| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| 5g |
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| Other Sizes |
| Targets |
Sodium copper chlorophyllin A does not target a specific protein receptor or enzyme in the classical sense but exerts its effects through multiple mechanisms, including antioxidant activity, metal chelation, and modulation of xenobiotic metabolism. The compound is a potent antioxidant that scavenges free radicals, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby protecting cells from oxidative damage. The copper ion in the porphyrin ring may contribute to the compound's redox activity, although the precise mechanisms are not fully understood. Sodium copper chlorophyllin A also exhibits metal-chelating properties, binding to heavy metals and other toxic ions, which may contribute to its detoxifying effects. The compound has been shown to modulate the activity of cytochrome P450 enzymes, including CYP1A1, CYP1A2, and CYP3A4, which are involved in the metabolism of xenobiotics and carcinogens. By inhibiting the activation of procarcinogens and enhancing the detoxification of carcinogens, sodium copper chlorophyllin A may exert chemopreventive effects. The compound also modulates the Nrf2/ARE signaling pathway, leading to the upregulation of antioxidant enzymes such as heme oxygenase-1 (HO-1), glutathione S-transferase (GST), and NAD(P)H:quinone oxidoreductase 1 (NQO1). In addition to its antioxidant and chemopreventive activities, sodium copper chlorophyllin A has been shown to inhibit the growth of certain bacteria and fungi, suggesting antimicrobial properties. The compound's anti-inflammatory effects are mediated through the suppression of pro-inflammatory cytokines and the inhibition of NF-κB activation. The diverse mechanisms of action of sodium copper chlorophyllin A contribute to its potential health benefits, although further studies are needed to fully elucidate its molecular targets and pathways.
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| ln Vitro |
In vitro studies have demonstrated that sodium copper chlorophyllin A exhibits a range of biological activities in various cell-based and cell-free systems. As an antioxidant, the compound effectively scavenges DPPH radicals, ABTS radicals, and superoxide anions in cell-free assays, with IC₅₀ values in the micromolar range. In cell culture models of oxidative stress, sodium copper chlorophyllin A protects against H₂O₂-, UV-, and chemical-induced oxidative damage by reducing intracellular ROS levels, maintaining mitochondrial membrane potential, and preventing lipid peroxidation. The compound's cytoprotective effects have been demonstrated in various cell lines, including hepatocytes (HepG2), fibroblasts (3T3), and keratinocytes (HaCaT). In models of inflammation, sodium copper chlorophyllin A inhibits LPS-induced production of NO, TNF-α, IL-1β, and IL-6 in macrophages by suppressing the activation of NF-κB and MAPK signaling pathways. The compound also inhibits the expression of COX-2 and iNOS, further contributing to its anti-inflammatory effects. In cancer cell lines, including colon cancer (HT-29, Caco-2), liver cancer (HepG2), and breast cancer (MCF-7), sodium copper chlorophyllin A has been shown to inhibit cell proliferation and induce apoptosis at concentrations of 10-100 µg/mL. The compound's anticancer effects are associated with the activation of the mitochondrial apoptotic pathway, characterized by Bax upregulation, Bcl-2 downregulation, cytochrome c release, and caspase-3/9 activation. Sodium copper chlorophyllin A also exhibits antimicrobial activity against various bacteria, including Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa, and against fungi such as Candida albicans. The compound's antimicrobial effects are attributed to its ability to disrupt microbial cell membranes and generate ROS. In addition to its biological activities, sodium copper chlorophyllin A is used as a photosensitizer in photodynamic therapy (PDT) for the treatment of certain cancers and skin conditions.
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| ln Vivo |
In vivo studies have investigated the therapeutic potential of sodium copper chlorophyllin A in various animal models, although the data are limited compared to its use as a food additive. In models of acute liver injury, oral administration of sodium copper chlorophyllin A at doses of 10-100 mg/kg significantly reduced serum ALT and AST levels, improved hepatic histology, and decreased oxidative stress markers in the liver. The compound's hepatoprotective effects were associated with the upregulation of antioxidant enzymes and the activation of the Nrf2 pathway. In models of chemically induced carcinogenesis, sodium copper chlorophyllin A has been shown to reduce the incidence and multiplicity of tumors in the colon, liver, and skin, indicating chemopreventive activity. The compound's chemopreventive effects are attributed to its ability to inhibit the activation of procarcinogens, enhance the detoxification of carcinogens, and scavenge free radicals. In models of wound healing, topical application of sodium copper chlorophyllin A promotes tissue repair and reduces inflammation, likely due to its antioxidant and anti-inflammatory properties. In models of inflammatory bowel disease (IBD), sodium copper chlorophyllin A reduced colonic inflammation, mucosal damage, and oxidative stress, suggesting potential for the management of IBD. In models of microbial infection, the compound has shown efficacy in reducing bacterial load and improving clinical outcomes. However, many of these in vivo studies have used relatively high doses of the compound, and the clinical relevance of these findings is uncertain. The compound is generally recognized as safe (GRAS) for use as a food additive, but its therapeutic applications have not been fully validated in clinical trials.
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| Enzyme Assay |
For in vitro antioxidant assays, sodium copper chlorophyllin A is typically evaluated using DPPH, ABTS, and superoxide radical scavenging assays. In the DPPH assay, the compound is dissolved in methanol or ethanol at concentrations ranging from 1 to 100 µg/mL, and an equal volume of DPPH solution (0.1 mM in ethanol) is added. The mixture is incubated at room temperature for 30 minutes in the dark, and the decrease in absorbance at 517 nm is measured using a spectrophotometer. The percentage of DPPH radical scavenging activity is calculated, and the IC₅₀ value is determined from dose-response curves, with ascorbic acid or Trolox as positive controls. In the ABTS assay, ABTS radical cation is generated by reacting ABTS with potassium persulfate, and the compound is added to the ABTS solution. The decrease in absorbance at 734 nm is measured after 6 minutes of incubation, and the IC₅₀ value is determined. For superoxide radical scavenging assays, the compound is tested using the NBT reduction method or the xanthine/xanthine oxidase system. For metal chelation assays, the compound's ability to chelate ferrous ions is measured using the ferrozine method. For antimicrobial assays, the compound is tested against various bacterial and fungal strains using the broth microdilution method to determine the minimum inhibitory concentration (MIC). For enzyme inhibition assays, sodium copper chlorophyllin A is tested against CYP1A1, CYP1A2, and CYP3A4 using microsomal preparations and specific substrates, and the IC₅₀ values are determined. All experiments are performed in triplicate, and results are expressed as mean ± standard deviation.
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| Cell Assay |
For in vitro cell-based assays, sodium copper chlorophyllin A is evaluated using a panel of cell lines relevant to its pharmacological activities. For cytotoxicity and cell proliferation assays, cells (e.g., HepG2, HT-29, MCF-7, HaCaT) are seeded in 96-well plates at 5 × 10³ cells per well, treated with the compound at concentrations of 1-100 µg/mL for 24-72 hours, and cell viability is determined using MTT or CCK-8 assays. For apoptosis assays, cells are treated with the compound for 24-48 hours, and apoptosis is assessed by flow cytometry using Annexin V-FITC/PI staining, caspase-3/7 activity assays, and Western blot analysis of apoptosis-related proteins. For oxidative stress studies, cells are pretreated with the compound for 24 hours and then exposed to H₂O₂ (200-500 µM) or other oxidants for 4-6 hours. Cell viability is measured using MTT assays, and intracellular ROS levels are measured using DCFH-DA fluorescent probes. The expression of antioxidant enzymes (SOD, CAT, GPx, HO-1) is assessed by Western blotting or qPCR. For anti-inflammatory studies, macrophages (e.g., RAW 264.7) are stimulated with LPS (1 µg/mL) in the presence or absence of the compound (1-50 µg/mL) for 24 hours, and NO production is measured using the Griess reaction, and TNF-α, IL-1β, and IL-6 levels are measured by ELISA. For antimicrobial studies, cells are not typically used; instead, the compound is tested against microbial cultures. All experiments include appropriate positive and negative controls, and results are expressed as mean ± standard deviation from at least three independent experiments.
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| Animal Protocol |
For in vivo animal experiments, sodium copper chlorophyllin A is typically administered orally (by gavage) or topically to rodents. For hepatoprotective studies, male ICR or C57BL/6 mice (20-25 g) are administered the compound orally at doses of 10, 50, or 100 mg/kg/day for 7 days prior to a single intraperitoneal injection of CCl₄ (0.1 mL/kg, 10% in olive oil) or acetaminophen (300 mg/kg). After 24 hours, blood samples are collected for serum ALT and AST measurement, and liver tissues are harvested for histopathological examination and measurement of oxidative stress markers (MDA, SOD, GSH). For chemoprevention studies, mice are treated with the compound orally at doses of 50-200 mg/kg/day for 2-4 weeks prior to and during carcinogen exposure (e.g., DMH, DMBA), and the incidence and multiplicity of tumors are assessed. For wound healing studies, full-thickness excisional wounds are created on the dorsal skin of rats or mice, and the compound is applied topically as a gel or cream (0.1-1%) once daily for 7-14 days. Wound closure is monitored by measuring the wound area, and the wound tissues are collected for histopathological analysis and measurement of inflammatory markers. For antimicrobial studies, mice are infected with pathogenic bacteria or fungi, and the compound is administered orally or topically, and the bacterial load and clinical outcomes are assessed. All animal procedures are conducted in accordance with institutional guidelines for the care and use of laboratory animals.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for sodium copper chlorophyllin A are limited, as the compound is primarily used as a food additive rather than a therapeutic agent. The compound has a molecular weight of approximately 724.15 g/mol and a molecular formula of C₃₄H₃₁CuN₄Na₃O₆. Following oral administration, sodium copper chlorophyllin A is poorly absorbed from the gastrointestinal tract due to its large size and hydrophilic nature. Most of the compound remains in the intestinal lumen and is excreted in the feces, which is consistent with its use as a food colorant. However, small amounts of the compound may be absorbed and distributed to various tissues, including the liver and kidneys. The absorbed compound is metabolized in the liver and excreted in urine. The compound is soluble in water (≥10 mg/mL), which facilitates its use in aqueous formulations. The compound is stable when stored as a powder at room temperature, protected from light and moisture. For in vivo administration, sodium copper chlorophyllin A can be formulated in saline, water, or other suitable vehicles. Further detailed pharmacokinetic studies are needed to fully characterize the absorption, distribution, metabolism, and excretion (ADME) properties of sodium copper chlorophyllin A.
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| Toxicity/Toxicokinetics |
Toxicological data for sodium copper chlorophyllin A indicate that it is generally recognized as safe (GRAS) for use as a food additive. The compound has been evaluated in various toxicological studies, and the acceptable daily intake (ADI) for chlorophyllin has been established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) and the European Food Safety Authority (EFSA). In acute toxicity studies, the oral LD₅₀ in rodents is greater than 5000 mg/kg, indicating very low acute toxicity. In subacute and chronic toxicity studies, animals fed with sodium copper chlorophyllin A at doses of up to 1000 mg/kg/day showed no significant adverse effects on body weight, organ weights, hematological parameters, or serum biochemistry. Histopathological examination of major organs revealed no treatment-related abnormalities. No genotoxicity was observed in the Ames test, the mouse micronucleus assay, or the chromosomal aberration test. No carcinogenicity or reproductive toxicity has been reported for sodium copper chlorophyllin A. However, the compound may cause discoloration of the skin, urine, or feces at high doses, which is a harmless cosmetic effect. As with all chemicals, appropriate safety precautions should be taken when handling sodium copper chlorophyllin A, including the use of personal protective equipment. The compound is for research use only and is not intended for human therapeutic use.
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| Additional Infomation |
See also: Chlorophyll (note moved to).
Sodium copper chlorophyllin A is a research-use only compound and has not been approved for clinical applications as a therapeutic agent. It is also known as chlorophyllin sodium copper salt, sodium copper chlorophyllin, and E141. The compound has a molecular formula of C₃₄H₃₁CuN₄Na₃O₆ and a molecular weight of approximately 724.15 g/mol. It is a semi-synthetic mixture of sodium copper salts derived from chlorophyll, the green pigment found in plants and algae. Sodium copper chlorophyllin A is widely used as a food additive (E141) and colorant in the food, pharmaceutical, and cosmetic industries. In alternative medicine, it has been used for its purported health benefits, including wound healing, anti-inflammatory effects, and as an internal deodorant. The compound is available from various research chemical suppliers with purities typically ≥95-98%. It is a dark green to black powder that is soluble in water (≥10 mg/mL). Storage recommendations include keeping the compound in a tightly sealed container, protected from light and moisture, at room temperature. The compound is of interest for research on its antioxidant, anti-inflammatory, hepatoprotective, and chemopreventive activities, although further studies are needed to fully elucidate its pharmacological profile and therapeutic potential. The compound is not intended for human therapeutic use. |
| Molecular Formula |
C34H31CUN4NA3O6
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|---|---|
| Molecular Weight |
724.1485
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| Exact Mass |
723.123
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| CAS # |
11006-34-1
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| PubChem CID |
23725082
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| Appearance |
Green to black solid powder
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| Boiling Point |
801.6ºC at 760 mmHg
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| Flash Point |
438.6ºC
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
48
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| Complexity |
1750
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| Defined Atom Stereocenter Count |
0
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| SMILES |
[Cu+2].[Na+].[Na+].[Na+].[O-]C(C([H])([H])C([H])([H])C1([H])C2=C(C([H])([H])C(=O)[O-])C3/C(=C(\[O-])/[O-])/C(C([H])([H])[H])=C(C([H])=C4C(C([H])([H])C([H])([H])[H])=C(C([H])([H])[H])C(=C([H])C5C(C([H])=C([H])[H])=C(C([H])([H])[H])C(=C([H])C(C1([H])C([H])([H])[H])=N2)N=5)[N-]4)N=3)=O |c:10,45,60,t:30|
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| InChi Key |
HWDGVJUIHRPKFR-UHFFFAOYSA-I
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| InChi Code |
InChI=1S/C34H36N4O6.Cu.3Na/c1-7-19-15(3)23-12-25-17(5)21(9-10-29(39)40)32(37-25)22(11-30(41)42)33-31(34(43)44)18(6)26(38-33)14-28-20(8-2)16(4)24(36-28)13-27(19)35-23;;;;/h7,12-14,17,21H,1,8-11H2,2-6H3,(H5,35,36,37,38,39,40,41,42,43,44);;;;/q;+2;3*+1/p-5
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| Chemical Name |
copper;trisodium;3-[20-(carboxylatomethyl)-18-(dioxidomethylidene)-8-ethenyl-13-ethyl-3,7,12,17-tetramethyl-2,3-dihydroporphyrin-23-id-2-yl]propanoate
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| 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) |
H2O : ≥ 66.66 mg/mL (~92.05 mM)
DMSO : ~1.2 mg/mL (~1.66 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 5 mg/mL (6.90 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.3809 mL | 6.9046 mL | 13.8093 mL | |
| 5 mM | 0.2762 mL | 1.3809 mL | 2.7619 mL | |
| 10 mM | 0.1381 mL | 0.6905 mL | 1.3809 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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