Indapamide 2.5mg tablets
Requires a prescription from a doctor or prescriber
Diuretics
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Indapamide
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Submit a Yellow Card report to the MHRA
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.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Indapamide
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
28 branded products available
Part of the Natrilix brand family (generic: Indapamide)
MHRA licensed products
View all licensed products for Indapamide on the MHRA register
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg tablets
Indapamide 2.5mg 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)
2.5 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 NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
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.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Indapamide
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). 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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
25 found
Half-life
13.9 to 18 hours
Mechanism
Indapamide acts on the nephron, specifically at the proximal segment of the dist…
Food interactions
3 warnings
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10%
[A203663][A203519]…
Half-life
13.9 to 18 hours
[A203663]
In healthy subjects, indapamide's elimination half-life can range from 13.9…
Protein binding
76-79%
[A203627][A203663]
Indapamide binds primarily to alpha 1-acid glycoprotein and less significantly to serum albumin and lipoproteins.
[A204041]…
Volume of distribution
25 L
[A203663][A203519][A204113]…
Metabolism
7%
[A203663]…
Elimination
60-70%
[A203627]
Clearance
1.71 mL/min
[A203627]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Thiazide-like diuretics such as indapamide are a valuable tool for the treatment of hypertension and continue to grow in popularity, falling behind only ACE inhibitors in terms of prescription frequency.[A204134] When compared to [hydrochlorothiazide] (another commonly prescribed diuretic), indapamide has been shown to be superior at lowering systolic blood pressure, reducing left ventricular mass index, lowering oxidative stress, inhibiting platelet aggregation, and reducing microalbuminuria associated with diabetes.[A204134] Interestingly, unlike thiazide diuretics, several sources suggest that indapamide is not associated with glucose or lipid disturbances.[A204134][A204161]
Indapamide is characterized by both a methylindoline and a sulfamoyl chlorobenzamide functional group, with the former being largely responsible for the molecule’s lipid solubility.[A204158]
[L13982]
It may also be used to treat fluid and salt retention associated with congestive heart failure.
[L13982]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1823 interactions
[L13982]
Other signs of overdose include respiratory depression and severe hypotension.
[L13982]
In cases of overdose, supportive care interventions may be necessary to manage symptoms.
[L13982]
Emesis and gastric lavage may be recommended to empty the stomach; however, patients should be monitored closely for any electrolyte or fluid imbalances.
[L13982]
Interestingly, it is likely that thiazide-like diuretics such as indapamide have additional blood pressure lowering mechanisms that are unrelated to diuresis.[A16729] This is exemplified by the observation that the antihypertensive effects of thiazides are sustained 4-6 weeks after initiation of therapy, despite recovering plasma and extracellular fluid volumes.[A16729]
Some studies have suggested that indapamide may decrease responsiveness to pressor agents while others have suggested it can decrease peripheral resistance.[A203627] Although it is clear that diuresis contributes to the antihypertensive effects of indapamide, further studies are needed to investigate the medication’s ability to decrease peripheral vascular resistance and relax vascular smooth muscle.[A203627]
Administration of indapamide produces water and electrolyte loss, with higher doses associated with increased diuresis.[A203627][A204068] Severe and clinically significant electrolyte disturbances may occur with indapamide use - for example, hypokalemia resulting from renal potassium loss may lead to QTc prolongation.[A203627][A204062] Further electrolyte imbalances may occur due to renal excretion of sodium, chloride, and magnesium.[A203627][A204062][A204068]
Other indapamide induced changes include increases in plasma renin and aldosterone, and reduced calcium excretion in the urine.[A203627][A204074][A204131] In many studies investigating the effects of indapamide in both non-diabetic and diabetic hypertensive patients, glucose tolerance was not significantly altered.[A203627] However, additional studies are necessary to assess the long term metabolic impacts of indapamide, since thiazide related impaired glucose tolerance can take several years to develop in non-diabetic patients.[A203627]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A203663][A203519]
Indapamide is highly lipid-soluble due to its indoline moiety - a characteristic that likely explains why indapamide’s renal clearance makes up less than 10% of its total systemic clearance.
[A203627][A203663][A203519]
The Tmax occurs approximately 2.3 hours after oral administration.
[A203663]
The Cmax and AUC0-24 values are 263 ng/mL and 2.95 ug/hr/mL, respectively.
[A203663]
[A203663]
In healthy subjects, indapamide's elimination half-life can range from 13.9 to 18 hours.
[A203627][A203519]
The long half-life is conducive to once-daily dosing.
[A203663]
[A203627][A203663]
Indapamide binds primarily to alpha 1-acid glycoprotein and less significantly to serum albumin and lipoproteins.
[A204041]
In the blood, indapamide is extensively and preferentially bound to erythrocytes.
[A203663][A204041][L13982]
[A203663][A203519][A204113]
[A203663]
In humans, as many as 19 distinct indapamide metabolites may be produced, although not all have been identified.
[A203627][A203663]
There are several metabolic routes through which indapamide may be metabolized, and CYP3A4 is the main enzyme involved in the corresponding hydroxylation, carboxylation, and dehydrogenation reactions.
[A34415]
Indapamide can undergo dehydrogenation to form M5, then oxidation to form M4, then further hydroxylation at the indole moiety to form M2.
[A17553]
These reactions are facilitated by CYP3A4.
[A17553]
Another route of metabolism occurs when indapamide is first hydroxylated to M1 by CYP3A4.
[A17553]
M1 then undergoes dehydrogenation to form M3 and is further oxidized to form M2.
[A17553]
Hydroxylation of indapamide’s indole moiety is thought to form the major metabolite (M1), which is less pharmacologically active compared to its parent compound according to animal studies.
[A203663]
Indapamide may also undergo epoxidation via CYP3A4 to form a reactive epoxide intermediate.
[A17553]
The unstable epoxide intermediate may then undergo dihydroxylation via microsomal epoxide hydrolase to form M6, or glutathione conjugation to form M7.
[A17553]
[A203627]
[A203627]
Proteins and enzymes this drug interacts with in the body
PMID:18270262 PMID:21613606 PMID:22009145 PMID:36351028 PMID:36792826
Also acts as a receptor for the pro-inflammatory cytokine IL18, thereby contributing to IL18-induced cytokine production, including IFNG, IL6, IL18 and CCL2 (By similarity). May act either independently of IL18R1, or in a complex with IL18R1 (By similarity)
PMID:10646604 PMID:25441029
Associates with KCNE beta subunits that modulates current kinetics .
PMID:10646604 PMID:11101505 PMID:19687231 PMID:8900283 PMID:9108097 PMID:9312006
Induces a voltage-dependent current by rapidly activating and slowly deactivating potassium-selective outward current .
PMID:10646604 PMID:11101505 PMID:25441029 PMID:8900283 PMID:9108097 PMID:9312006
Also promotes a delayed voltage activated potassium current showing outward rectification characteristic (By similarity). During beta-adrenergic receptor stimulation, participates in cardiac repolarization by associating with KCNE1 to form the I(Ks) cardiac potassium current that increases the amplitude and slows down the activation kinetics of outward potassium current I(Ks) (By similarity) .
PMID:10646604 PMID:11101505 PMID:8900283 PMID:9108097 PMID:9312006
Muscarinic agonist oxotremorine-M strongly suppresses KCNQ1/KCNE1 current .
PMID:10713961
When associated with KCNE3, forms the potassium channel that is important for cyclic AMP-stimulated intestinal secretion of chloride ions .
PMID:10646604
This interaction with KCNE3 is reduced by 17beta-estradiol, resulting in the reduction of currents (By similarity). During conditions of increased substrate load, maintains the driving force for proximal tubular and intestinal sodium ions absorption, gastric acid secretion, and cAMP-induced jejunal chloride ions secretion (By similarity).
Allows the provision of potassium ions to the luminal membrane of the secretory canaliculus in the resting state as well as during stimulated acid secretion (By similarity). When associated with KCNE2, forms a heterooligomer complex leading to currents with an apparently instantaneous activation, a rapid deactivation process and a linear current-voltage relationship and decreases the amplitude of the outward current .
PMID:11101505
When associated with KCNE4, inhibits voltage-gated potassium channel activity .
PMID:19687231
When associated with KCNE5, this complex only conducts current upon strong and continued depolarization .
PMID:12324418
Also forms a heterotetramer with KCNQ5; has a voltage-gated potassium channel activity .
PMID:24855057
Binds with phosphatidylinositol 4,5-bisphosphate .
PMID:25037568
KCNQ1-KCNE2 channel associates with Na(+)-coupled myo-inositol symporter in the apical membrane of choroid plexus epithelium and regulates the myo-inositol gradient between blood and cerebrospinal fluid with an impact on neuron excitability (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
Appears to function in modulating the activity of the immune system during the acute-phase reaction
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Involved compounds
ATC C03BA11
ATC C09BX01
ATC G01AE10
ATC C10BX13
ATC C09BX06
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)
Indapamide
Additional database identifiers
Drugs Product Database (DPD)
1960
ChemSpider
3574
BindingDB
25901
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10912
GenAtlas
SLC12A3
GeneCards
SLC12A3
GenBank Gene Database
U44128
GenBank Protein Database
1172161
UniProt Accession
S12A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6294
GenAtlas
KCNQ1
GeneCards
KCNQ1
GenBank Gene Database
AF000571
GenBank Protein Database
2465531
Guide to Pharmacology
560
UniProt Accession
KCNQ1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3401
GeneCards
EPHX1
UniProt Accession
HYEP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
International reference pricing
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
2 active patents
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: