Copper sulfate 50mg/50ml solution for infusion vials
Requires a prescription from a doctor or prescriber
Cupric sulfate is a salt created by treating cupric oxide with sulfuric acid.
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Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 30 studies.
Reviews & meta-analyses: 2 · 2016–2025
Showing all 30 studies, sorted by most relevant.
M. Basuini, A. El-Hais, M. Dawood, et al.
Aquaculture, 2016
Maria Arena, D. Auteri, S. Barmaz, et al.
EFSA Journal, 2018
The conclusions of the EFSA following the peer review of the initial risk assessments carried out by the competent authorities of the rapporteur Member State, France, and co-rapporteur Member State, Germany, for the pesticide active substance copper compounds are reported. The context of the peer review was that required by Commission Implementing Regulation (EU) No 844/2012. The conclusions were reached on the basis of the evaluation of the representative uses of copper compounds as a fungicide on grapes, tomatoes and cucurbits. The reliable end points appropriate for use in regulatory risk assessment are presented. Missing information identified as being required by the regulatory framework is listed. Concerns are identified.
Abstract licence: CC BY-ND
Hongbin Wu, Hongrui Guo, Huan Liu, et al.
Ecotoxicology and environmental safety, 2020
- Endoplasmic Reticulum Chaperone BiP
- Liver
- Mice, Inbred ICR
Yanliang Zhao, F. Liu, Kaijin Zhu, et al.
Advanced Composites and Hybrid Materials, 2022
Seyyed Morteza Hoseini, A. Hedayati, Ali Taheri Mirghaed, et al.
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie, 2016
- Carps
- Copper
- Kidney
Samaneh Hajimohammadi, S. Gharibi, Vahid Pourbarkhordar, et al.
The Egyptian Journal of Internal Medicine, 2022
Abstract Background Copper sulfate is a bright blue crystal used primarily for agricultural purposes, as a pesticide, disinfectant, feed, and soil additive. Acute volunteer poisoning of copper sulfate is not common in the world and in Iran. Case presentation We reported the case of a 15-year-old girl who presented to the emergency department after ingestion of an unknown amount of copper sulfate following a struggle at school. She had become acquainted with the toxic compound through school textbooks. On admission to the hospital, she had abdominal pain and a sore throat with a normal serum copper level. The patient stated that she had three episodes of bluish vomiting. She underwent symptomatic treatment and was monitored for 3 days. The outcome was favorable, and she had no signs and symptoms of organ failure. Conclusions As a result, copper sulfate poisoning depending on the consumed dose can be mild or very severe with a high mortality rate. The authors discuss the various pathogenesis and treatments of this rare poisoning by reviewing the available literature.
Abstract licence: CC BY
S. Naz, Riaz Hussain, Guangbin Zhang, et al.
Frontiers in Veterinary Science, 2023
Despite being an essential trace element for numerous metabolic processes and micronutrients, copper (Cu) has induced adverse effects on the environment and public health due to its continuous and widespread use for the last several decades. The current study assessed the hematological and histopathological alterations in the freshwater fish ( Labeo rohita ) exposed to graded concentrations of copper sulfate. For this purpose, L. rohita fish ( n = 72), weighing ~200–215 g, were randomly divided into four experimental groups and then exposed to acute doses of CuSO 4 , i.e., control, 0.28, 0.42, and 0.56 μgL −1 . For comparative analysis of hematological and biochemical changes, blood/serum samples were obtained on 12, 24, and 36 days. Overall, the body weight of fish decreased with the time and dose of CuSO 4 ; as the dose increases, body weight decreases. Dose and time-dependent results were observed in other parameters also. Results showed a significant increase in leukocytes, whereas red blood cells count, Hb, and Hct were significantly reduced in treated groups compared to the control. The mean corpuscular hemoglobin (MHC) and mean corpuscular hemoglobin concentration (MCHC) showed a non-significant decrease in treated groups compared to the control group. Serum biochemical parameters, including total proteins, albumin, and globulin, decreased significantly ( p < 0.05). At the same time, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glucose, and cholesterol were significantly ( p < 0.05) increased in the treated groups compared to the control group. Significantly ( p < 0.05) increased levels of lipid peroxidation while decreased values of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (RGSH) in the blood of fish were recorded. Histopathological examination of fish gills, liver, and kidneys showed inflammation and degenerative changes due to CuSO 4 exposure. In the brain tissue, degenerative changes like neuron necrosis, intracellular edema, cytoplasmic vacuolization, and congestion were observed. In conclusion, the study indicates that exposure to copper sulfate, even in smaller concentrations, can cause adverse hematological and histopathological changes in L. rohita fish.
Abstract licence: CC BY
R. Guo, Hui Wang, Y. Suh, et al.
BMC Genomics, 2016
- Genome
- Antioxidants
- Gene Expression Regulation
BACKGROUND: Harmful algal blooms (HABs) caused by the dinoflagellate Cochlodinium polykrikoides lead to severe environmental impacts in oceans worldwide followed by huge economic losses. Algicide agent copper sulfate (CuSO4) is regard as an economical and effective agent for HABs mitigation; its biochemical and physiological effects were revealed in C. polykrikoides. However, molecular mechanisms of CuSO4 effect on the C. polykrikoides, even other HAB species, have not been investigated. The present study investigated the transcriptional response of C. polykrikoides against CuSO4 treatments, with the aim of providing certain molecular mechanism of CuSO4 effect on the C. polykrikoides blooms. RESULTS: RNA-seq generated 173 million reads, which were further assembled to 191,212 contigs. 43.3 %, 33.9 %, and 15.6 % of contigs were annotated with NCBI NR, GO, and KEGG database, respectively. Transcriptomic analysis revealed 20.6 % differential expressed contigs, which grouped into 8 clusters according to K-means clustering analysis, responding to CuSO4; 848 contigs were up-regulated and 746 contigs were down-regulated more than 2-fold changes from 12 h to 48 h exposure. KEGG pathway analysis of eukaryotic homologous genes revealed the differentially expressed genes (DEGs) were involved in diverse pathway; amongst, the genes involved in the translation, spliceosome, and/or signal transduction genes were highly regulated. Most of photosystem related genes were down-regulated and most of mitochondria related genes were up-regulated. In addition, the genes involved in the copper ion binding or transporting and antioxidant systems were identified. Measurement of chlorophyll fluorescence showed that photosynthesis was significantly inhibited by CuSO4 exposure. CONCLUSIONS: This study reported the first transcriptome of the C. polykrikoides. The widely differential expressed photosystem genes suggested photosynthetic machinery were severely affected, and may further contribute to the cell death. Furthermore, gene translation and transcription processes may be disrupted, inhibiting cell growth and proliferation, and possibly accelerating cell death. However, antioxidant systems resistant to CuSO4 caused stress; mitochondrion may compensate for photosynthesis efficiency decreasing caused energy deficiency. In addition, various signal transduction pathways may be involved in the CuSO4 induced regulation network in the C. polykrikoides. These data provide the potential transcriptomic mechanism to explain the algicide CuSO4 effect on the harmful dinoflagellate C. polykrikoides.
Abstract licence: CC BY
N. Mroczek-Sosnowska, M. Łukasiewicz, A. Wnuk, et al.
Journal of the science of food and agriculture, 2016
Zhifei Yang, Fangfang Feng, Wenwen Jiang, et al.
Materials science & engineering. C, Materials for biological applications, 2021
- Cellulose
- Copper
- Anti-Bacterial Agents
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
13-33 days
Mechanism
This drug is an essential trace element for the functioning of many metalloenzym…
Food interactions
None known
Human targets
None mapped
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 to 3 hours
[L1823]
Based on studies with radioactive isotopes of copper, most copper is absorbed from the stomach
and duodenum of the gastrointestinal tract.…
Half-life
13-33 days
[A32221]
Protein binding
65-70%
[L1838]
The…
Volume of distribution
110 mg
Metabolism
1 to 3 hours
Elimination
80%
[L1823]
Metabolism…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Copper is an essential trace element and an important catalyst for heme synthesis and iron absorption. After zinc and iron, copper is the third most abundant trace element found in the human body. Copper is a noble metal and its properties include high thermal and electrical conductivity, low corrosion, alloying ability, and malleability. Copper is a component of intrauterine contraceptive devices (IUD) and the release of copper is necessary for their important contraceptive effects. The average daily intake of copper in the USA is approximately 1 mg Cu with the diet being a primary source [A32221].
Interestingly, the dysregulation of copper has been studied with a focus on neurodegenerative diseases, such as Wilson’s disease, Alzheimer’s disease, and Parkinson’s disease. Data from clinical observations of the neurotoxic effects of copper may provide the basis for future treatments affecting copper and its homeostasis [L1830].
Copper and copper containing compounds are broadly used in medical practice. Metallic copper is used already for many years in dental fillings and in copper intrauterine devices (IUD) for reversible contraception. Ointments containing copper, which release copper ions that are absorbed by the skin in the management of cramps, disturbances of renal function, peripheral, venous hypostatic circulatory disturbances, rheumatic disease and swelling associated with trauma.
There are also cosmetic facial creams containing copper as their main active ingredient .
[L1828]
Copper sulfate ingestion (accidental or deliberate) is a rare form of poisoning usually limited to the Indian subcontinent. Though the rates are on the decline, it is essential that physicians are aware of its lethal complications and management strategies. The main complications of copper sulfate ingestion include intravascular hemolysis, methemoglobinaemia, acute kidney injury, and rhabdomyolysis .
[L1827]
Severe gastrointestinal effects may occur with acute overdosage.
In extreme or long-term overdosage, symptoms may be similar to those of Wilson's disease, a disease in which the liver does not filter copper adequately and copper accumulates in the liver, brain, eyes, and other organs. Gradually, high copper levels may cause life-threatening organ damage .
[L1823]
Ingestion of more than 15 mg of copper has been reported to be toxic to humans. In a survey of human clinical case studies, 5.3 mg/day was the lowest oral dose at which local gastrointestinal irritation was seen.
Ingestion of gram quantities of copper sulfate resulted in death by suicide, whereas less severe effects were reported from estimated copper doses of 40 to 50 mg from ingestion of carbonated beverages in contact with copper containers. Limited data are available on the chronic toxicity of copper. The hazard from dietary intakes of up to 5 mg/day appears to be low .
[L1838]
Treatment of cupric sulfate toxicity is symptomatic and may involve the use of a chelating agent (e.g. penicillamine, trientine and zinc) to remove any excessive metal that has been absorbed.
In addition, dialysis may be useful .
[L1821][L1823]
It is involved in erythropoiesis & leukopoiesis, bone mineralization, elastin and collagen cross-linking, oxidative phosphorylation, catecholamine metabolism, melanin formation & antioxidant protection of cells [L1828].
Cupric sulfate may also have a role in iron turnover, ascorbic acid metabolism, phospholipid metabolism, myelin formation, glucose homeostasis, and cellular immune defense [L1823].
After the metal passes through the basolateral membrane it is transported to the liver, attached to serum albumin. The liver is the critical organ for the homeostasis of copper. The copper is then prepared for excretion through the bile or incorporation into various proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes [L1829].
In the dermis, copper promotes dermal fibroblasts proliferation, upregulates collagen (types I, II, and V) and elastin fiber components (elastin, fibrillins) production by fibroblasts, through the induction of TGF-β, promotes heat shock protein-47, important for collagen fibril formation, serves as a cofactor of LOX enzyme required for extracellular matrix protein cross-linking, stabilizes the skin ECM once formed, as increased crosslinking of collagen and elastin matrices occurs in a copper dose dependant manner, serves as a cofactor of superoxide dismutase, an antioxidant enzyme in the skin, essential for protection against free radicals, inhibits cellular oxidative effects such as membrane damage and lipid peroxidation, acts as a cofactor of tyrosinase, a melanin biosynthesis essential enzyme responsible for skin and hair pigmentation [L1828].
In reference to its role as a biocide, copper is an essential nutrient for many organisms. It acts as a cofactor in respiration, and therefore copper is required for aerobic metabolism. Accumulation of copper ions or intracellular release of free copper ions from proteins lead to cell damage. Copper catalyzes reactions that result in the production of hydroxyl radicals through the Fenton and Haber-Weiss reactions. The highly reactive oxygen intermediates lead to lipid peroxidation and oxidation of proteins. Free copper ions oxidize sulfhydryl groups, such as cysteine, in proteins or the cellular redox buffer glutathione. In particular, copper ions inactivate proteins by damaging Fe-S clusters in cytoplasmic hydratases [L1841].
Copper is one of the nine essential minerals for humans, as it plays an imperative role in various physiological pathways in basically all human tissue, as well as in the health of the dermis and epidermis [L1828].
In addition to the above, copper is essential in wound healing, as it promotes angiogenesis and skin extracellular matrix formation and stabilization [L1828].
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L1823]
Based on studies with radioactive isotopes of copper, most copper is absorbed from the stomach
and duodenum of the gastrointestinal tract.
Maximum blood copper levels are observed within 1 to 3 hours following oral administration, and about 50 percent of ingested copper was absorbed. Copper absorption is proposed to occur by two mechanisms, one energy- dependent and the other enzymatic. Factors that can interfere with copper absorption include competition for binding sites with zinc, interactions with molybdenum and sulfates, chelation with phytates, and inhibition by ascorbic acid (vitamin C) .
[L1838]
Copper absorbed from the gastrointestinal tract is transported rapidly to blood serum and deposited in the liver bound to metallothionein .
[L1838]
From 20 to 60% of the dietary copper is absorbed .
[L1819]
[A32221]
[L1838]
The bioavailability of copper from the diet is about 65-70% depending on a variety of factors including chemical form, interaction with other metals, and dietary components .
[A32221]
[L1828]
The distribution of copper is affected by sex, age, and the amount of copper in the diet. Brain and liver have the highest tissue levels (about one-third of the total body burden), with lesser concentrations found in the heart, spleen, kidneys, and blood. The iris and choroid of the eye have very high copper levels .
[L1838]
Erythrocyte copper levels are generally stable, however, plasma levels fluctuate widely in association with the synthesis and release of ceruloplasmin.
Plasma copper levels during gestation may be 2-3 times levels measured before pregnancy, due to the increased synthesis of ceruloplasmin .
[L1838]
[L1838]
Copper absorbed from the intestine is transported quickly into blood serum and deposited in the liver bound to metallothionein.
It is released and incorporated into ceruloplasmin, a copper-specific transport protein. The remaining copper in the serum binds to albumin or amino acids or is contained in the erythrocytes. About 80 percent of the absorbed copper is bound to liver metallothionein; the remainder is included into cytochrome c oxidase or sequestered by lysosomes .
[L1838]
[L1823]
Metabolism studies show that persons with daily intakes of 2-5 mg of copper per day absorbed 0.6 to 1.6 mg (32%), excreted 0.5 to 1.3 mg in the bile, passed 0.1 to 0.3 mg directly into the bowel, and excreted 0.01 to 0.06 mg in the urine. As the data indicate, urinary excretion plays a negligible role in copper clearance, and the main route of excretion is in the bile.
Other nonsignificant excretory routes include saliva, sweat, menstrual flow, and excretion into the intestine from the blood .
[L1838]
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
PMID:16150804
Copper ions provide a large number of enzymatic activites.
Oxidizes highly toxic ferrous ions to the ferric state for further incorporation onto apo-transferrins, catalyzes Cu(+) oxidation and promotes the oxidation of biogenic amines such as norepinephrin and serotonin .
PMID:14623105 PMID:4643313 PMID:5912351
Provides Cu(2+) ions for the ascorbate-mediated deaminase degradation of the heparan sulfate chains of GPC1 (By similarity). Has glutathione peroxidase-like activity, can remove both hydrogen peroxide and lipid hydroperoxide in the presence of thiols .
PMID:10481051
Also shows NO-oxidase and NO2 synthase activities that determine endocrine NO homeostasis PMID:16906150
ATC V03AB20
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Cupric sulfate
Matched from: Copper sulfate
Additional database identifiers
Drugs Product Database (DPD)
582
Drugs Product Database (DPD)
6989
Drugs Product Database (DPD)
6990
ChemSpider
22870
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8582
GenAtlas
PAH
GeneCards
PAH
GenBank Gene Database
K03020
GenBank Protein Database
189937
Guide to Pharmacology
1240
UniProt Accession
PH4H_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6664
GeneCards
LOX
Guide to Pharmacology
3097
UniProt Accession
LYOX_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7419
GenAtlas
MT-CO1
GeneCards
MT-CO1
GenBank Gene Database
V00662
GenBank Protein Database
13006
UniProt Accession
COX1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2295
GenAtlas
CP
GeneCards
CP
GenBank Gene Database
M13699
GenBank Protein Database
180256
UniProt Accession
CERU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Molecular structure
ATC classifications (Wikidata)
Linked open data from Wikidata (Q107184), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. Molecular structure images from Wikimedia Commons.