Ferrous gluconate 300mg/5ml oral solution
Requires a prescription from a doctor or prescriber
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
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Suspected adverse reactions reported for Ferrous gluconate
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1 branded products available
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
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. 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: 3 · Randomised trials: 2 · 1991–2026
Showing the 50 most relevant studies, sorted by most relevant.
Zoe Tolkien, Lynne Stecher, Adrian Mander, et al.
PLoS ONE, 2015
- Clinical Trials as Topic
- Ferrous Compounds
- Gastrointestinal Diseases
Christofi MD, Giannakou K, Mpouzika M, et al.
2024
BackgroundPatients with a low serum blood hemoglobin concentration suffer from a pathologic state that contributes significantly to morbidity and mortality figures worldwide. Oral iron supplementation, the most common method of treatment, is reported to have poor patient adherence, due to its unwanted side effects. Lactoferrin is a globular glycoprotein of the transferrin family that has shown promising results in patients with a low hemoglobin profile. This systematic review and meta-analysis of randomized clinical trials explore its effect on blood hemoglobin compared to conventional iron preparations.MethodsWe followed the PRISMA Guidelines for reporting systematic reviews and meta-analyses. A systematic search was conducted in electronic databases (PubMed, CINAHL, Scopus, and Cochrane) from inception to June 2022. Meta-analysis was performed on studies where the primary outcome was the mean Hb concentration, comparing lactoferrin to ferrous sulfate subgroups. We assessed the methodological quality of the trials using the Jadad scoring scale.ResultsNineteen trials published between 2006 and 2022 met the eligibility criteria. It has been found that the levels of Hb concentration in different populations with varying health conditions undergo a moderate to significant change after treatment with all types of trialed interventions, including both iron and lactoferrin treatment, in both the intervention group and the comparison group. Most of the studies report that LF showed a statistically significant increase in Hb concentration levels, compared to those in the iron group. The meta-analysis included seven trials comparing the effectiveness of lactoferrin to ferrous sulfate for patients with low Hb concentration. The analysis showed a statistically significant increase in Hb levels in the oral bovine lactoferrin group compared to ferrous sulfate (SMD -0.81, 95% CI: -1.21, -0.42, p 2 = 95.8%, P heterogeneity ConclusionsLactoferrin is an effective intervention at doses of 100-250 ng/day, for patients with a low Hb concentration. As a safer option and with high compliance evidence, lactoferrin can serve as an iron replacement treatment for patients who may be experiencing adverse side effects due to iron intake.
Abstract licence: CC BY
D. Henry, N. Dahl, M. Auerbach, et al.
The oncologist, 2007
- Epoetin Alfa
- Anemia
- Antineoplastic Agents
Palacios Santiago
The Scientific World JOURNAL, 2012
- Ferrous Compounds
- Anemia, Iron-Deficiency
- Iron, Dietary
Vahid Falahati, Ali Asghar Ghasemi, Kazem Ghaffari, et al.
Journal of Education and Health Promotion, 2022
Peter P. Mueller, Tobias May, Angela Perz, et al.
Biomaterials, 2005
- Stents
- Cell Proliferation
- Cell Cycle
Anna A. Wawer, Linda J. Harvey, J. Dainty, et al.
PLoS ONE, 2014
- Alginates
- Calcium
- Enzyme-Linked Immunosorbent Assay
Leone G, Arrabito M, Russo G, et al.
2026
Background/Objectives: Iron deficiency (ID) is the most common nutritional disorder in childhood worldwide. It has profound consequences for growth, neurodevelopment, behaviour, and overall health. Despite the long-standing efficacy of oral ferrous salts, their poor gastrointestinal tolerability and adherence challenges have spurred the development of alternative formulations and innovative dosing strategies. Methods: We conducted a narrative review of national and international guidelines, pediatric randomized controlled trials, observational and cohort studies, cost-effectiveness analyses, diagnostic method papers, and reviews, with emphasis on diagnostic innovations, therapeutic outcomes, tolerability, and formulation-specific efficacy. Results: Ferrous salts remain the gold standard for efficacy, low cost, and guideline endorsement, but up to 40% of children experience GI intolerance. Therefore, a lower dosage of ferrous salts has been proposed for IDA as still being an efficacious and better-tolerated schedule. Also, alternate-day dosing improves absorption and tolerability and is supported by a recent pediatric RCT. Newer formulations-ferric polymaltose, ferrous bisglycinate, co-processed bisglycinate with alginate (Feralgine™), and vesicular encapsulated forms such as sucrosomial and liposomal ferric pyrophosphate-showed improved tolerability and palatability, supporting adherence with hematologic outcomes comparable to ferrous salts, particularly in children with intolerance, malabsorption, or inflammatory comorbidities. Intravenous iron is effective and safe with modern preparations and is reserved for severe anemia, malabsorption, or oral therapy failure. Conclusions: Oral ferrous salts should remain the first-line therapy in pediatric ID/IDA. Future pediatric trials should prioritize head-to-head comparisons of formulations, hepcidin-guided dosing, and patient-centred outcomes, including neurocognitive trajectories and quality of life.
Abstract licence: CC BY
Pantopoulos K
2024
- Anemia, Iron-Deficiency
- Iron
- Dietary Supplements
Iron-deficiency anemia and pre-anemic iron deficiency are the most frequent pathologies. The first line of treatment involves oral iron supplementation. The simplest, least expensive, and most commonly prescribed drug is ferrous sulfate, while other ferrous salts and ferric complexes with polysaccharides or succinylated milk proteins are also widely used. In recent years, novel iron formulations have been developed, such as the lipophilic iron donor ferric maltol, or nanoparticle encapsulated sucrosomial® iron. Oral iron supplementation is usually efficacious in correcting iron-deficiency anemia and replenishing iron stores but causes gastrointestinal side effects that reduce compliance. When oral iron supplementation is contraindicated, intravenous iron therapy can rapidly achieve therapeutic targets without gastrointestinal complications. Herein, we critically review literature on relative efficacy and tolerability of currently available oral iron supplements, and summarize recent data on optimal dosage and frequency.
Abstract licence: CC BY-NC
Wenhui Jing, Rongxian Guo, Xiaolin Zhu, et al.
Microbiological Research, 2024
- Ferroptosis
- DNA Damage
- Escherichia coli
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 128 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 B03AD05
ATC B03AA03
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)
Ferrous gluconate
Additional database identifiers
Drugs Product Database (DPD)
309
Drugs Product Database (DPD)
246
ChemSpider
19953133
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
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q421291), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.