Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
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17 branded products available
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View all licensed products for Enalapril + Hydrochlorothiazide on the MHRA register
Innozide 20mg/12.5mg tablets
Innozide 20mg/12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
Enalapril 20mg / Hydrochlorothiazide 12.5mg tablets
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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.
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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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: 7 · Randomised trials: 5 · 1982–2026
Showing the 50 most relevant studies, sorted by most relevant.
Cicero AFG, ALGhasab NS, Tocci G, et al.
2024
Objectives: This systematic review and meta-analysis aimed to assess the blood pressure (BP)-lowering effect and the safety profile of low-dose bisoprolol/hydrochlorothiazide combination treatment in patients with hypertension. Methods: Multiple electronic databases were systematically searched, and five clinical studies were included in the meta-analysis. Results: Treatment with bisoprolol/hydrochlorothiazide significantly reduced systolic BP (SBP) [mean difference (MD): -8.35 mmHg, 95% confidence interval (CI): -11.44, -5.25 mmHg versus control; MD: -9.88 mmHg, 95%CI: -12.62, -7.14 mmHg versus placebo] and diastolic BP (DBP) [MD: -7.62 mmHg, 95%CI: -11.20, -4.04 mmHg, versus control; MD: -8.79 mmHg, 95%CI: -11.92, -5.67 mmHg versus placebo]. Moreover, BP response rate and BP control rate after low-dose bisoprolol/hydrochlorothiazide combination treatment were significantly greater compared to control [odd ratio (OR) for response rate: 4.86, 95%CI: 2.52, 9.37; OR for control rate: 1.67, 95%CI: 1.11, 2.51]. Finally, treatment with low-dose bisoprolol/hydrochlorothiazide was associated with a reduced risk of any adverse event (AE) and peripheral edema compared to control. Conclusions: Overall, our results reaffirm the safety and efficiency of prescribing bisoprolol/hydrochlorothiazide combination treatment in stage I and II hypertension.
Abstract licence: CC BY
Popat A, Pethe G, Yadav S, et al.
2025
- Carotid Stenosis
- Cardiovascular Diseases
- Hypertension
Cardiovascular conditions disrupt the normal functioning of the heart and blood vessels, often due to underlying conditions like atherosclerosis or hypertension. Antihypertensive medications are essential in cardiovascular disease management, encompassing several major drug classes with distinct mechanisms of action. Hence, this review evaluated the impact of various antihypertensive treatments on cardiovascular event reduction in asymptomatic carotid artery stenosis (CAS) patients. A comprehensive literature search was conducted from inception to 2024 on various databases by using specific keywords, and based on the eligibility criteria, three observational cohort studies and six randomized controlled trials (RCTs) of the 540 records retrieved were incorporated in this systematic review. The Newcastle-Ottawa scale was used to assess the methodological quality of the cohort studies, and the risk of bias visualization tool was used for RCTs. Data were then systematically extracted and analyzed. The results reported that enalapril and fosinopril demonstrated dual benefits in blood pressure (BP) reduction and vascular remodeling, though meta-analysis showed statistically insignificant improvements in regional cerebral blood flow (CI: -0.84, 6.08, P = 0.14, I2= 94%). Similarly, isradipine, lacidipine, and amlodipine improved carotid hemodynamics and cerebral perfusion, with meta-analysis favoring calcium channel blocker intervention for blood pressure management (CI: -3.25 to 7.64, P = 0.43). On the other hand, thiazide diuretics effectively reduced BP but showed limited efficacy in preventing atherosclerosis progression. In addition, angiotensin II receptor blockers (ARBs) significantly reduced 5-year stroke rates from 11% to 3.5%. Moreover, beta-blockers showed specific benefits, with metoprolol improving plaque echogenicity (57.3 ± 16.8 vs. 51.8 ± 20.0, p = 0.006) and reducing cardiovascular events (17% vs. 37% placebo, p = 0.011), while labetalol effectively managed post-endarterectomy hypertension. In conclusion, antihypertensive treatments showed varying effectiveness in cardiovascular event reduction and improvements in vessel measures.
Abstract licence: CC BY
Dalane W. Kitzman, W. Gregory Hundley, Peter H. Brubaker, et al.
Circulation Heart Failure, 2010
- Angiotensin-Converting Enzyme Inhibitors
- Blood Pressure
- Carotid Arteries
Tol ID, Khalil A, Cairns AE, et al.
2025
Abstract Objective: To assess the effectiveness and safety of management strategies for postpartum hypertension. Data sources: We searched the Cochrane Pregnancy and Childbirth’s Trials Register in collaboration with their Information Specialist, on 20/October/2022. As the Pregnancy and Childbirth Review Group closed (2023), we updated our literature search on 17/September/2024, using a strategy developed with an information specialist from the Royal College of Physicians, United Kingdom. Study eligibility criteria: We included randomised controlled trials (RCTs) assessing any intervention (pharmacological, surgical, or models of care) used to reduce maternal blood pressure (BP) in participants with postpartum hypertension. Study appraisal and synthesis methods: Search results were screened independently by two authors, with any disagreement resolved by consensus. Data were extracted independently, onto a Cochrane-based bespoke form which included Cochrane’s Trustworthiness Screening Tool. Random-effects meta-analysis was performed in RevMan. Results: Of 538 studies identified, 39 were included. Evidence was low/very low certainty. There were no safety concerns. In seven trials (n=1113 participants) of diuretics (primarily furosemide) vs. placebo/no therapy, BP control was better, due to trials administering antihypertensives to both groups. In three trials (n=96) of antihypertensive vs. placebo, data were insufficient to inform effectiveness. In eight trials (n=749) of antihypertensive (4 types) vs. another (2 types) for non-severe hypertension, additional antihypertensive need was similar in comparisons with either nifedipine or methyldopa, but greater when amlodipine or enalapril were compared with nifedipine. In eight trials (n=403) of antihypertensive vs. another for severe hypertension, BP was lower with diltiazem (vs. nifedipine). In four trials (n=668) of uterine curettage vs. usual care, small improvements in some laboratory parameters were of unclear clinical importance. In nine trials (n=1263) of models of postnatal care (usually BP self-monitoring/management, N=6) vs. usual care, BP was lower eight months postpartum following BP self-monitoring/management or lifestyle change. Conclusions: Diuretics cannot be recommended as monotherapy. There is little to guide choice of antihypertensive. Of greatest relevance to current practice is whether enalapril and amlodipine are as effective as nifedipine, and the role of BP self-measurement/management and lifestyle change in preventing longer-term cardiovascular outcomes.
Abstract licence: CC BY
Katogiannis K, Ikonomidis I, Farmakis D, et al.
2025
BackgroundIn patients with bone marrow transplantation (BMT) for hematologic malignancies, evidence for prevention of cancer therapy-related cardiac dysfunction (CTRCD) remains limited.ObjectivesThe authors investigated whether early initiation of sacubitril/valsartan or enalapril could be helpful to prevent CTRCD in patients undergoing BMT.MethodsWe randomized 90 patients with preserved left ventricular ejection fraction (LVEF) after BMT to sacubitril/valsartan, enalapril, or no cardioprotective medication (controls). The primary endpoints included i) LVEF, ii) LV global longitudinal strain (GLS), iii) myocardial wasted work (GWW), and work efficiency (GWE) by speckle tracking echocardiography. Secondary endpoints included changes in LV volumes.ResultsPatients treated with sacubitril/valsartan or enalapril for 6 months did not show a deterioration of LV GLS or LVEF (P > 0.05). Conversely, controls showed impaired LV GLS (-20.9% ± 2.1% vs -18.8% ± 2.6%, P = 0.001) and reduced LVEF (P = 0.045) at 6 months post-BMT. The percent improvement of GWW and GWE was greater in the sacubitril/valsartan compared to enalapril or control group (P = 0.044 and P = 0.011, respectively) at 6 months. Conversely, in controls, GWW increased (80.7 ± 60.6 vs 115.3 ± 52.1 mm Hg%, P = 0.045), and GWE was compromised (P = 0.030) at 6 months post-BMT. Among the 3 treatment groups, only sacubitril/valsartan group showed a reduction in LV end-diastolic and systolic volume compared to baseline (102.3 ± 26.9 vs 93.2 ± 18.9 mL, P = 0.042 and 44.5 ± 15.4 vs 39.1 ± 10.1 mL, P = 0.012, respectively).ConclusionsTreatment with sacubitril/valsartan or enalapril prevented deterioration of myocardial function at 6 months in patients with hematologic malignancies treated with BMT. Moreover, sacubitril/valsartan showed a more favorable effect on myocardial work indices. (Effect of Angiotensin Converting Enzyme and Sacubitril Valsartan in Patients After Bone Marrow Transplantation; NCT04092309).
Abstract licence: CC BY-NC-ND
Bertram Pitt, Nathaniel Reichek, Roland Willenbrock, et al.
Circulation, 2003
- Eplerenone
- Mineralocorticoid Receptor Antagonists
- Angiotensin-Converting Enzyme Inhibitors
S Björck, H. Mulec, Svend Aage Johnsen, et al.
BMJ, 1992
- Blood Pressure
- Diabetic Nephropathies
- Enalapril
John G.F. Cleland, Henry J. Dargie, Stephen G. Ball, et al.
Heart, 1985
- Angiotensin-Converting Enzyme Inhibitors
- Angiotensin II
- Clinical Trials as Topic
Peter A. Todd, R.C. Heel
Drugs, 1986
- Drug Interactions
- Enalapril
- Heart Failure
Marcia A. Testa, Richard B. Anderson, Johanna F. Nackley, et al.
New England Journal of Medicine, 1993
- Quality of Life
- Affective Symptoms
- Captopril
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
101 found
Half-life
5.6-14.8h
Mechanism
Hydrochlorothiazide is transported from the circulation into epithelial cells of…
Food interactions
6 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
65-75%
[L8447][L8450]…
Half-life
5.6-14.8h
[L8447]
Protein binding
40-68%
[L8447][L8450]
Hydrochlorothiazide has been shown to bind to human serum albumin.
[A185201]
Volume of distribution
0.83-4.19L/kg
[A185213]
Metabolism
[L8447][L8450]
Elimination
[L8447][L8450]
Clearance
285mL/min
[A185207]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Hydrochlorothiazide was granted FDA approval on 12 February 1959.[L8444]
[L8447][L8450]
Hydrochlorothiazide is also indicated alone or in combination for the management of hypertension.
[A185138][L8447][L8450][L45663]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1950 interactions
[L8447][L8450]
Patients experiencing an overdose may present with hypokalemia, hypochloremia, and hyponatremia.
[L8447][L8450][A185138]
Treat patients with symptomatic and supportive treatment including fluids and electrolytes.
[L8447][L8450][A185138]
Vasopressors may be administered to treat hypotension and oxygen may be given for respiratory impairment.
[A185138][L8447][L8450]
Normally, sodium is reabsorbed into epithelial cells of the distal convoluted tubule and pumped into the basolateral interstitium by a sodium-potassium ATPase, creating a concentration gradient between the epithelial cell and the distal convoluted tubule that promotes the reabsorption of water.[A16730]
Hydrochlorothiazide acts on the proximal region of the distal convoluted tubule, inhibiting reabsorption by the sodium-chloride symporter, also known as Solute Carrier Family 12 Member 3 (SLC12A3).[A185138][A185180][A16730] Inhibition of SLC12A3 reduces the magnitude of the concentration gradient between the epithelial cell and distal convoluted tubule, reducing the reabsorption of water.[A16730]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L8447][L8450]
When taken with a meal, bioavailability is 10% lower, Cmax is 20% lower, and Tmax increases from 1.6 to 2.9 hours.
[L8450]
[L8447]
[L8447][L8450]
Hydrochlorothiazide has been shown to bind to human serum albumin.
[A185201]
[A185213]
[L8447][L8450]
[L8447][L8450]
[A185207]
Patients with a creatinine clearance of 31-80mL/min have an average hydroxychlorothiazide renal clearance of 75mL/min, and patients with a creatinine clearance of ≤30mL/min have an average hydroxychlorothiazide renal clearance of 17mL/min.
[A185207]
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:14523450 PMID:29330545 PMID:31152168
It is also activated by the concentration of cytosolic Mg(2+). Its activation dampens the excitatory events that elevate the cytosolic Ca(2+) concentration and/or depolarize the cell membrane. It therefore contributes to repolarization of the membrane potential.
Plays a key role in controlling excitability in a number of systems, such as regulation of the contraction of smooth muscle, the tuning of hair cells in the cochlea, regulation of transmitter release, and innate immunity. In smooth muscles, its activation by high level of Ca(2+), caused by ryanodine receptors in the sarcoplasmic reticulum, regulates the membrane potential. In cochlea cells, its number and kinetic properties partly determine the characteristic frequency of each hair cell and thereby helps to establish a tonotopic map.
Kinetics of KCNMA1 channels are determined by alternative splicing, phosphorylation status and its combination with modulating beta subunits. Highly sensitive to both iberiotoxin (IbTx) and charybdotoxin (CTX). Possibly induces sleep when activated by melatonin and through melatonin receptor MTNR1A-dependent dissociation of G-beta and G-gamma subunits, leading to increased sensitivity to Ca(2+) and reduced synaptic transmission PMID:32958651
PMID:15615692 PMID:20826823 PMID:2558109 PMID:4322742 PMID:7523412 PMID:7683654
Composed of two similar catalytic domains, each possessing a functional active site, with different selectivity for substrates .
PMID:10913258 PMID:1320019 PMID:1851160 PMID:19773553 PMID:7683654 PMID:7876104
Plays a major role in the angiotensin-renin system that regulates blood pressure and sodium retention by the kidney by converting angiotensin I to angiotensin II, resulting in an increase of the vasoconstrictor activity of angiotensin .
PMID:11432860 PMID:1851160 PMID:19773553 PMID:23056909 PMID:4322742
Also able to inactivate bradykinin, a potent vasodilator, and therefore enhance the blood pressure response .
PMID:15615692 PMID:2558109 PMID:4322742 PMID:6055465 PMID:6270633 PMID:7683654
Acts as a regulator of synaptic transmission by mediating cleavage of neuropeptide hormones, such as substance P, neurotensin or enkephalins .
PMID:15615692 PMID:6208535 PMID:6270633 PMID:656131
Catalyzes degradation of different enkephalin neuropeptides (Met-enkephalin, Leu-enkephalin, Met-enkephalin-Arg-Phe and possibly Met-enkephalin-Arg-Gly-Leu) .
PMID:2982830 PMID:6270633 PMID:656131
Acts as a regulator of synaptic plasticity in the nucleus accumbens of the brain by mediating cleavage of Met-enkephalin-Arg-Phe, a strong ligand of Mu-type opioid receptor OPRM1, into Met-enkephalin (By similarity). Met-enkephalin-Arg-Phe cleavage by ACE decreases activation of OPRM1, leading to long-term synaptic potentiation of glutamate release (By similarity). Also acts as a regulator of hematopoietic stem cell differentiation by mediating degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) .
PMID:26403559 PMID:7876104 PMID:8257427 PMID:8609242
Acts as a regulator of cannabinoid signaling pathway by mediating degradation of hemopressin, an antagonist peptide of the cannabinoid receptor CNR1 .
PMID:18077343
Involved in amyloid-beta metabolism by catalyzing degradation of Amyloid-beta protein 40 and Amyloid-beta protein 42 peptides, thereby preventing plaque formation .
PMID:11604391 PMID:16154999 PMID:19773553
Catalyzes cleavage of cholecystokinin (maturation of Cholecystokinin-8 and Cholecystokinin-5) and Gonadoliberin-1 (both maturation and degradation) hormones .
PMID:10336644 PMID:2983326 PMID:7683654 PMID:9371719
Degradation of hemoregulatory peptide N-acetyl-SDKP (AcSDKP) and amyloid-beta proteins is mediated by the N-terminal catalytic domain, while angiotensin I and cholecystokinin cleavage is mediated by the C-terminal catalytic region PMID:10336644 PMID:19773553 PMID:7876104
Proteins that transport this drug across cell membranes
PMID:11669456 PMID:11907186 PMID:14675047 PMID:22108572 PMID:23832370 PMID:28534121 PMID:9950961
Mediates the uptake of OA across the basolateral side of proximal tubule epithelial cells, thereby contributing to the renal elimination of endogenous OA from the systemic circulation into the urine .
PMID:9887087
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
Transports prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) and may contribute to their renal excretion .
PMID:11907186
Also mediates the uptake of cyclic nucleotides such as cAMP and cGMP .
PMID:26377792
Involved in the transport of neuroactive tryptophan metabolites kynurenate (KYNA) and xanthurenate (XA) and may contribute to their secretion from the brain .
PMID:22108572 PMID:23832370
May transport glutamate .
PMID:26377792
Also involved in the disposition of uremic toxins and potentially toxic xenobiotics by the renal organic anion secretory pathway, helping reduce their undesired toxicological effects on the body .
PMID:11669456 PMID:14675047
Uremic toxins include the indoxyl sulfate (IS), hippurate/N-benzoylglycine (HA), indole acetate (IA), 3-carboxy-4- methyl-5-propyl-2-furanpropionate (CMPF) and urate .
PMID:14675047 PMID:26377792
Xenobiotics include the mycotoxin ochratoxin (OTA) .
PMID:11669456
May also contribute to the transport of organic compounds in testes across the blood-testis-barrier PMID:35307651
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
PMID:10660625 PMID:11907186 PMID:15037815 PMID:15102942 PMID:15291761 PMID:15576633 PMID:17229912 PMID:18501590 PMID:26277985 PMID:28027879
May be responsible for placental absorption of fetal-derived steroid sulfates such as estrone sulfate (E1S) and the steroid hormone precursor dehydroepiandrosterone sulfate (DHEA-S), as well as clearing waste products and xenobiotics from the fetus .
PMID:12409283
Maybe also be involved in placental urate homeostasis .
PMID:17229912
Facilitates the renal reabsorption of organic anions such as urate and derived steroid sulfates .
PMID:15037815 PMID:17229912
Organic anion glutarate acts as conteranion for E1S renal uptake .
PMID:15037815 PMID:17229912
Possible transport mode may also include DHEA-S/E1S exchange .
PMID:28027879
Also interacts with inorganic anions such as chloride and hydroxyl ions, therefore possible transport modes may include E1S/Cl(-), E1S/OH(-), urate/Cl(-) and urate/OH(-) .
PMID:17229912
Also mediates the transport of prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) and may be involved in their renal excretion .
PMID:11907186
Also able to uptake anionic drugs, diuretics, bile salts and ochratoxin A .
PMID:10660625 PMID:26277985
Mediates the unidirectional efflux of glutamate and aspartate .
PMID:28027879
Glutamate efflux down its transmembrane gradient may drive SLC22A11/OAT4-mediated placental uptake of E1S PMID:26277985
PMID:11856762 PMID:12523936 PMID:12835412 PMID:12883481 PMID:15364914 PMID:15454390 PMID:16282361 PMID:17959747 PMID:18300232 PMID:26721430
Mediates the ATP-dependent efflux of glutathione conjugates such as leukotriene C4 (LTC4) and leukotriene B4 (LTB4) too. The presence of GSH is necessary for the ATP-dependent transport of LTB4, whereas GSH is not required for the transport of LTC4 .
PMID:17959747
Mediates the cotransport of bile acids with reduced glutathione (GSH) .
PMID:12523936 PMID:12883481 PMID:16282361
Transports a wide range of drugs and their metabolites, including anticancer, antiviral and antibiotics molecules .
PMID:11856762 PMID:12105214 PMID:15454390 PMID:17344354 PMID:18300232
Confers resistance to anticancer agents such as methotrexate PMID:11106685
Proteins that carry this drug through the body
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
ATC C09BX03
ATC C03AX01
ATC C03AB03
ATC C09DX03
ATC C03EA01
ATC C09DX06
ATC C09XA52
ATC G01AE10
ATC C09DX01
ATC C03AA03
ATC C09XA54
ATC C09DX08
ATC C09DX07
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q4229451), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.