Ferrous citrate 62mg tablets
Tablet
62mg
Oral
Anaemias and some other blood disorders
Active ingredients:
Ferrous citrate
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Updated 3 months ago(16 Jan 2026)Safety monitoring data
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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Clinical guidelines and formulary information
British National Formulary
Ferrous citrate
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
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Active and completed clinical studies from ClinicalTrials.gov
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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%
Approximately 5 – 10% of dietary iron is absorbed, and this absorption rate increases to up to 30% in iron deficiency states.…
Half-life
2-4 months
The half-life of orally administered iron is not readily available in the literature, with total effects lasting 2-4 months (congruent with the…
Protein binding
90%
The protein binding for ferrous sulfate is equal to or greater than 90%.
[L2240]…
[L2240]…
Volume of distribution
60%
About 60% of iron is distributed the erythrocytes.
[A32524]
The remainder of the iron is found in muscle tissues (as a part of myoglobin),…
[A32524]
The remainder of the iron is found in muscle tissues (as a part of myoglobin),…
Metabolism
The metabolism of iron is complex. Normally, iron exists in the ferrous (Fe2+) or ferric (Fe3+) state, but since Fe2+ is oxidized to Fe3+, which…
Elimination
Oral iron is recycled, with some loss in the urine, sweat, and desquamation.…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Iron deficiency anemia is a large public health concern worldwide, especially in young children, infants, and women of childbearing age.[A190804] This type of anemia occurs when iron intake, iron stores, and iron loss do not adequately support the formation of erythrocytes, also known as red blood cells.[A190528]
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]
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]
Properties:
solid
Avg. mass: 151.91 Da
DrugBank indication
Ferrous sulfate is used for the prevention and treatment of iron deficiency anemia in adults and children.
[A190804][L2240][L11800]
[A190804][L2240][L11800]
Also known as(51)
Ferrous sulfate anhydrous
iron sulfate
iron sulfate (1:1)
iron(2+) sulfate (anhydrous)
iron(II) sulfate
Alpha-globin
Hemoglobin alpha chain
p90
Dosage forms(63)
Syrup (Oral)
Tablet, film coated (Oral) — 100 mg/1
Lotion (Topical)
Solution (Oral) — 15 mg/1mL
Tablet, sugar coated (Oral) — 200 mg
Solution / drops (Oral) — 125 mg / mL
Tablet, coated (Oral) — 0.34 g
Tablet, extended release (Oral) — 105 mg
Molecular properties(16)
Drug interactions(130)
Known interactions with other medications. Always consult a healthcare professional.
Dimercaprol
Moderate
Dimercaprol may increase the nephrotoxic activities of Ferrous sulfate anhydrous.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Cefdinir resulting in a reduced serum concentration and potentially a decrease in efficacy.
Deferiprone
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Deferiprone resulting in a reduced serum concentration and potentially a decrease in efficacy.
Dolutegravir
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Dolutegravir resulting in a reduced serum concentration and potentially a decrease in efficacy.
Eltrombopag
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Eltrombopag resulting in a reduced serum concentration and potentially a decrease in efficacy.
The bioavailability of Levodopa can be decreased when combined with Ferrous sulfate anhydrous.
Levothyroxine
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Levothyroxine resulting in a reduced serum concentration and potentially a decrease in efficacy.
Methyldopa
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Methyldopa resulting in a reduced serum concentration and potentially a decrease in efficacy.
Penicillamine
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Penicillamine resulting in a reduced serum concentration and potentially a decrease in efficacy.
Lipoic acid
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Lipoic acid resulting in a reduced serum concentration and potentially a decrease in efficacy.
Moxifloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Moxifloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Grepafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Grepafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Enoxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pefloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Pefloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ciprofloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Ciprofloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Trovafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Trovafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Nalidixic acid
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Nalidixic acid resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Rosoxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Cinoxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Lomefloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Lomefloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Gatifloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Gatifloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Norfloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Norfloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Levofloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Levofloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Gemifloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Gemifloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Ofloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Sparfloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Sparfloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Temafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Temafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Fleroxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Fleroxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Ferrous sulfate anhydrous can cause a decrease in the absorption of Technetium Tc-99m ciprofloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Garenoxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Garenoxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Nemonoxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Nemonoxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Flumequine
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Flumequine resulting in a reduced serum concentration and potentially a decrease in efficacy.
Enrofloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Enrofloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Orbifloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Orbifloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Sarafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Sarafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Difloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Difloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pazufloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Pazufloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Prulifloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Prulifloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Delafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Delafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Sitafloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Sitafloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Oxolinic acid
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Oxolinic acid resulting in a reduced serum concentration and potentially a decrease in efficacy.
Rufloxacin
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Rufloxacin resulting in a reduced serum concentration and potentially a decrease in efficacy.
Pipemidic acid
Moderate
Ferrous sulfate anhydrous can cause a decrease in the absorption of Pipemidic acid resulting in a reduced serum concentration and potentially a decrease in efficacy.
Doxycycline
Moderate
Doxycycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Lymecycline
Moderate
Lymecycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Clomocycline
Moderate
Clomocycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Oxytetracycline
Moderate
Oxytetracycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Demeclocycline
Moderate
Demeclocycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Tetracycline
Moderate
Tetracycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Metacycline
Moderate
Metacycline can cause a decrease in the absorption of Ferrous sulfate anhydrous resulting in a reduced serum concentration and potentially a decrease in efficacy.
Showing 50 of 130 interactions
Food & lifestyle interactions
Advice
Avoid milk and dairy products. Take ferrous sulfate at least 2 hours before or after milk.
Caffeine Notice
Limit caffeine intake. Food and beverages containing caffeine may reduce iron absorption.
Advice
Take at least 2 hours before or after calcium supplements.
Advice
Take separate from antacids. Take ferrous sulfate at least 2 hours before or after antacids.
Take With Food
Take with food. This may reduce gastric irritation.
Take With Food
Take with foods containing vitamin C. Foods rich in vitamin C increase the absorption of iron.
Toxicity & overdose
The toxicity of ferrous sulfate in humans depends on the amount of iron ingested. Up to 20 mg/kg of elemental iron is not toxic, 20-60 mg/kg has mild toxicity, and more than 60 mg/kg can lead to severe symptoms and morbidity.
[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.
[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.
How it works
Mechanism of action
Iron is required to maintain optimal health, particularly for helping to form red blood cells (RBC) that carry oxygen around the body. A deficiency in iron indicates that the body cannot produce enough normal red blood cells.[A32514][L11800] Iron deficiency anemia occurs when body stores of iron decrease to very low levels, and the stored iron is insufficient to support normal red blood cell (RBC) production. Insufficient dietary iron, impaired iron absorption, bleeding, pregnancy, or loss of iron through the urine can lead to iron deficiency.[A32514][L11794] Symptoms of iron deficiency anemia include fatigue, breathlessness, palpitations, dizziness, and headache.
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]
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]
Pharmacodynamics
Ferrous sulfate replenishes iron, an essential component in hemoglobin, myoglobin, and various enzymes. It replaces the iron that is usually found in hemoglobin and myoglobin. Iron participates in oxygen transport and storage, electron transport and energy metabolism, antioxidant and beneficial pro-oxidant functions, oxygen sensing, tissue proliferation and growth, as well as DNA replication and repair.[A32524][A32514]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Approximately 5 – 10% of dietary iron is absorbed, and this absorption rate increases to up to 30% in iron deficiency states. Oral iron supplements are absorbed up to 60% via active and passive transport processes.
[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]
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]
Half-life
The half-life of orally administered iron is not readily available in the literature, with total effects lasting 2-4 months (congruent with the red blood cell life span)[A190945] with an onset of action of 4 days and peak activity at 7-10 days.
[L2240]
[L2240]
Protein binding
The protein binding for ferrous sulfate is equal to or greater than 90%.
[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]
[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]
Volume of distribution
About 60% of iron is distributed the erythrocytes.
[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]
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]
Metabolism
The metabolism of iron is complex. Normally, iron exists in the ferrous (Fe2+) or ferric (Fe3+) state, but since Fe2+ is oxidized to Fe3+, which hydrolyzes to insoluble iron(III)hydroxides in neutral aqueous solutions, iron binds to plasma proteins and is either transported or stored throughout the body.
[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]
[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]
Route of elimination
Oral iron is recycled, with some loss in the urine, sweat, and desquamation. Some iron can be lost during menstrual bleeding[A32514][L2240] This loss is balanced by changes in intestinal absorption. The enzyme hepcidin promotes the excretion of iron via the sloughing of enterocytes with ferritin stores into the feces.
[L11794]
[L11794]
Drug targets(2)
Proteins and enzymes this drug interacts with in the body
Hemoglobin subunit alpha
HBA1
binder
Specific functionheme binding
General function & pharmacology
Involved in oxygen transport from the lung to the various peripheral tissues
Transferrin receptor protein 2
TFR2
substrate
Specific functionco-receptor binding
Cellular location
Cell membrane
General function & pharmacology
Mediates cellular uptake of transferrin-bound iron in a non-iron dependent manner. May be involved in iron metabolism, hepatocyte function and erythrocyte differentiation
Metabolizing enzymes(5)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CPCeruloplasmin
substrate
HAMPHepcidin
substrate
TFSerotransferrin
substrate
HEPHHephaestin
substrate
CYBRD1Plasma membrane ascorbate-dependent reductase CYBRD1
substrate
Transporters(2)
Proteins that transport this drug across cell membranes
Natural resistance-associated macrophage protein 2
SLC11A2
substrate
Specific functioncadmium ion binding
Cellular location
Early endosome membrane
General function & pharmacology
Proton-coupled metal ion symporter operating with a proton to metal ion stoichiometry of 1:1 .
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: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
Ferroportin
SLC40A1
substrate
Specific functionferrous iron transmembrane transporter activity
Cellular location
Cell membrane
General function & pharmacology
Transports Fe(2+) from the inside of a cell to the outside of the cell, playing a key role for maintaining systemic iron homeostasis .
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
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
Scientific references(11)
Leary A., Barthe L., Clavel T., Sanchez C., Oulmi-Castel M., Paillard B., Edmond J.M., Brunner V.
Pharmacokinetics of Ferrous Sulphate (Tardyferon(R)) after Single Oral Dose Administration in Women with Iron Deficiency Anaemia.
Drug Research (Stuttg)
2016 Jan66(1):51-6. doi: 10.1055/s-0035-1549934. Epub 2015 May 19
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Affected organisms(1)
Humans and other mammals
International brands(46)
Salt forms(4)
Ferrous sulfate(DBSALT002666)
Ferrous sulfate dihydrate(DBSALT002463)
Ferrous sulfate monohydrate(DBSALT002667)
Ferrous sulfate sesquihydrate(DBSALT002668)
Experimental properties(5)
Commercial products(102)
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 sulfate anhydrous
Matched from: Ferrous citrate
Normalized synonym
80% confidenceAdditional 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 the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 27 days ago(8 Mar 2026)