Ferric maltol (iron 30mg) capsules
Requires a prescription from a doctor or prescriber
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1 branded products available
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Feraccru 30mg capsules
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
60 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
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
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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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. 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 the 50 most relevant studies.
Reviews & meta-analyses: 9 · Randomised trials: 9 · 1993–2026
Showing the 50 most relevant studies, sorted by most relevant.
P. Kalra, J. Cleland, M. Petrie, et al.
Lancet, 2022
Malireddi A, Abera M, Suresh SB, et al.
2024
Ulcerative colitis and Crohn's disease, two types of inflammatory bowel disease (IBD), often cause anemia, primarily due to iron deficiency and chronic inflammation. Anemia negatively affects patients' daily functioning and quality of life, causing symptoms including headaches, exhaustion, and dyspnea. In IBD, iron deficiency arises from reduced intake, chronic blood loss, and impaired absorption. While oral iron supplements are commonly used, their poor absorption and gastrointestinal side effects limit their effectiveness, especially in IBD patients. The European Crohn's and Colitis Organization (ECCO) recommends intravenous iron, such as ferric carboxymaltose (FCM), as iron deficiency anemia in IBD can be managed using a safe and efficient substitute. With regard to treating iron deficiency anemia in patients with IBD, the purpose of this study is to investigate the safety and effectiveness of intravenous ferric carboxymaltose. We conducted a thorough search of medical databases, such as the Cochrane library, PubMed, and ResearchGate, to gather relevant literature. Using the databases, we found a total of 297 relevant articles. The identified studies have been screened, eligibility criteria have been introduced, and 14 research studies were selected for inclusion. This review adhered to the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines, with quality assessments conducted using the Cochrane risk of bias 2 scale for randomized tests and the Newcastle-Ottawa scale for observational examination. We reviewed 14 research articles involving 2,493 patients. Among these, five were randomized controlled trials (RCTs), and the remaining nine were observational studies. The primary outcomes assessed were the therapeutic response (defined as hemoglobin ≥2 g/dL rise or normalization, improvement in iron profile parameters) and any adverse effects after FCM is administered to IBD patients. FCM was found to be highly effective in improving hemoglobin and iron profile parameters, with a generally good safety profile. Ferric carboxymaltose was the most efficient and well-tolerated intravenous (IV) iron formulation, proving safer and more effective than other iron therapies in patients suffering from IBD. However, severe hypophosphatemia can lead to serious complications, including heart failure, pulmonary failure, rhabdomyolysis, fractures, and osteomalacia, which may worsen its long-term impact. Therefore, the risk of hypophosphatemia associated with prolonged FCM use requires careful monitoring and further research to ensure its long-term safety and assess its effects on patients' quality of life.
Abstract licence: CC BY
S. Anker, T. Friede, Javed Butler, et al.
JAMA, 2025
R. Mentz, Jyotsna Garg, F. Rockhold, et al.
The New England journal of medicine, 2023
Savarese G, von Haehling S, Butler J, et al.
2023
- Cardiovascular Diseases
- Anemia
- Anemia, Iron-Deficiency
Iron deficiency (ID) is common in patients with cardiovascular disease. Up to 60% of patients with coronary artery disease, and an even higher proportion of those with heart failure (HF) or pulmonary hypertension have ID; the evidence for cerebrovascular disease, aortic stenosis and atrial fibrillation is less robust. The prevalence of ID increases with the severity of cardiac and renal dysfunction and is probably more common amongst women. Insufficient dietary iron, reduced iron absorption due to increases in hepcidin secondary to the low-grade inflammation associated with atherosclerosis and congestion or reduced gastric acidity, and increased blood loss due to anti-thrombotic therapy or gastro-intestinal or renal disease may all cause ID. For older people in the general population and patients with HF with reduced ejection fraction (HFrEF), both anaemia and ID are associated with a poor prognosis; each may confer independent risk. There is growing evidence that ID is an important therapeutic target for patients with HFrEF, even if they do not have anaemia. Whether this is also true for other HF phenotypes or patients with cardiovascular disease in general is currently unknown. Randomized trials showed that intravenous ferric carboxymaltose improved symptoms, health-related quality of life and exercise capacity and reduced hospitalizations for worsening HF in patients with HFrEF and mildly reduced ejection fraction (<50%). Since ID is easy to treat and is effective for patients with HFrEF, such patients should be investigated for possible ID. This recommendation may extend to other populations in the light of evidence from future trials.
Abstract licence: CC BY-NC
T. Jones, A. Forsythe, M. Sampson, et al.
Value in Health, 2018
Koppelman LJM, Loveikyte R, Goetgebuer RL, et al.
2026
- Inflammatory Bowel Diseases
- Anemia, Iron-Deficiency
- Iron
BackgroundIron deficiency anaemia (IDA) is common in inflammatory bowel disease (IBD) and impairs quality of life. Hepcidin, the regulator of systemic iron homeostasis, may predict response to iron therapy; however, its utility in IBD remains unclear. This study evaluated whether baseline hepcidin predicts response to oral and intravenous (IV) iron in active IBD to guide personalised treatment.MethodsNinety adults with active IBD and iron deficiency (with or without anaemia) from two randomised trials received IV iron, oral ferrous fumarate (FF) or oral ferric maltol (FM). Response at 12 weeks was defined as haemoglobin increase ≥ 1.2 mmol/L (19.3 g/L) or normalisation in IDA or ferritin > 100 μg/L and transferrin saturation > 20% in iron deficient patients. Baseline iron indices including ferritin, hepcidin, and soluble transferrin receptor (sTfR) were measured. Logistic regression and receiver operating curve analyses evaluated predictive performance.ResultsBaseline hepcidin strongly predicted response to iron therapy: AUC(FF): 0.86, 95% CI: 0.71-1.00 and AUC(IV): 0.63, 95% CI: 0.30-0.96. Hepcidin > 2.68 μg/mL identified non-responders to FF with 89% sensitivity and 77% specificity. Each twofold increase in baseline hepcidin or ferritin reduced the odds of response [log2(hepcidin) OR: 0.71, 95% CI: 0.56-0.89; log2(ferritin) OR: 0.38, 95% CI: 0.21-0.69]. Higher transferrin/log10(ferritin) (OR: 2.95, 95% CI: 1.38-6.30) and sTfR/log10(ferritin) ratios (OR: 1.29, 95% CI: 1.05-1.59) increased likelihood of response.ConclusionBaseline hepcidin supports route selection for iron therapy: higher levels favour IV iron, while lower levels indicate likely oral response. Ferritin-based indices, notably transferrin/log10(ferritin), offer pragmatic alternatives where hepcidin testing is unavailable.Trial registrationClinicalTrials.gov identifier: NCT05581420 and NCT05456932.
Abstract licence: CC BY
Gass D, Freiberg A, Auth MKH, et al.
2026
Alexandra Marley, E. Dickson, Blessing Oduh, et al.
Flash Posters, 2026
P. Pergola, N. Kopyt
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2021
- Anemia, Iron-Deficiency
- Renal Insufficiency, Chronic
- Iron Deficiencies
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
0.7h
Mechanism
Ferric maltol dissociates as the iron atom is donated to unknown iron uptake mec…
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.5-3.0 hours
Half-life
0.7h
[L11010]
Protein binding
[L10974][L11010]
Volume of distribution
[L10974][L11010]
Metabolism
[L10974]
Elimination
39.8-60%
[L10974]
…
Clearance
[L10974][L11010]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ferric maltol was granted FDA Approval on 25 July 2019.[L10974]
[L10974]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 134 interactions
[L10974]
Patients experiencing an overdose may present with nausea, vomiting, abdominal pain, diarrhea, hypoperfusion, metabolic acidosis, and systemic toxicity.
[L10974]
Overdoses should be treated with symptomatic and supportive measures which may include the use of desferroxamine.
[L11010]
Hemodialysis will not remove iron but will remove the iron-desferroxamine complex.
[L11010]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A189306][L10974]
Mean serum iron increases by 14±6µmol/L in iron deficient patients following a single dose.
[A189288]
a 60mg dose is approximately 14% bioavailable.
[A189300]
60 minutes after injection of radiolabelled ferric maltol, 11+2% of the dose is present in the bone marrow, 18±1% is present in the liver, and 2.6±1% is in the urine.
[A189297]
Maltol has an AUC of 0.022-0.205h\*µg/mL and maltol glucuronide has an AUC of 9.83-30.9h\*µg/mL.
[L11010]
[L11010]
[L10974][L11010]
[L10974][L11010]
[L10974]
[L10974]
Iron and ferric maltol are not excreted in the urine and unabsorbed ferric maltol is eliminated in the feces.
[A189306]
[L10974][L11010]
Proteins and enzymes this drug interacts with in the body
Integrin alpha-IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain (By similarity). Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen .
PMID:9111081
This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. Fibrinogen binding enhances SELP expression in activated platelets (By similarity).
ITGAV:ITGB3 binds to fractalkine (CX3CL1) and acts as its coreceptor in CX3CR1-dependent fractalkine signaling .
PMID:23125415 PMID:24789099
ITGAV:ITGB3 binds to NRG1 (via EGF domain) and this binding is essential for NRG1-ERBB signaling .
PMID:20682778
ITGAV:ITGB3 binds to FGF1 and this binding is essential for FGF1 signaling .
PMID:18441324
ITGAV:ITGB3 binds to FGF2 and this binding is essential for FGF2 signaling .
PMID:28302677
ITGAV:ITGB3 binds to IGF1 and this binding is essential for IGF1 signaling .
PMID:19578119
ITGAV:ITGB3 binds to IGF2 and this binding is essential for IGF2 signaling .
PMID:28873464
ITGAV:ITGB3 binds to IL1B and this binding is essential for IL1B signaling .
PMID:29030430
ITGAV:ITGB3 binds to PLA2G2A via a site (site 2) which is distinct from the classical ligand-binding site (site 1) and this induces integrin conformational changes and enhanced ligand binding to site 1 .
PMID:18635536 PMID:25398877
ITGAV:ITGB3 acts as a receptor for fibrillin-1 (FBN1) and mediates R-G-D-dependent cell adhesion to FBN1 .
PMID:12807887
In brain, plays a role in synaptic transmission and plasticity. Involved in the regulation of the serotonin neurotransmission, is required to localize to specific compartments within the synapse the serotonin receptor SLC6A4 and for an appropriate reuptake of serotonin. Controls excitatory synaptic strength by regulating GRIA2-containing AMPAR endocytosis, which affects AMPAR abundance and composition (By similarity).
ITGAV:ITGB3 act as a receptor for CD40LG .
PMID:31331973
ITGAV:ITGB3 acts as a receptor for IBSP and promotes cell adhesion and migration to IBSP PMID:10640428
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
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
Integrin alpha-IIb/beta-3 recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain (By similarity). Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen .
PMID:9111081
This step leads to rapid platelet aggregation which physically plugs ruptured endothelial surface. Fibrinogen binding enhances SELP expression in activated platelets (By similarity).
ITGAV:ITGB3 binds to fractalkine (CX3CL1) and acts as its coreceptor in CX3CR1-dependent fractalkine signaling .
PMID:23125415 PMID:24789099
ITGAV:ITGB3 binds to NRG1 (via EGF domain) and this binding is essential for NRG1-ERBB signaling .
PMID:20682778
ITGAV:ITGB3 binds to FGF1 and this binding is essential for FGF1 signaling .
PMID:18441324
ITGAV:ITGB3 binds to FGF2 and this binding is essential for FGF2 signaling .
PMID:28302677
ITGAV:ITGB3 binds to IGF1 and this binding is essential for IGF1 signaling .
PMID:19578119
ITGAV:ITGB3 binds to IGF2 and this binding is essential for IGF2 signaling .
PMID:28873464
ITGAV:ITGB3 binds to IL1B and this binding is essential for IL1B signaling .
PMID:29030430
ITGAV:ITGB3 binds to PLA2G2A via a site (site 2) which is distinct from the classical ligand-binding site (site 1) and this induces integrin conformational changes and enhanced ligand binding to site 1 .
PMID:18635536 PMID:25398877
ITGAV:ITGB3 acts as a receptor for fibrillin-1 (FBN1) and mediates R-G-D-dependent cell adhesion to FBN1 .
PMID:12807887
In brain, plays a role in synaptic transmission and plasticity. Involved in the regulation of the serotonin neurotransmission, is required to localize to specific compartments within the synapse the serotonin receptor SLC6A4 and for an appropriate reuptake of serotonin. Controls excitatory synaptic strength by regulating GRIA2-containing AMPAR endocytosis, which affects AMPAR abundance and composition (By similarity).
ITGAV:ITGB3 act as a receptor for CD40LG .
PMID:31331973
ITGAV:ITGB3 acts as a receptor for IBSP and promotes cell adhesion and migration to IBSP PMID:10640428
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
ATC B03AB10
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)
Ferric maltol
Additional database identifiers
Drugs Product Database (DPD)
309
ChemSpider
148265
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6156
GenAtlas
ITGB3
GeneCards
ITGB3
GenBank Gene Database
J02703
GenBank Protein Database
306786
Guide to Pharmacology
2457
UniProt Accession
ITB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10908
GeneCards
SLC11A2
Guide to Pharmacology
967
UniProt Accession
NRAM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12538
GeneCards
UGT1A6
UniProt Accession
UD16_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6156
GenAtlas
ITGB3
GeneCards
ITGB3
GenBank Gene Database
J02703
GenBank Protein Database
306786
Guide to Pharmacology
2457
UniProt Accession
ITB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10908
GeneCards
SLC11A2
Guide to Pharmacology
967
UniProt Accession
NRAM2_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