Damnacanthal
Based on 1 Customer Validation
Damnacanthal is an anthraquinone isolated from the root of Morinda citrifolia. Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activity. Natural Damnacanthal inhibits p56 lck autophosphorylation and phosphorylation of exogenous substrates with IC50s of 46 nM and 220 nM, respectively. Damnacanthal is a potent inducer of apoptosis with anticancer activity. Damnacanthal also has antinociceptive, anti-inflammatory effects in mice and anti-fungal activity against Candida albicans.
For research use only. We do not sell to patients.
- Purity : 99.40%
- CAS No.: 477-84-9
- Formula: C16H10O5
- Molecular Weight:282.25
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Storage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
IC50 & Target
IC50: 46 nM (p56 lck autophosphorylation) and 220 nM (phosphorylation of exogenous substrates by p56 lck)[1];
Apoptosis[2];
Candida albicans[2]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| DU-145 | IC50 |
26 μM
Compound: 26, damnacanthal
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Cytotoxicity against Homo sapiens (human) DU145 cells assessed as inhibition of cell survival after 96 hr by MTT assay
Cytotoxicity against Homo sapiens (human) DU145 cells assessed as inhibition of cell survival after 96 hr by MTT assay
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10.1007/s00044-012-0197-5 |
| Jurkat | IC50 |
17 nM
Compound: Damnacanthal
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Inhibition of p56 Lck tyrosine kinase in Jurkat cells where p56lck autophosphorylation is inhibited.
Inhibition of p56 Lck tyrosine kinase in Jurkat cells where p56lck autophosphorylation is inhibited.
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10.1016/S0960-894X(97)00034-6 |
| MCF7 | IC50 |
11 μM
Compound: 26, damnacanthal
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Cytotoxicity against Homo sapiens (human) MCF7 cells assessed as inhibition of cell survival after 96 hr by MTT assay
Cytotoxicity against Homo sapiens (human) MCF7 cells assessed as inhibition of cell survival after 96 hr by MTT assay
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10.1007/s00044-012-0197-5 |
| NCI-H460 | IC50 |
25 μM
Compound: 26, damnacanthal
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Cytotoxicity against Homo sapiens (human) H460 cells assessed as inhibition of cell survival after 96 hr by MTT assay
Cytotoxicity against Homo sapiens (human) H460 cells assessed as inhibition of cell survival after 96 hr by MTT assay
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10.1007/s00044-012-0197-5 |
| THP-1 | CC50 |
31.47 μM
Compound: 5
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Cytotoxicity against human THP1 cells assessed as cell viability after 72 hrs by MTT assay
Cytotoxicity against human THP1 cells assessed as cell viability after 72 hrs by MTT assay
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[PMID: 26906638] |
| THP-1 | IC50 |
39.51 μM
Compound: 5
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Antiprotozoan activity against intracellular amastigote stage of Trypanosoma cruzi Tulahuen infected in human THP1 cells assessed as reduction in parasite viability after 48 hrs by microplate based assay
Antiprotozoan activity against intracellular amastigote stage of Trypanosoma cruzi Tulahuen infected in human THP1 cells assessed as reduction in parasite viability after 48 hrs by microplate based assay
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[PMID: 26906638] |
In Vitro
Damnacanthal has > 100-fold selectivity for p56lck over the serine/threonine kinases, protein kinase A and protein kinase C, and > 40-fold selectivity for p56lck over four receptor tyrosine kinases. Damnacanthal also demonstrates modest (7-20-fold), but highly statistically significant, selectivity for p56lck over the homologous enzymes p60src and p59fyn[1].
Damnacanthal (0.1-100 μM; 1-4 days; HCT-116 and SW480 cells) treatment results in a significant reduction of cell proliferation in a concentration- and time-dependent manner[2].
Damnacanthal (1-50 μM; 72 hours; HCT-116 cells) treatment results in a significant enrichment in the number of cells in the S/G1 and G2/G1 phases at concentration of 50 μM[2].
Damnacanthal (10 μM; 24 hours; HCT-116 cells) treatment significantly increases caspase 3/7 activity. Damnacanthal-induced apoptosis[2].
Damnacanthal (0.1-10 μM; 24 hours; HCT-116 cells) treatment induces NAG-1 expression in HCT-116 cells. Cyclin D1 expression is reduced at 10 μM of Damnacanthal, whereas p21 and p53 does not alter their expression. PARP cleavage is seen at 10 μM Damnacanthal treatment only in HCT-116 cells, where NAG-1 is induced[2].
Damnacanthal treatment for 2 weeks shows significant decreasing colony number in HCT-116 cells in a concentration-dependent manner. Damnacanthal-treated cells show a dramatic inhibition of clonogenic capacity. Damnacanthal-treated (1-50 μM; 48 hours) cells significantly inhibits the migration of HCT-116 cells in a concentration-dependent manner[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HCT-116 and SW480 cells
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Concentration:0.1 μM, 1 μM, 10 μM, 100 μM
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Incubation Time:1, 2, and 4 days
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Result:Resulted in a significant reduction of cell proliferation in a concentration- and time-dependent manner.
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Cell Line:HCT-116 cells
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Concentration:1 μM, 10 μM and 50 μM
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Incubation Time:72 hours
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Result:Resulted in a significant enrichment in the number of cells in the S/G1 and G2/G1 phases at concentration of 50 μM.
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Cell Line:HCT-116 cells
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Concentration:10 μM
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Incubation Time:24 hours
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Result:Significantly increased caspase 3/7 activity.
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Cell Line:HCT-116 cells
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Concentration:0.1 μM, 1 μM and 10 μM
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Incubation Time:24 hours
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Result:NAG-1 was induced in HCT-116 cells in a dose- and time-dependent manner. Cyclin D1 expression was reduced at 10 μM.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male ddY mice (5-6 weeks) injected with formalin or Histamine[4]
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Dosage:10 mg/kg, 30 mg/kg and 100 mg/kg
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Administration:Oral administration; for 10 minutes, 30 minutes, 60 minutes or 300 minutes
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Result:Significantly reduced the growth of human lung tumor without acute toxicity.
Chemical Information
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CAS No. 477-84-9
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Appearance Solid
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Molecular Weight 282.25
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Formula C16H10O5
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Color Light yellow to yellow
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SMILES
O=CC(C(OC)=C1C2=O)=C(O)C=C1C(C3=C2C=CC=C3)=O
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Solvent & Solubility
In Vitro:
DMSO : 5 mg/mL (17.71 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
For the following dissolution methods, please prepare the working solution directly:
It is recommended to prepare fresh solutions and use them promptly within a short period of time.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocols
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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (293 KB)
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SDS (392 KB)
- English - EN (392 KB)
- Français - FR (392 KB)
- Deutsch - DE (392 KB)
- Norwegian - NO (392 KB)
- Español - ES (392 KB)
- Swedish - SV (392 KB)
- Italian - IT (392 KB)
- Korean - KR (392 KB)
- Portuguese - PT (392 KB)
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Handling Instructions (2659 KB)
References
[1]. Faltynek CR, et al. Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activity. Biochemistry. 1995 Sep 26;34(38):12404-10. [Content Brief]
[2]. Nualsanit T, et al. Damnacanthal, a noni component, exhibits antitumorigenic activity in human colorectal cancer cells. J Nutr Biochem. 2012 Aug;23(8):915-23. [Content Brief]
[3]. Aziz MY, et al. Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells. Oncol Lett. 2014 May;7(5):1479-1484. [Content Brief]
[4]. Okusada K, et al. The antinociceptive and anti-inflammatory action of the CHCl3-soluble phase and its main active component, damnacanthal, isolated from the root of Morinda citrifolia. Biol Pharm Bull. 2011;34(1):103-7. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.5430 mL | 17.7148 mL | 35.4296 mL | 88.5740 mL |
| 5 mM | 0.7086 mL | 3.5430 mL | 7.0859 mL | 17.7148 mL | |
| 10 mM | 0.3543 mL | 1.7715 mL | 3.5430 mL | 8.8574 mL | |
| 15 mM | 0.2362 mL | 1.1810 mL | 2.3620 mL | 5.9049 mL |
Damnacanthal Related Classifications
HY-108485 Related Classifications
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