Ferrous fumarate 210mg tablets
Available from a pharmacy with pharmacist advice
Used in treatment of iron deficiency anemia.
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Suspected adverse reactions reported for Ferrous fumarate
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15 branded products available
Part of the AadFer brand family (generic: Ferrous fumarate)
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View all licensed products for Ferrous fumarate on the MHRA register
Ferrous fumarate 210mg tablets
Ferrous fumarate 210mg tablets
Ferrous fumarate 210mg tablets
Ferrous fumarate 210mg tablets
Ferrous fumarate 210mg tablets
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)
200 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 BNF/ATC 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
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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 the 50 most relevant studies.
Reviews & meta-analyses: 5 · Randomised trials: 15 · 1989–2026
Showing the 50 most relevant studies, sorted by most relevant.
Guerra Toro HI, Jaramillo AP, Pazmino G, et al.
2026
Iron-deficiency anemia is the most common hematologic disorder in pregnancy. Slow iron repletion, poor gastrointestinal tolerance, and late presentation during gestation often limit the effectiveness of oral ferrous salts, which remain the traditional first-line treatment. Intravenous iron offers faster iron delivery, but its role in routine antenatal care remains uncertain, particularly regarding its long-term safety and cost-effectiveness compared to traditional oral iron treatments. This qualitative systematic review included 10 randomized controlled trials published within the last decade that enrolled pregnant women with iron-deficiency anemia or persistent iron deficiency (defined, where applicable, as ferritin <30 μg/L after approximately four weeks of oral iron therapy) and compared intravenous iron with oral iron or one intravenous formulation with another. Across the included trials, intravenous iron generally produced more rapid ferritin replenishment and, in many studies, a faster rise in hemoglobin than oral therapy. Oral ferrous preparations were associated with more gastrointestinal adverse effects; for example, in one study, gastrointestinal treatment-related events were reported in more women receiving oral ferrous sulfate versus those receiving ferric carboxymaltose. In another trial, nausea/vomiting occurred in greater number of oral-iron recipients versus intravenous ones, while constipation and epigastric discomfort were reported only in the oral group. By contrast, serious intravenous treatment-related events were uncommon in the larger trials. Smaller and medium-sized trials generally favored parenteral iron for hematologic recovery, but the largest pragmatic studies from India, Malawi, and Nigeria showed that biochemical superiority did not consistently translate into lower rates of late-pregnancy anemia or improved major maternal and neonatal outcomes. One head-to-head intravenous trial also suggested practical and hematologic advantages of ferric carboxymaltose over iron sucrose. From a hematology perspective, intravenous iron appears most useful when rapid restoration of iron stores is needed, when adherence to oral therapy is doubtful, or when little time remains before delivery. Future trials should standardize ferritin-based diagnostic criteria, clearly distinguish hematologic from obstetric endpoints, and better define which patients are most likely to derive clinically meaningful benefit from parenteral iron.
Abstract licence: CC BY
Nikolaou A, Assunção R, Cvetković B, et al.
2026
This systematic review, conducted under the COST Action CA20218 "Promoting Innovation of fermented foods" (PIMENTO), aimed to evaluate whether sourdough- and regular-bread fermentation improve iron bioavailability, absorption, and status in humans. Screening of PubMed, Scopus, and Cochrane Library (January 1970-December 2024) identified 8 human intervention studies, in healthy or iron-deficient participants, that met inclusion criteria. EFSA's scientific guidance for health claim applications, which integrates product characteristics and mechanisms of action to the human studies, was followed, and the extracted data were narratively presented. Results were inconclusive as acute postprandial studies increased non-haem iron bioavailability (especially in low-phytate breads); for example, low-phytate white bread produced a greater 2 h increase in serum iron than high-phytate wholemeal bread (59 vs. 30 μg Fe/100 mL), while exogenous phytase increased iron absorption by 50% for ferrous sulfate and 61% for iron bis-glycine chelate. However, long-term trials did not improve, and in one case even decreased, ferritin and total body iron; specifically, in the low-phytate sourdough rye bread group, ferritin declined from 32 ± 7 to 27 ± 6 μg/L and total body iron from 6.9 ± 1.4 to 5.4 ± 1.1 mg/kg over 12 weeks. On the other hand, phytate reduction combined with iron fortification showed positive effects on haemoglobin or prevented iron depletion; in anaemic children, fermented amaranth bread increased haemoglobin [adjusted β = 8.9 g/L (95% CI: 3.5-14.3)] and reduced anaemia prevalence (32% vs. 56%) compared to control bread. Despite convincing mechanistic evidence that the sourdough-fermentation process in bread fabrication improves iron bioavailability, through reduction of phytate, no human studies address this research question with the appropriate control and study quality.Systematic review registrationosf.io/gzt8m.
Abstract licence: CC BY
Patel PN, Mangal D, Singh D
2025
Iron deficiency (ID) is a common and clinically significant comorbidity in patients with heart failure (HF), contributing to reduced exercise capacity, poor quality of life, and increased hospitalization risk. Although intravenous (IV) iron therapy has demonstrated efficacy in improving functional outcomes, the comparative effectiveness of IV vs. oral (per os, or PO) iron supplementation remains uncertain. We conducted a systematic review and network meta-analysis (NMA) of 13 randomized controlled trials (RCTs) evaluating IV iron (ferric carboxymaltose, ferric derisomaltose, iron sucrose), PO iron (ferrous sulfate, ferrous fumarate, polysaccharide, sucrosomial, ferric polymaltose), and placebo in HF patients with ID, analyzed as route-specific class effects. Outcomes analyzed included six-minute walk distance (6MWD), ferritin, transferrin saturation (TSAT), HF hospitalization, all-cause mortality, and cardiovascular (CV) mortality. We used a Hartung-Knapp random-effects framework with Sidik-Jonkman variance, assessed heterogeneity and inconsistency using I2, τ2, design-by-treatment interaction, and node-splitting. Risk of bias was assessed independently by two reviewers using Risk of Bias 2 (RoB 2), and certainty of evidence for all outcomes was graded using GRADE adapted for NMA. Because most contrasts included fewer than 10 RCTs, formal tests for publication bias were not feasible, and potential small-study effects were considered qualitatively in the GRADE assessments. Trials that reported outcomes only as medians and interquartile ranges (IQRs), or baseline values without follow-up data, were excluded from quantitative pooling and described narratively. IV iron significantly improved 6MWD compared to placebo (mean difference (MD) +26.0 m; 95% confidence interval (CI): 18.1 to 33.9), increased ferritin (MD +237.2 μg/L), and reduced the risk of HF hospitalization (risk ratio (RR) 0.79; 95% CI: 0.66 to 0.93), with moderate to high certainty. PO iron showed a comparable, but not statistically significant, mean improvement in 6MWD (MD +35.1 m; 95% CI: -5.2 to +75.4), with wider CIs and inconsistent ferritin and TSAT gains. Neither IV nor PO iron was associated with a significant reduction in all-cause or CV mortality, although a trend toward benefit was observed with IV therapy. Numerical SUCRA values favored IV iron for HF hospitalization (77.9 vs. 57.6 for PO, 14.5 for placebo), ferritin (100.0 vs. 50.0 vs. 0.0), and TSAT (74.0 vs. 75.8 vs. 0.2), while PO iron ranked slightly higher for 6MWD (76.3 vs. 73.7 vs. 0.0). Included PO formulations encompassed both traditional preparations (ferrous sulfate/fumarate, polysaccharide) and newer agents such as sucrosomial iron and ferric polymaltose. Adverse events were comparable across groups: IV iron was not associated with excess mortality or serious adverse events, and PO iron was primarily limited by gastrointestinal intolerance. Sensitivity analyses restricting outcomes to trials with 3-12 months of follow-up showed consistent results, while longer studies mainly influenced event counts rather than the direction of effect. Our findings support the use of IV iron as the preferred strategy to improve symptoms and reduce hospitalizations in HF patients with ID, whereas PO iron may be considered when IV therapy is inaccessible. Further large-scale trials are needed to clarify long-term mortality impact and the role of newer PO formulations.
Abstract licence: CC BY
Maria Andersson, Prashanth Thankachan, Sumithra Muthayya, et al.
American Journal of Clinical Nutrition, 2008
- Food, Fortified
- Iron Deficiencies
- Biological Availability
Shruti B Bhavi, PB Jaju
BMC Pregnancy and Childbirth, 2017
- Ferric Oxide, Saccharated
- Ferric Compounds
- Ferritins
Anna Christofides, Kwaku Poku Asante, Claudia Schauer, et al.
Maternal and Child Nutrition, 2006
- Capsules
- Ferrous Compounds
- Food, Fortified
Siddhibhong Jongkraijakra, Thitima Doungngern, Warunsuda Sripakdee, et al.
Annals of Hematology, 2023
- Anemia
- Anemia, Iron-Deficiency
- Ferrous Compounds
Goh YE, Duggal M, Das R, et al.
2025
- Sodium Chloride, Dietary
- Micronutrients
- Nutritional Status
BackgroundInnovative fortification solutions are needed to address micronutrient deficiencies, which remain highly prevalent among adult females in India.ObjectivesThe objective of this trial was to evaluate the effects of quintuply-fortified salt (QFS) compared with iodized salt on the micronutrient status of nonpregnant females of reproductive age (NPFRA) in Punjab, India.MethodsWe conducted a double-blind, randomized, controlled, community-based trial. A total of 998 NPFRA were randomly assigned to receive: 1) QFS with iron as encapsulated ferrous fumarate, zinc, vitamin B12, folic acid, and iodine (eFF-QFS); 2) QFS with the same micronutrients, but iron as encapsulated ferric pyrophosphate plus ethylenediaminetetraacetic acid (eFePP-QFS); or 3) iodized salt. Biomarkers of micronutrient status were assessed at enrollment, 6 mo and 12 mo.ResultsAt enrollment, the prevalence of anemia, iron deficiency, hypozincemia, vitamin B12 insufficiency, and folate insufficiency among trial participants was 47.9%, 59.7%, 35.5%, 61.5%, and 69.7%, respectively. Mean household salt disappearance, measured at monthly home visits, was 6.0 g/adult female equivalent/day [95% confidence interval (CI): 5.9, 6.1] and did not vary across groups or time. At 6 mo, the odds of vitamin B12 insufficiency, folate insufficiency, and hypozincemia were, respectively, 80% [odds ratio (OR): 0.20; 95% CI: 0.13, 0.31], 86% (OR: 0.14; 95% CI: 0.09, 0.21), and 38% (OR: 0.62; 95% CI: 0.41, 0.93) lower in the eFF-QFS compared with the iodized salt group. Effects on vitamin B12 and folate status were sustained at 12 mo, and were comparable in the eFePP-QFS compared with the iodized salt group. There was a small, marginally significant, reduction in iron deficiency in the eFF-QFS compared with the iodized salt group at 6 (OR: 0.64; 95% CI: 0.42, 0.98; P = 0.08) and 12 mo (OR: 0.58; 95% CI: 0.35, 0.95; P = 0.06), but not in the eFePP-QFS compared with the iodized salt group. There were no groupwise differences in anemia at either time point.ConclusionsMultiple micronutrient salt fortification may be an effective strategy to improve micronutrient status, especially vitamin B12 and folate, among NPFRA at high risk of deficiency.Trial registration numberThis study was registered at clinicaltrials.gov, with NCT05166980 and at Clinical Trials Registry-India with CTRI/2022/02/040333.
Abstract licence: CC BY
F.E. O'Toole, F.M. McAuliffe, J.M. Fitzgerald, et al.
Contemporary Clinical Trials Communications, 2025
Secrest AH, Norgan Radler C, Kelly J, et al.
2025
Introduction The biotransformation of minerals through glycosylation by microorganisms, such as yeast or probiotics, can produce nutrients bound to a food matrix, potentially enhancing their bioavailability. This study aimed to compare the absorption kinetics of iron bound to a glycoprotein matrix (GPM) with those of ferrous bisglycinate chelate (FBC) and ferrous fumarate (FF). Methods In a double-blind, crossover design, 17 participants ingested 11 mg of iron in one of three forms: GPM (Pharmachem Innovation, Kearny, NJ, USA), FBC (Ferrochel®, Balchem Corp., Montvale, NJ, USA), or FF (FerroPharma Chemicals Ltd, Hungary). Blood samples were collected at baseline and 30-, 60-, 90-, 120-, 180-, 240-, 300-, 360-, 420-, and 480-minutes post-ingestion. Water intake was standardized throughout the protocol, and an iron-free snack was provided at four hours post-ingestion. Pharmacokinetic analysis was performed, with key outcome variables including the incremental area under the concentration vs. time curve (iAUC), maximum concentration (Cmax), and time to maximum concentration (Tmax). The a priori significance level was set at p < 0.05. Results Linear mixed-effects models indicated statistically significant effects of the GPM condition for both raw iron concentrations and changes from baseline (p = 0.03). On average, participants had iron concentrations that were 27.1 mcg/dL (95% CI: 2.8 to 51.4) higher after consuming GPM iron compared to the FF reference condition. Changes in iron concentrations from the baseline were 16.6 mcg/dL (95% CI: 1.5 to 31.7) higher after GPM consumption compared to FF. In contrast, iron concentrations and changes in iron levels after FBC consumption did not significantly differ from those observed with FF. Significant effects of time were also observed in both linear mixed-effects models. When expressed as percentage changes from baseline, iron concentrations in the GPM condition were 9.4% to 35.0% higher than FF and 5.9% to 32.6% higher than FBC. Pharmacokinetic analysis revealed a significant effect of condition on the iAUC (p = 0.047), but no significant effects for Cmax (p = 0.15) or Tmax (p = 0.81). Post hoc tests for the iAUC indicated a trend (p = 0.07) for a difference between the GPM and FBC conditions, but no significant differences between GPM and FF (p = 0.17) or FBC and FF (p = 0.75). Conclusion These findings suggest that iron bound to a glycoprotein matrix can improve absorption kinetics without any associated side effects. This data could have important implications for addressing iron deficiency or absorption disorders in a variety of populations.
Abstract licence: CC BY
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
Not available
Mechanism
Iron is necessary for the production of hemoglobin.
Food interactions
6 warnings
Human targets
13 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 125 interactions
The second phase may occur at 6-24 hours after ingestion and is characterized by a temporary remission. In the third phase, gastrointestinal symptoms recur accompanied by shock, metabolic acidosis, coma, hepatic necrosis and jaundice, hypoglycemia, renal failure and pulmonary edema. The fourth phase may occur several weeks after ingestion and is characterized by gastrointestinal obstruction and liver damage.
In a young child, 75 milligrams per kilogram is considered extremely dangerous. A dose of 30 milligrams per kilogram can lead to symptoms of toxicity. Estimates of a lethal dosage range from 180 milligrams per kilogram and upwards.
A peak serum iron concentration of five micrograms or more per ml is associated with moderate to severe poisoning in many.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:26214738
Endosomal acidification leads to iron release. The apotransferrin-receptor complex is then recycled to the cell surface with a return to neutral pH and the concomitant loss of affinity of apotransferrin for its receptor. Transferrin receptor is necessary for development of erythrocytes and the nervous system (By similarity).
A second ligand, the hereditary hemochromatosis protein HFE, competes for binding with transferrin for an overlapping C-terminal binding site. Positively regulates T and B cell proliferation through iron uptake .
PMID:26642240
Acts as a lipid sensor that regulates mitochondrial fusion by regulating activation of the JNK pathway .
PMID:26214738
When dietary levels of stearate (C18:0) are low, promotes activation of the JNK pathway, resulting in HUWE1-mediated ubiquitination and subsequent degradation of the mitofusin MFN2 and inhibition of mitochondrial fusion .
PMID:26214738
When dietary levels of stearate (C18:0) are high, TFRC stearoylation inhibits activation of the JNK pathway and thus degradation of the mitofusin MFN2 .
PMID:26214738
Mediates uptake of NICOL1 into fibroblasts where it may regulate extracellular matrix production (By similarity)
Has a preference for the CODD site for both HIF1A and HIF1B. Hydroxylated HIFs are then targeted for proteasomal degradation via the von Hippel-Lindau ubiquitination complex. Under hypoxic conditions, the hydroxylation reaction is attenuated allowing HIFs to escape degradation resulting in their translocation to the nucleus, heterodimerization with HIF1B, and increased expression of hypoxy-inducible genes.
EGLN1 is the most important isozyme under normoxia and, through regulating the stability of HIF1, involved in various hypoxia-influenced processes such as angiogenesis in retinal and cardiac functionality. Target proteins are preferentially recognized via a LXXLAP motif
PMID:10748112 PMID:10922473 PMID:10926844 PMID:14701748 PMID:28497810
Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression and developmental events .
PMID:10748112 PMID:10922473 PMID:10926844 PMID:14701748
Histone deacetylases act via the formation of large multiprotein complexes .
PMID:10748112 PMID:10922473 PMID:10926844 PMID:14701748
Also involved in the deacetylation of cohesin complex protein SMC3 regulating release of cohesin complexes from chromatin .
PMID:22885700
May play a role in smooth muscle cell contractility .
PMID:15772115
In addition to protein deacetylase activity, also has protein-lysine deacylase activity: acts as a protein decrotonylase by mediating decrotonylation ((2E)-butenoyl) of histones PMID:28497810
ATC B03AA02
ATC B03AD02
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 fumarate
Additional database identifiers
Drugs Product Database (DPD)
4845
Drugs Product Database (DPD)
309
ChemSpider
10607713
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11763
GeneCards
TFRC
UniProt Accession
TFR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1232
GenAtlas
EGLN1
GeneCards
EGLN1
GenBank Gene Database
AF246631
GenBank Protein Database
11345052
Guide to Pharmacology
2833
UniProt Accession
EGLN1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13315
GenAtlas
HDAC8
GeneCards
HDAC8
GenBank Gene Database
AF230097
GenBank Protein Database
8118721
Guide to Pharmacology
2619
UniProt Accession
HDAC8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18075
GeneCards
AHSP
UniProt Accession
AHSP_HUMAN
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:3951
GeneCards
FXN
UniProt Accession
FRDA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3976
GenAtlas
FTH1
GeneCards
FTH1
GenBank Gene Database
X00318
GenBank Protein Database
28435
UniProt Accession
FRIH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3650
GeneCards
FEN1
UniProt Accession
FEN1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18448
GenAtlas
NEIL1
GeneCards
NEIL1
GenBank Gene Database
AB079068
UniProt Accession
NEIL1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18956
GeneCards
NEIL2
UniProt Accession
NEIL2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9174
GenAtlas
POLB
GeneCards
POLB
GenBank Gene Database
L11607
GenBank Protein Database
292397
Guide to Pharmacology
3231
UniProt Accession
DPOLB_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:11740
GenAtlas
TF
GeneCards
TF
GenBank Gene Database
M12530
GenBank Protein Database
339453
UniProt Accession
TRFE_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: