Dihydrotanshinone ICAS# 87205-99-0 |
2D Structure
Quality Control & MSDS
3D structure
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Number of papers citing our products
Cas No. | 87205-99-0 | SDF | Download SDF |
PubChem ID | 11425923 | Appearance | Red powder |
Formula | C18H14O3 | M.Wt | 278.3 |
Type of Compound | Diterpenoids | Storage | Desiccate at -20°C |
Solubility | DMSO : 4.76 mg/mL (17.10 mM; Need ultrasonic) | ||
Chemical Name | (1R)-1,6-dimethyl-1,2-dihydronaphtho[1,2-g][1]benzofuran-10,11-dione | ||
SMILES | CC1COC2=C1C(=O)C(=O)C3=C2C=CC4=C3C=CC=C4C | ||
Standard InChIKey | HARGZZNYNSYSGJ-JTQLQIEISA-N | ||
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 | 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 | Antibacterial activities of cryptotanshinone and dihydrotanshinone I from a medicinal herb, Salvia miltiorrhiza Bunge.[Pubmed: 10664860 ]Biosci Biotechnol Biochem. 1999 Dec;63(12):2236-9.Cryptotanshinone and Dihydrotanshinone I, constituents of a medicinal plant, Salvia miltiorrhiza Bunge, had antibacterial activity against a broad range of Gram positive bacteria.
Dihydrotanshinone I inhibits angiogenesis both in vitro and in vivo.[Pubmed: 18180848]Acta Biochim Biophys Sin (Shanghai). 2008 Jan;40(1):1-6.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.
Combination treatment with dihydrotanshinone I and irradiation enhances apoptotic effects in human cervical cancer by HPV E6 down-regulation and caspases activation.[Pubmed: 22147199 ]Mol Cell Biochem. 2012 Apr;363(1-2):191-202.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.
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In vivo | Dihydrotanshinone I induced apoptosis and autophagy through caspase dependent pathway in colon cancer.[Pubmed: 26547530 ]Phytomedicine. 2015 Nov 15;22(12):1079-87.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.
|
Kinase Assay | Dihydrotanshinone I Exhibits Strong Inhibition Towards UDP-glucuronosyltransferase (UGT) 1A7.[Reference: WebLink]Blockade of TNF-α-induced NF-κB signaling pathway and anti-cancer therapeutic response of dihydrotanshinone I.[Pubmed: 26283590]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]Cryptotanshinone and dihydrotanshinone I exhibit strong inhibition towards human liver microsome (HLM)-catalyzed propofol glucuronidation.[Pubmed: 23333907]Fitoterapia. 2013 Mar;85:109-13.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.
J Mol Neurosci. 2014 Jul;53(3):506-10.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.
Int Immunopharmacol. 2015 Sep;28(1):764-72.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.
Latin Am. J. Pharm., 2012, 31(7):1060-3.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.
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Cell Research | Biological activity of dihydrotanshinone I: effect on apoptosis.[Pubmed: 16232748]J Biosci Bioeng. 2000;89(3):292-3.Recently, we have found for the first time that Dihydrotanshinone I, isolated from Salvia miltiorrhiza, exhibited cytotoxicity against various tumor cell lines.
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Dihydrotanshinone I Dilution Calculator
Dihydrotanshinone I Molarity Calculator
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 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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Dihydrotanshinone I is a natural compound extracted from Salvia miltiorrhiza Bunge which has been widely used for treating cardiovascular diseases.
In Vitro:In lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs), DHT (10 nM) decreases lectin-like ox-LDL receptor-1 (LOX-1) and NADPH oxidase 4 (NOX4) expression, reactive oxygen species (ROS) production, NF-κB nuclear translocation, ox-LDL endocytosis and monocytes adhesion[1]. Dihydrotanshinone I induces caspase dependent apoptosis induced in HCT116 cells. Dihydrotanshinone I induces concentration and ROS dependent caspase activation. Apoptosis induced by Dihydrotanshinone I is completely prevented by Z-VAD-fmk. Apoptosis induced by Dihydrotanshinone I is significantly inhibited by pretreatment of Z-LEHD-fmk but only is partially inhibited by Z-IETD-fmk. Apoptosis induced by Dihydrotanshinone I is significantly increased by caspase-2 knockdown[3].
In Vivo:DHT (10 and 25 mg/kg) significantly attenuates atherosclerotic plaque formation, alteres serum lipid profile, decreases oxidative stress and shrinks necrotic core areas in ApoE-/- mice. DHT dramatically inhibits the enhanced expression of LOX-1, NOX4, and NF-κB in aorta[1]. Dihydrotanshinone I (1, 2, 4 mg/kg) treatment can improve cardiac function, reduce infarct size, ameliorate the variations in myocardial zymogram and histopathological disorders, decrease 20-HETE generation, and regulate apoptosis-related protein in myocardial ischemia-reperfusion rats[2].
References:
[1]. Zhao W, et al. Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium. Front Pharmacol. 2016 Nov 8;7:418. eCollection 2016.
[2]. Wei Y, et al. The cardioprotection of dihydrotanshinone I against myocardial ischemia-reperfusion injury via inhibition of arachidonic acid ω-hydroxylase. Can J Physiol Pharmacol. 2016 Dec;94(12):1267-1275. Epub 2016 Jun 24.
[3]. Wang L, et al. Dihydrotanshinone I induced apoptosis and autophagy through caspase dependent pathway in colon cancer. Phytomedicine. 2015 Nov 15;22(12):1079-87.
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Biological activity of dihydrotanshinone I: effect on apoptosis.[Pubmed:16232748]
J Biosci Bioeng. 2000;89(3):292-3.
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.
Dihydrotanshinone I induced apoptosis and autophagy through caspase dependent pathway in colon cancer.[Pubmed:26547530]
Phytomedicine. 2015 Nov 15;22(12):1079-87.
BACKGROUND: 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. PURPOSE: To further study the anti-cancer activity of DHTS and its molecular mechanisms of action in colon cancer both in vitro and in vivo. METHODS: 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. RESULTS: 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. CONCLUSION: 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 interferes with the RNA-binding activity of HuR affecting its post-transcriptional function.[Pubmed:26553968]
Sci Rep. 2015 Nov 10;5:16478.
Post-transcriptional regulation is an essential determinant of gene expression programs in physiological and pathological conditions. HuR is a RNA-binding protein that orchestrates the stabilization and translation of mRNAs, critical in inflammation and tumor progression, including tumor necrosis factor-alpha (TNF). We identified the low molecular weight compound 15,16-dihydrotanshinone-I (DHTS), well known in traditional Chinese medicine practice, through a validated high throughput screening on a set of anti-inflammatory agents for its ability to prevent HuR:RNA complex formation. We found that DHTS interferes with the association step between HuR and the RNA with an equilibrium dissociation constant in the nanomolar range in vitro (Ki = 3.74 +/- 1.63 nM). In breast cancer cell lines, short term exposure to DHTS influences mRNA stability and translational efficiency of TNF in a HuR-dependent manner and also other functional readouts of its post-transcriptional control, such as the stability of selected pre-mRNAs. Importantly, we show that migration and sensitivity of breast cancer cells to DHTS are modulated by HuR expression, indicating that HuR is among the preferential intracellular targets of DHTS. Here, we disclose a previously unrecognized molecular mechanism exerted by DHTS, opening new perspectives to therapeutically target the HuR mediated, post-transcriptional control in inflammation and cancer cells.
Antibacterial activities of cryptotanshinone and dihydrotanshinone I from a medicinal herb, Salvia miltiorrhiza Bunge.[Pubmed:10664860]
Biosci Biotechnol Biochem. 1999 Dec;63(12):2236-9.
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.
Combination treatment with dihydrotanshinone I and irradiation enhances apoptotic effects in human cervical cancer by HPV E6 down-regulation and caspases activation.[Pubmed:22147199]
Mol Cell Biochem. 2012 Apr;363(1-2):191-202.
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.
Dihydrotanshinone I inhibits angiogenesis both in vitro and in vivo.[Pubmed:18180848]
Acta Biochim Biophys Sin (Shanghai). 2008 Jan;40(1):1-6.
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.
Blockade of TNF-alpha-induced NF-kappaB signaling pathway and anti-cancer therapeutic response of dihydrotanshinone I.[Pubmed:26283590]
Int Immunopharmacol. 2015 Sep;28(1):764-72.
The nuclear factor-kappaB (NF-kappaB) transcription factors control many physiological processes including inflammation, immunity, apoptosis, and angiogenesis. We identified Dihydrotanshinone I as an inhibitor of NF-kappaB activation through our research on Salvia miltiorrhiza Bunge. In this study, we found that Dihydrotanshinone I significantly inhibited the expression of NF-kappaB reporter gene induced by TNF-alpha in a dose-dependent manner. And Dihydrotanshinone I also inhibited TNF-alpha induced phosphorylation and degradation of IkappaBalpha, phosphorylation and nuclear translocation of p65. Furthermore, pretreatment of cells with this compound prevented the TNF-alpha-induced expression of NF-kappaB target genes, such as anti-apoptosis (cIAP-1 and FLIP), proliferation (COX-2), invasion (MMP-9), angiogenesis (VEGF), and major inflammatory cytokines (TNF-alpha, IL-6, and MCP1). We also demonstrated that Dihydrotanshinone I potentiated TNF-alpha-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-alpha production. Taken together, Dihydrotanshinone I could be a valuable candidate for the intervention of NF-kappaB-dependent pathological conditions such as inflammation and cancer.
Cryptotanshinone and dihydrotanshinone I exhibit strong inhibition towards human liver microsome (HLM)-catalyzed propofol glucuronidation.[Pubmed:23333907]
Fitoterapia. 2013 Mar;85:109-13.
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 1.7muM, 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.
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]
J Mol Neurosci. 2014 Jul;53(3):506-10.
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.