DehydrocorydalinCAS# 30045-16-0 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 30045-16-0 | SDF | Download SDF |
PubChem ID | 34781 | Appearance | Cryst. |
Formula | C22H24NO4 | M.Wt | 366.44 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Synonyms | Dehydrocorydaline | ||
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | 2,3,9,10-tetramethoxy-13-methyl-5,6-dihydroisoquinolino[2,1-b]isoquinolin-7-ium | ||
SMILES | CC1=C2C=CC(=C(C2=C[N+]3=C1C4=CC(=C(C=C4CC3)OC)OC)OC)OC | ||
Standard InChIKey | RFKQJTRWODZPHF-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C22H24NO4/c1-13-15-6-7-18(24-2)22(27-5)17(15)12-23-9-8-14-10-19(25-3)20(26-4)11-16(14)21(13)23/h6-7,10-12H,8-9H2,1-5H3/q+1 | ||
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 | Dehydrocorydalin has anti-inflammatory,antinociceptive,antiplatelet,and anti-tumor effects and can protect the cardiovascular system. Dehydrocorydaline stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP. |
Targets | MMP(e.g.TIMP) | Bcl-2/Bax | Caspase | TNF-α | p38MAPK | IL Receptor | PARP | MyoD | MyoE |
In vitro | Anti-Metastatic Effect of Dehydrocorydaline on H1299 Non-Small Cell Lung Carcinoma Cells via Inhibition of Matrix Metalloproteinases and B Cell Lymphoma 2.[Pubmed: 28144994 ]Phytother Res. 2017 Mar;31(3):441-448.Though Dehydrocorydaline, an alkaloid isolated from Corydalis turtschaninovii tuber, was known to have anti-coronary artery disease, anti-inflammatory, apoptotic, anti-allergic, anti-acetylcholinesterase, and antitumor effects, the underlying anti-metastatic mechanism of Dehydrocorydalin was never elucidated in lung cancer cells so far. Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation.[Pubmed: 27573543]Mol Med Rep. 2016 Oct;14(4):3029-36.Muscle regeneration is a coordinated process that involves proliferation and differentiation of muscle progenitor cells. Activation of MyoD is a key event in myogenic differentiation, which is regulated by p38 mitogen‑activated protein kinases (MAPK). In a screen of natural compounds for the enhancement of MyoD activity, Dehydrocorydaline (DHC) from the Corydalis tuber was identified. |
In vivo | Antinociceptive effects of dehydrocorydaline in mouse models of inflammatory pain involve the opioid receptor and inflammatory cytokines.[Pubmed: 27272194 ]Sci Rep. 2016 Jun 7;6:27129.Dehydrocorydaline (DHC) is an alkaloidal component isolated from Rhizoma corydalis. Previous studies have shown that DHC has anti-inflammatory and anti-tumor effects and that it can protect the cardiovascular system. However, there are few studies of the antinociceptive effects of DHC in vivo. |
Kinase Assay | Dehydrocorydaline inhibits elevated mitochondrial membrane potential in lipopolysaccharide-stimulated macrophages.[Pubmed: 21575743]Int Immunopharmacol. 2011 Sep;11(9):1362-7.Activated macrophages play a critical role in the pathogenesis of numerous diseases by producing pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6. While the mechanisms of bacterial component recognition and signal transduction have been well investigated, viability regulation in activated macrophages remains unclear. |
Cell Research | Dehydrocorydaline inhibits breast cancer cells proliferation by inducing apoptosis in MCF-7 cells.[Pubmed: 22298457 ]Am J Chin Med. 2012;40(1):177-85.Dehydrocorydaline is an alkaloid isolated from traditional Chinese herb Corydalis yanhusuo W.T. Wang. We discovered that it possessed anti-tumor potential during screening of anti-tumor natural products from Chinese medicine. In this study, its anti-tumor potential was investigated with breast cancer line cells MCF-7 in vitro. |
Dehydrocorydalin Dilution Calculator
Dehydrocorydalin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.729 mL | 13.6448 mL | 27.2896 mL | 54.5792 mL | 68.224 mL |
5 mM | 0.5458 mL | 2.729 mL | 5.4579 mL | 10.9158 mL | 13.6448 mL |
10 mM | 0.2729 mL | 1.3645 mL | 2.729 mL | 5.4579 mL | 6.8224 mL |
50 mM | 0.0546 mL | 0.2729 mL | 0.5458 mL | 1.0916 mL | 1.3645 mL |
100 mM | 0.0273 mL | 0.1364 mL | 0.2729 mL | 0.5458 mL | 0.6822 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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Antinociceptive effects of dehydrocorydaline in mouse models of inflammatory pain involve the opioid receptor and inflammatory cytokines.[Pubmed:27272194]
Sci Rep. 2016 Jun 7;6:27129.
Dehydrocorydaline (DHC) is an alkaloidal component isolated from Rhizoma corydalis. Previous studies have shown that DHC has anti-inflammatory and anti-tumor effects and that it can protect the cardiovascular system. However, there are few studies of the antinociceptive effects of DHC in vivo. This study explored the antinociceptive effects and possible mechanisms of DHC in mice using two inflammatory pain models: the acetic acid-induced writhing test and the formalin paw test. The intraperitoneal administration of DHC (3.6, 6 or 10 mg/kg) showed a dose-dependent antinociceptive effect in the acetic acid-induced writhing test and significantly attenuated the formalin-induced pain responses in mice. The antinociceptive effects of DHC were not associated with changes in the locomotor activity or motor responses of animals, and no obvious acute or chronic toxic effects were observed in the mice. Furthermore, the use of naloxone confirmed the involvement of the opioid receptor in the central antinociceptive effects of DHC. DHC reduced formalin-induced paw edema, which indicated that DHC may produce an anti-inflammatory effect in the periphery. In the formalin test, DHC decreased the expression of caspase 6 (CASP6), TNF-alpha, IL-1beta and IL-6 proteins in the spinal cord. These findings confirm that DHC has antinociceptive effects in mice.
Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation.[Pubmed:27573543]
Mol Med Rep. 2016 Oct;14(4):3029-36.
Muscle regeneration is a coordinated process that involves proliferation and differentiation of muscle progenitor cells. Activation of MyoD is a key event in myogenic differentiation, which is regulated by p38 mitogenactivated protein kinases (MAPK). In a screen of natural compounds for the enhancement of MyoD activity, Dehydrocorydaline (DHC) from the Corydalis tuber was identified. Treatment of C2C12 myoblasts with DHC increased the expression levels of musclespecific proteins, including MyoD, myogenin and myosin heavy chain. In addition, C2C12 myoblasts exhibited enhanced multinucleated myotube formation without any cytotoxicity. Treatment with DHC elevated p38 MAPK activation and the interaction of MyoD with an E protein, which is likely to result in activation of MyoD and promotion of myoblast differentiation. Furthermore, defects in differentiationinduced p38 MAPK activation and myoblast differentiation induced by depletion of the promyogenic receptor protein Cdo in C2C12 myoblasts were restored by DHC treatment. In conclusion, these results indicated that DHC stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. These findings suggested that DHC may be considered a potential therapeutic compound for the improvement of muscle stem cell regenerative capacity in injured muscle.
Anti-Metastatic Effect of Dehydrocorydaline on H1299 Non-Small Cell Lung Carcinoma Cells via Inhibition of Matrix Metalloproteinases and B Cell Lymphoma 2.[Pubmed:28144994]
Phytother Res. 2017 Mar;31(3):441-448.
Though Dehydrocorydaline, an alkaloid isolated from Corydalis turtschaninovii tuber, was known to have anti-coronary artery disease, anti-inflammatory, apoptotic, anti-allergic, anti-acetylcholinesterase, and antitumor effects, the underlying anti-metastatic mechanism of Dehydrocorydalin was never elucidated in lung cancer cells so far. Thus, in the present study, the anti-metastatic effect of Dehydrocorydaline was examined in non-small cell lung carcinoma (NSCLC) cells, mainly targeting matrix metalloproteinases (MMPs) and B cell lymphoma-2 (Bcl-2) signaling. Here, Dehydrocorydaline exerted weak cytotoxicity and attenuated the protein expression of Bcl-2 and activated Bax in a concentration-dependent manner in NSCLC cells, such as A549, H460, H1299, and H596 cells. Also, Dehydrocorydaline suppressed the migration of H1299 cells by wound healing assay and transwell migration assay. Consistently, Dehydrocorydaline attenuated mRNA and protein levels of MMP7 and MMP9 as metastasis biomarkers in H1299 cells by quantitative reverse transcription polymerase chain reaction. Of note, Bcl-2 overexpression reduced the cytotoxic and anti-metastatic effects of Dehydrocorydaline on pCDNA-Bcl-2 transfected H1299 cells. Overall, our findings provide scientific evidence that Dehydrocorydaline exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSCLC cells. Copyright (c) 2017 John Wiley & Sons, Ltd.
Dehydrocorydaline inhibits breast cancer cells proliferation by inducing apoptosis in MCF-7 cells.[Pubmed:22298457]
Am J Chin Med. 2012;40(1):177-85.
Dehydrocorydaline is an alkaloid isolated from traditional Chinese herb Corydalis yanhusuo W.T. Wang. We discovered that it possessed anti-tumor potential during screening of anti-tumor natural products from Chinese medicine. In this study, its anti-tumor potential was investigated with breast cancer line cells MCF-7 in vitro. The anti-proliferative effect of Dehydrocorydaline was determined by MTT assay and the mitochondrial membrane potential (Delta Psi m) was monitored by JC-1 staining. DNA fragments were visualized by Hoechst 33342 staining and DNA ladder assay. Apoptotic related protein expressions were measured by Western blotting. Dehydrocorydaline significantly inhibited MCF-7 cell proliferation in a dose- dependent manner, which could be reversed by a caspase-8 inhibitor, Z-IETD-FMK. Dehydrocorydaline increased DNA fragments without affecting DeltaPsim. Western blotting assay showed that Dehydrocorydaline dose-dependently increased Bax protein expression and decreased Bcl-2 protein expression. Furthermore, Dehydrocorydaline induced activation of caspase-7,-8 and the cleavage of PARP without affecting caspase-9. These results showed that Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.
Dehydrocorydaline inhibits elevated mitochondrial membrane potential in lipopolysaccharide-stimulated macrophages.[Pubmed:21575743]
Int Immunopharmacol. 2011 Sep;11(9):1362-7.
Activated macrophages play a critical role in the pathogenesis of numerous diseases by producing pro-inflammatory cytokines such as interleukin (IL)-1beta and IL-6. While the mechanisms of bacterial component recognition and signal transduction have been well investigated, viability regulation in activated macrophages remains unclear. We screened herbal ingredients to find an agent that reduces the viability of lipopolysaccharide (LPS)-stimulated macrophages and observed that Dehydrocorydaline, a component of Corydalis yanhusuo, reduced the viability of macrophage-derived RAW264.7 cells and primary macrophages in the presence of LPS. Dehydrocorydaline inhibited the elevation of mitochondrial membrane potential and induced ATP depletion in LPS-stimulated macrophages but neither affected basal mitochondrial membrane potential nor ATP content in non-stimulated macrophages. Dehydrocorydaline also prevented increased concentrations of IL-1beta and IL-6 in culture media of LPS-stimulated macrophages. Mode of Dehydrocorydaline action indicates that elevated mitochondrial membrane potential may be a novel target to specifically reduce viability and suppress cytokine production in LPS-stimulated macrophages.