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| Targets |
Columbianadin targets multiple cellular pathways. It exhibits strong inhibitory activity against the inflammatory response of IL-1β-treated A549 cells and LPS-treated MH-S cells. It functions as a calcium channel blocker. In colon cancer cells, it induces apoptosis and, at high concentrations (50 µM), induces necroptosis. The induction of apoptosis is correlated with the modulation of caspase-9, caspase-3, Bax, Bcl-2, RIP-3, and caspase-8, Bim, and Bid.
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| ln Vitro |
Colon cancer cell proliferation is significantly inhibited by colonnadin (CBN). At moderate concentrations (up to 25 μM), colondinadin produces apoptosis; at high concentrations (50 μM), it induces necroptosis. The regulation of caspase-9, caspase-3, Bax, Bcl-2, Bim, and Bid is linked to the induction of apoptosis by Columbianadin, while RIP-3 and caspase-8 are linked to the generation of necroptosis. Furthermore, columbanadin causes an imbalance in internal antioxidant enzymes as catalase, GPx-1, SOD-1, and SOD-2 as well as the buildup of ROS. The most effective growth inhibitory action on human colorectal cancer cells was demonstrated by colonidin. Consequently, in order to provide a comprehensive mechanism of Columbianadin-mediated growth inhibition, additional research was carried out employing HCT116 cells. Following 48 and 72 hours of incubation, respectively, cells treated with varying doses of Columbianadin (0-100 μM) displayed dose- and time-dependent growth inhibition, with IC50 values of 47.2 and 32.4 μM. Following a 48-hour treatment with Columbianadin at varying doses (12.5, 25 and 50 μM), HCT116 cells showed a reduction in the number of cells and an increase in floating cells. Round and dead cells showed noticeable morphological alterations when exposed to 25 and 50 μM Columbianadin [1].
In vitro, Columbianadin possesses strong inhibitory activity against the inflammatory response of IL-1β-treated A549 cells and LPS-treated MH-S cells. It effectively suppresses the growth of colon cancer cells. It exhibits cytotoxic activity against various cancer cell lines. It also shows analgesic activities. At high concentrations (50 µM), Columbianadin induces necroptosis. |
| ln Vivo |
The tissue distribution of intravenous given Columbianadin (CBN) and Columbianetin (CBT) in rats was effectively studied using this analytical approach. The study's findings demonstrate that, following an intravenous injection, colondanadin can be found in all of the tissues that were chosen. Columbianadin is quickly absorbed by rat tissues, and in the majority of those tissues, it can be converted to CBT via metabolism. The heart had the largest absorption of Columbianadin among the tissues tested, indicating that it could be one of Columbianadin's primary target tissues [2].
In vivo, Columbianadin has been shown to possess significant inhibitory activity against LPS-induced inflammation at a dose of 20-60 mg/kg. It exhibits analgesic activities in animal models. It is a metabolite in rodents and plants. |
| Enzyme Assay |
The in vitro activity of Columbianadin is assessed using various cell-based assays. The anti-inflammatory activity is assessed in A549 lung epithelial cells treated with IL-1β or in MH-S alveolar macrophage cells treated with LPS. Cells are treated with various concentrations of Columbianadin (typically ranging from 1 to 100 µM) for different time periods, and the production of pro-inflammatory cytokines (e.g., IL-6, TNF-α) is measured by ELISA. The expression of inflammatory mediators (e.g., COX-2, iNOS) is analyzed by quantitative real-time PCR or Western blotting. The anti-cancer activity is assessed in various cancer cell lines (e.g., colon cancer cells) by measuring cell viability using the MTT assay, apoptosis using flow cytometry with Annexin V staining, and the expression of apoptosis-related proteins (e.g., caspase-3, caspase-9, Bax, Bcl-2) by Western blotting.
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| Cell Assay |
For cellular assays, A549 lung epithelial cells, MH-S alveolar macrophages, or colon cancer cell lines are used. Cells are cultured in appropriate media (e.g., RPMI-1640 or DMEM with 10% fetal bovine serum) and treated with various concentrations of Columbianadin (typically ranging from 1 to 100 µM) for different time periods (e.g., 24-72 hours). Cell viability is assessed using the MTT or CCK-8 assay. Apoptosis is assessed by measuring caspase-3/7 activity, by flow cytometry using Annexin V/PI staining, or by Western blotting for cleaved caspases and PARP. The effect on calcium channels can be assessed using calcium imaging with fluorescent dyes such as Fluo-4.
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| Animal Protocol |
In vivo, Columbianadin is typically administered to animal models via intraperitoneal or oral administration. For anti-inflammatory studies, mice are treated with LPS to induce systemic inflammation. Columbianadin is administered at doses ranging from 20 to 60 mg/kg before or after LPS treatment. The levels of pro-inflammatory cytokines in serum are measured by ELISA, and the expression of inflammatory mediators in tissues is analyzed. For analgesic studies, animal models such as the acetic acid-induced writhing test or the hot plate test are used. The compound is administered, and the pain response is measured.
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| ADME/Pharmacokinetics |
Specific pharmacokinetic data for Columbianadin is not detailed in the provided search results. As a small molecule with a molecular weight of 328.36 g/mol, it is expected to have reasonable oral bioavailability. Its intestinal absorption has been studied. Its metabolism and excretion would require further investigation.
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| Toxicity/Toxicokinetics |
Specific toxicity data for Columbianadin is not available in the provided search results. In in vitro studies, it has been shown to induce apoptosis and necroptosis in cancer cells at higher concentrations, indicating potential cytotoxicity. Comprehensive toxicological studies are required to establish its full safety profile.
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| References | |
| Additional Infomation |
Columbianadin is an α,β-unsaturated carboxylic acid ester formed by the condensation of the carboxyl group of angelic acid with the hydroxyl group of 2-[(8S)-2-oxo-8,9-dihydro-2H-furano[2,3-h][1]benzopyran-8-yl]prop-2-ol. It possesses various activities including anti-inflammatory, apoptosis-inducing, hepatoprotective, and antitumor effects, and is a metabolite in rodents and plants. It is a furanocoumarin compound and also an α,β-unsaturated carboxylic acid ester. Its function is related to angelic acid. Columbianadin has been reported to exist in Semenovia dasycarpa, Cnidium monnieri, and other organisms with relevant data.
Columbianadin is a natural coumarin with diverse biological activities, including anti-inflammatory, anti-cancer, analgesic, and calcium-channel blocking effects. It is a research compound used to study these various pharmacological effects and is not approved for clinical use. Its presence in plants such as Angelica decursiva, which is used in traditional medicine, makes it a compound of interest for drug discovery and development. |
| Molecular Formula |
C19H20O5
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|---|---|
| Molecular Weight |
328.364
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| Exact Mass |
328.131
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| CAS # |
5058-13-9
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| PubChem CID |
6436246
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| Appearance |
White to off-white solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
482.3±45.0 °C at 760 mmHg
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| Melting Point |
166ºC
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| Flash Point |
212.7±28.8 °C
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| Vapour Pressure |
0.0±1.2 mmHg at 25°C
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| Index of Refraction |
1.569
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| LogP |
3.95
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
24
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| Complexity |
589
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C/C=C(/C)\C(=O)OC(C)(C)[C@@H]1CC2=C(O1)C=CC3=C2OC(=O)C=C3
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| InChi Key |
JRIBPWOXWIRQOQ-GHAIFCDISA-N
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| InChi Code |
InChI=1S/C19H20O5/c1-5-11(2)18(21)24-19(3,4)15-10-13-14(22-15)8-6-12-7-9-16(20)23-17(12)13/h5-9,15H,10H2,1-4H3/b11-5-/t15-/m0/s1
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| Chemical Name |
2-[(8S)-2-oxo-8,9-dihydrofuro[2,3-h]chromen-8-yl]propan-2-yl (Z)-2-methylbut-2-enoate
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| Synonyms |
CBN; Columbianadin
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~25 mg/mL (~76.14 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 3.5 mg/mL (10.66 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 35.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.0454 mL | 15.2272 mL | 30.4544 mL | |
| 5 mM | 0.6091 mL | 3.0454 mL | 6.0909 mL | |
| 10 mM | 0.3045 mL | 1.5227 mL | 3.0454 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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