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1 branded products available
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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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0.
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 the 50 most relevant studies.
Reviews & meta-analyses: 12 · Randomised trials: 7 · 1966–2025
Showing the 50 most relevant studies, sorted by most relevant.
Ding X, Sun S, Zhang J, et al.
2024
Background: The application of ferric citrate therapy has yielded unexpected benefits in recent years for Chronic kidney disease patients suffering from hyperphosphatemia and iron deficiency -anaemia. Despite this, earlier research on the impact of ferric citrate on NDD-CKD has been contentious. Objective: The goal of the meta-analysis is to evaluate the evidence regarding the advantages and dangers of ferric citrate for the treatment of hyperphosphatemia and iron deficiency anaemia in NDD-CKD patients. Methods: Between the start of the study and June 2022, we searched PubMed, Embase, Cochrane, EBSCO, Scopus, Web of Science, Wan Fang Data, CNKI, and VIP databases for randomised controlled trials of iron citrate for hyperphosphatemia and anaemia in patients with NDD-CKD. For binary categorical data, risk ratios (OR) were employed, and for continuous variables, weighted mean differences The effect sizes for both count and measurement data were expressed using 95% confidence intervals Results: The meta-analysis includes eight trials with a total of 1281 NDD-CKD patients. The phosphorus-lowering effect of ferric citrate was greater compared to the control group (WMD, -0.55, 95% CI, -0.81 to -0.28; I2 = 86%, p p > 0.05; I2 = 61.9%), PTH (WMD, -0.10; 95% CI, -0.44 to 0.23; I2 = 75%, p > 0.05) and iFGF23 (WMD, -7.62; 95% CI, -21.18 to 5.94; I2 = 20%, p > 0.05) levels were not statistically different after ferric citrate treatment compared to control treatment. Furthermore, ferric citrate increased iron reserves and haemoglobin. The ferric citrate group had considerably greater levels than the controls. Ferric citrate, on the other hand, may raise the risk of constipation, diarrhoea, and nausea. Conclusion: This meta-analysis found that ferric citrate had a beneficial effect in the treatment of NDD-CKD, particularly in reducing blood phosphorus levels when compared to a control intervention. It also shown that ferric citrate has a favourable effect on iron intake and anaemia management. In terms of safety, ferric citrate may increase the likelihood of gastrointestinal side effects.
Abstract licence: CC BY
Khashayar Sakhaee, Taft Bhuket, Beverley Adams-Huet, et al.
American Journal of Therapeutics, 1999
Li Li, Xin Zheng, Jin Deng, et al.
Renal Failure, 2022
M. Attinger, Stefanie von Felten, Claudia Lourenço Rodrigues, et al.
Clinical and Translational Science, 2025
- Magnesium Compounds
- Citric Acid
- Thyroxine
Maryam Taheri, Sanaz Tavasoli, Saba Jalali, et al.
2024
Abstract Background Calcium supplementation is only recommended to treat enteric hyperoxaluria, and its effect on idiopathic hyperoxaluria has not been thoroughly assessed. In this study, we compare the effect of calcium citrate supplementation with adequate dietary calcium intake on 24-hour urine (24-U) oxalate, calcium, and calcium oxalate supersaturation index (Ca Ox SS). Subjects: In a parallel-group controlled randomized clinical trial, 72 recurrent calcium stone formers with idiopathic hyperoxaluria were recruited from a tertiary stone prevention clinic in 2019–2020. 24-hour urine analyses and filling the 24-hour food recall were done at baseline and after eight weeks of intervention. Finally, 44 patients completed the study protocol. The participants were randomly assigned to receive adequate calcium through diet or taking 800 mg calcium citrate (in two divided doses with lunch and dinner) with a limited intake of dairy products. The study’s outcome was the change of 24-U Ox, Ca, and CaOx SS index after intervention. Results Findings showed that both interventions significantly reduced 24-U Ox (B Time effect: -10.06, 95% CI: -13.70, -6.42; p < 0.001) and CaOx SS index (B Time effect: -2.54, 95% CI: -4.06, -1.02; p = 0.001). After adjusting the effect of potential confounders through a Random-effects ML regression, the reduction of 24-U Ox remained significant. There was no significant increase in 24-U Ca in both intervention groups (p = 0.269). Conclusions Calcium citrate supplementation effectively reduces 24-U Ox levels comparably to adequate dietary calcium intake, without significantly raising 24-U Ca levels, offering a viable management option for calcium stone formers with idiopathic hyperoxaluria.
Abstract licence: CC BY 4.0
J. D. Cook, S. Dassenko, P. Whittaker
The American journal of clinical nutrition, 1991
R. Womack, Fabian Berru, Bhupesh Panwar, et al.
Clinical journal of the American Society of Nephrology : CJASN, 2020
Qiao-Feng Tian, Yan Fan, Li Hao, et al.
Critical Reviews in Food Science and Nutrition, 2021
A. Naciu, G. Tabacco, J. Bilezikian, et al.
Journal of Bone and Mineral Research, 2022
S. Bristow, G. Gamble, A. Stewart, et al.
The British journal of nutrition, 2014
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
4 days
Mechanism
Iron is required to maintain optimal health, particularly for helping to form re…
Food interactions
6 warnings
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
5 – 10%
Half-life
2-4 months
Protein binding
90%
[L2240]
…
Volume of distribution
60%
[A32524]
The remainder of the iron is found in muscle tissues (as a part of myoglobin), and…
Metabolism
Elimination
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ferrous sulfate is a synthetic agent used in the treatment of iron deficiency. It is the gold standard of oral iron therapy in the UK and many other countries.[L2234][L2246]
[A190804][L2240][L11800]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 130 interactions
[L2233]
Overdose information
Iron containing products are the primary cause of drug overdose in children under 6 years of age.
[L11767]
Iron is toxic to the gastrointestinal system, cardiovascular system, in addition to central nervous system. The most early reported effects following the excess ingestion of iron include nausea, flatulence, abdominal pain, diarrhea, constipation, and black/tarry stools.
[L2234]
Symptoms of overdose in the later stages include bluish lips, fingernails, and palms, drowsiness, tachycardia, seizures, metabolic acidosis, hepatic injury, and cardiovascular dysfunction.
Sequelae of iron sulfate overdose include intestinal obstruction, pyloric stenosis, and gastric scarring.
[L2240]
If the patient is comatose or seizing, gastric lavage with sodium bicarbonate should be performed. Deferoxamine is the antidote for iron poisoning. Other supportive treatments to support fluid and electrolyte balance and correct metabolic acidosis are also advised.
[L2240]
Hospitalization should continue for 24 h after the patient becomes asymptomatic to monitor for delayed onset of shock/gastrointestinal bleeding.
Taking iron in supplement form, such as ferrous sulfate, allows for more rapid increases in iron levels when dietary supply and stores are not sufficient.[L2175] Iron is transported by the divalent metal transporter 1 (DMT1) across the endolysosomal membrane to enter the macrophage. It can then can be incorporated into ferritin and be stored in the macrophage or carried of the macrophage by ferroportin. This exported iron is oxidized by the enzyme to ceruloplasmin to Fe3+, followed by sequestration by transferrin for transport in the serum to various sites, including the bone marrow for hemoglobin synthesis or into the liver.[A32524] Iron combines with porphyrin and globin chains to form hemoglobin, which is critical for oxygen delivery from the lungs to other tissues.[L2263]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L2240]
Gastrointestinal absorption of iron occurs via strict regulation by the enterocyte and duodenal cytochrome and ferric reductase enzymes.
[A32524][L11794]
The hormone hepcidin heavily regulates iron absorption and distribution throughout the body.
[L11800]
The median time to maximum serum concentration (Tmax) is generally 4 hours after administration. Between 2-8 hours post administration, average serum iron concentrations fluctuate by 20%, according to one study.
[A32500]
Bioavailability of iron depends on whether it is administered in a film coated tablet or enteric coated tablet.
One pharmacokinetic study in healthy volunteers revealed a 30% bioavailability for enteric coated tablets. The AUC of enteric coated tablets varied between a lower limit of -46.93 to 5.25 µmolxh/l. Cmax is higher for film coated tablets, ranging from 3.4 to 22.1 µmol/h/l.
[A190933]
It is advisable to take ferrous sulfate with ascorbic acid, as this practice may increase absorption.
[L11800][L11794]
Avoid antacids, tea, coffee,tea, dairy products, eggs, and whole-grain bread for at least an hour after taking ferrous sulfate.
Calcium can decrease iron absorption by 33% if taken concomitantly.
[L2240]
[L2240]
[L2240]
It is bound to transferrin and ferritin, ferroportin, myoglobin, and other enzymes.
[L11800][L11794]
Approximately 60% of iron is located in the erythrocytes as part of hemoglobin.
[A32524]
[A32524]
The remainder of the iron is found in muscle tissues (as a part of myoglobin), and in a variety of different enzymes, as well as in storage form. Most stored iron is in the form of ferritin, which can be found in the liver, bone marrow, spleen and, and muscle. Iron crosses the placenta and is also found in breast milk.
[L2240]
[A32524]
There are three proteins that serve to regulate the storage and transport of ingested iron. The first protein , transferrin, transports iron in both the plasma and extracellular fluid.
Ceruloplasmin in the plasma and hephaestin on the enterocyte participate in the oxidation and binding of iron to transferrin. The main role of transferrin is the chelation of iron to prevent the production of reactive oxygen species, while facilitating its transport into cells.
[L11794]
The transferrin receptor, located on many cells that require iron, binds the transferrin complex and internalizes this complex. Ferritin is a protein that stores iron, making it readily available for body requirements.
[A32524]
[L11794]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:17109629 PMID:17293870 PMID:22736759 PMID:25326704 PMID:25491917
Selectively transports various divalent metal cations, in decreasing affinity: Cd(2+) > Fe(2+) > Co(2+), Mn(2+) >> Zn(2+), Ni(2+), VO(2+) .
PMID:17109629 PMID:17293870 PMID:22736759 PMID:25326704 PMID:25491917
Essential for maintenance of iron homeostasis by modulating intestinal absorption of dietary Fe(2+) and TF-associated endosomal Fe(2+) transport in erythroid precursors and other cells (By similarity). Enables Fe(2+) and Mn(2+) ion entry into mitochondria, and is thus expected to promote mitochondrial heme synthesis, iron-sulfur cluster biogenesis and antioxidant defense (By similarity) .
PMID:24448823
Can mediate uncoupled fluxes of either protons or metal ions
PMID:15692071 PMID:22178646 PMID:22682227 PMID:24304836 PMID:29237594 PMID:29599243 PMID:30247984
Transports iron from intestinal, splenic, hepatic cells, macrophages and erythrocytes into the blood to provide iron to other tissues (By similarity). Controls therefore dietary iron uptake, iron recycling by macrophages and erythrocytes, and release of iron stores in hepatocytes (By similarity). When iron is in excess in serum, circulating HAMP/hepcidin levels increase resulting in a degradation of SLC40A1, thus limiting the iron efflux to plasma PMID:22682227 PMID:29237594 PMID:32814342
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Ferrous sulfate anhydrous
Matched from: Ferrous calcium citrate
Additional database identifiers
Drugs Product Database (DPD)
309
Drugs Product Database (DPD)
4839
ChemSpider
22804
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4824
GenAtlas
HBA1
GeneCards
HBA2
GenBank Gene Database
J00153
GenBank Protein Database
386764
UniProt Accession
HBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11763
GeneCards
TFRC
UniProt Accession
TFR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11762
GeneCards
TFR2
UniProt Accession
TFR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2295
GenAtlas
CP
GeneCards
CP
GenBank Gene Database
M13699
GenBank Protein Database
180256
UniProt Accession
CERU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15598
GeneCards
HAMP
UniProt Accession
HEPC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11740
GenAtlas
TF
GeneCards
TF
GenBank Gene Database
M12530
GenBank Protein Database
339453
UniProt Accession
TRFE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4866
GeneCards
HEPH
UniProt Accession
HEPH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:20797
GeneCards
CYBRD1
UniProt Accession
CYBR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10908
GeneCards
SLC11A2
Guide to Pharmacology
967
UniProt Accession
NRAM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10909
GeneCards
SLC40A1
UniProt Accession
S40A1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72