Ferrous glycine sulfate 141mg/5ml oral solution
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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.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
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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: 11 · 1958–2025
Showing the 50 most relevant studies, sorted by most relevant.
Jordie A. J. Fischer, Arlin Cherian, Jeffrey N. Bone, et al.
Nutrition Reviews, 2023
- Iron Deficiencies
- Iron
- Ferritins
J. Powers, G. Buchanan, L. Adix, et al.
JAMA, 2017
Xiya Zhao, Xu Zhang, Teng Xu, et al.
Nutrients, 2022
E. Bisbe, L. Moltó, R. Arroyo, et al.
British journal of anaesthesia, 2014
Adeola M Awomolo, A. McWhirter, L. Sadler, et al.
American journal of obstetrics & gynecology MFM, 2023
Cirigliano E, Saint A, Pei LX, et al.
2025
- Streptococcus agalactiae
- Ferrous Compounds
- Glycine
BackgroundIron deficiency in women of reproductive age can have severe adverse perinatal consequences. Although iron supplementation can be effective at treating iron deficiency, excess unabsorbed iron in the gut may also promote colonization by enteropathogens such as Group B Streptococcus (GBS), increasing the potential risk of maternal and neonatal infection.ObjectivesWe examined whether 12 wk of supplementation with 18 mg elemental iron as ferrous bisglycinate, 60 mg as ferrous sulfate, or a placebo differentially influences GBS colonization in Cambodian women of reproductive age.MethodsThis study is a secondary analysis of a randomized controlled trial conducted in 25 villages in 3 districts of Kampong Thom province, Cambodia, including 144 nonpregnant women (18‒45 y) who received 18 mg of elemental iron as ferrous bisglycinate, 60 mg ferrous sulfate, or placebo for 12 wk. GBS colonization was assessed by real-time quantitative polymerase chain reaction targeting the cfb gene (which encodes the Christie-Atkins-Munch-Peterson [CAMP] factor, an indicator of GBS colonization) from stool collected at baseline and 12 wk. Cycle threshold values were compared within and across groups using Kruskal-Wallis and Wilcoxon signed-rank tests.ResultsNo changes in cfb expression were detected between baseline and endline within any treatment arm, nor were there differences across groups at 12 wk. However, regional differences in cfb expression were detected, with participants from the Srayov district exhibiting lower baseline and endline expression, than those from Prey Kuy and Tboung Krapeu.ConclusionsOral iron supplementation for 12 wk did not increase cfb expression in this population of predominantly iron-replete Cambodian women, compared with placebo. However, the observed geographic variation in cfb expression across districts suggests that environmental or behavioral factors may contribute to GBS colonization risk. These findings highlight the need to further investigate region-specific risk factors and provide a foundation for future research into GBS screening in Cambodia. This trial was registered at clinicaltrials.gov as NCT04017598.
Abstract licence: CC BY
Fischer JAJ, Pei LX, Elango R, et al.
2023
- Anemia
- Anemia, Iron-Deficiency
- Inflammation
Ali Hussain, Ali Hasan, Arshad Javid, et al.
3 Biotech, 2016
Akkarach Bumrungpert, Patcharanee Pavadhgul, Theera Piromsawasdi, et al.
Nutrients, 2022
- Iron Deficiencies
- Ferrous Compounds
- Pregnancy Complications
Rajagopal V. Sekhar, Siripoom McKay, Sanjeet Patel, et al.
Diabetes Care, 2010
- Cysteine
- Diabetes Mellitus, Type 2
- Glutathione
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
None known
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
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 B03AA01
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 glycine sulfate
Additional database identifiers
ChemSpider
146251
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 (Q27261422), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.