited the expression of NF-κB reporter gene induced by TNF-α in a dose-dependent manner. And Dihydrotanshinone I also inhibited TNF-α induced phosphorylation and degradation of IκBα, phosphorylation and nuclear translocation of p65. Furthermore, pretreatment of cells with this compound prevented the TNF-α-induced expression of NF-κB target genes, such as anti-apoptosis (cIAP-1 and FLIP), proliferation (COX-2), invasion (MMP-9), angiogenesis (VEGF), and major inflammatory cytokines (TNF-α, IL-6, and MCP1). We also demonstrated that Dihydrotanshinone I potentiated TNF-α-induced apoptosis. Moreover, Dihydrotanshinone I significantly impaired activation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and stress-activated protein kinase/c-Jun NH2-terminal kinase (JNK/SAPK). In vivo studies demonstrated that Dihydrotanshinone I suppressed the growth of HeLa cells in a xenograft tumor model, which could be correlated with its modulation of TNF-α production.
    Taken together, Dihydrotanshinone I could be a valuable candidate for the intervention of NF-κB-dependent pathological conditions such as inflammation and cancer.
    Latin Am. J. Pharm., 2012, 31(7):1060-3.
    Dihydrotanshinone I Exhibits Strong Inhibition Towards UDP-glucuronosyltransferase (UGT) 1A7.[Reference: WebLink]
    Inhibition of the activity of UDP-glucuronosyltransferases (UGTs) can induce severe drugdrug interaction and metabolic disorders of endogenous substances. The aim of the present study is to investigate the inhibition of important UGT isoforms by Dihydrotanshinone I, which is an important bioactive component isolated from danshen.
    The nonselective probe substrate 4-methylumbelliferone (4-MU), and the recombinant UGT isoforms were used in the present study. The results showed that 100 M of Dihydrotanshinone I inhibited the activity of UGT1A1, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A10, and UGT2B7 by 32.7, 61.5, 61.1, 77.5, 47.9, 62.8, and 55.9 %, respectively. Further inhibition kinetic study was performed for the inhibition of UGT1A7 by Dihydrotanshinone I. Dose-dependent inhibition of UGT1A7 by Dihydrotanshinone I was detected, and Dixon and Lineweaver-Burk plots showed that the inhibition of UGT1A7 by Dihydrotanshinone I was best fit to competitive inhibition type. The inhibition kinetic parameter (Ki) was determined to be 2.8 μM. Using the in vivo maximum plasma concentration (Cmax) of Dihydrotanshinone I (11.29 ng/mL, 0.04 μM), the the change of AUC ranged from 0.14 to 1.42 % when the contribution of UGT1A7 towards the metabolism of drugs (fm) ranged from 0.1 to 1.
    Given that UGT1A7 is one of the most important gastrointestinal UGT isoforms and has high correlation with the occurence of cancer, the potential danshen-drug interaction due to the inhibition of UGT1A7 by Dihydrotanshinone I should be given more attention.
    Cell Research:
    J Biosci Bioeng. 2000;89(3):292-3.
    Biological activity of dihydrotanshinone I: effect on apoptosis.[Pubmed: 16232748]
    Recently, we have found for the first time that Dihydrotanshinone I, isolated from Salvia miltiorrhiza, exhibited cytotoxicity against various tumor cell lines.
    To investigate whether the mechanism underlying Dihydrotanshinone I toxicity involved apoptosis in cancer cell lines, we examined cell growth arrest and cell death by flow cytometric analysis and DNA fragmentation assay. Dihydrotanshinone I induced cell growth arrest during the S phase and subsequently, apoptosis, following its application to K562/ADR cells, whereas cryptotanshinone did not have these effects.
    These results suggest that the mode of action of Dihydrotanshinone I involves apoptotic pathways that are different from those involved in cryptotanshinone toxicity.