Methyldopa 50mg/5ml oral solution
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Methyldopa
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 Methyldopa
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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.
EudraVigilance
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Suspected adverse reactions reported for Methyldopa
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1 branded products available
WHO defined daily dose (DDD)
1 gram
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 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
Guidelines from the National Institute for Health and Care Excellence
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.
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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. 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: 9 · Randomised trials: 10 · 1962–2026
Showing the 50 most relevant studies, sorted by most relevant.
T. Easterling, S. Mundle, H. Bracken, et al.
Lancet (London, England), 2019
Hup RJ, Damen JAA, Terstappen J, et al.
2025
- Hypertension, Pregnancy-Induced
- Labetalol
- Methyldopa
ObjectiveConsidering safety and effectiveness of oral antihypertensive agents when treating hypertensive disorders of pregnancy, no preference can be stated between the 3 agents currently available. Therefore, this systematic review and network meta-analysis aims to determine the effects of antenatal treatment with methyldopa, labetalol, or nifedipine for hypertensive disorders of pregnancy regarding maternal or fetal/neonatal morbidity and mortality.Data sourcesOn August 25, 2023, an electronic search in PubMed/Medline, Embase, and CENTRAL was performed.Study eligibility criteriaRandomized controlled trials reporting on perinatal outcomes in hypertensive pregnancies treated with oral antihypertensive agents of interest (methyldopa, labetalol, or nifedipine) or placebo/no treatment were identified.Study appraisal and synthesis methodsQuality assessment was performed using the Cochrane Risk of Bias tool for randomized controlled trials and trustworthiness was assessed with the Trustworthiness in RAndomised Controlled Trials Checklist. Data on our predefined outcomes were extracted and relative risks were calculated in network estimates if possible.ResultsTwenty three trials (3989 women) were included in our network meta-analysis with an overall low-to-moderate quality. Compared to placebo/no treatment, labetalol and methyldopa significantly reduced the incidence of severe hypertension (including 8 studies, relative risk 0.20 [95% confidence interval 0.09-0.48] and 0.44 [0.20-0.99], respectively). In the network meta-analysis, labetalol vs nifedipine was associated with a reduction in preeclampsia (relative risk, 0.50 [0.28-0.87]; 15 studies) and preterm birth (relative risk, 0.68 [0.52-0.90]; 14 studies). No significant differences could be detected for any of the other outcomes of interest.ConclusionWhen comparing the oral antihypertensive agents currently available head-to-head, no significant differences in the primary outcome, severe hypertension, could be detected as well as on most of the secondary outcomes of interest. Considering the preference of labetalol over nifedipine regarding the outcomes preeclampsia and preterm birth, a modest favor for labetalol could be stated. Included studies however were of low overall quality warranting caution when interpreting results.
Abstract licence: CC BY
Tol ID, Khalil A, Cairns AE, et al.
2026
- Hypertension, Pregnancy-Induced
- Puerperal Disorders
- Hypertension
ObjectiveTo assess the effectiveness and safety of management strategies for postpartum hypertension.Data sourcesWe searched the Cochrane Pregnancy and Childbirth's Trials Register in collaboration with their Information Specialist, on October 20, 2022. As the Pregnancy and Childbirth Review Group closed (2023), we updated our literature search on September 17, 2024 (topped up on September 25, 2025), using a strategy developed with an information specialist from the Royal College of Physicians, United Kingdom.Study eligibility criteriaWe included randomized controlled trials assessing any intervention (pharmacological, surgical, or models of care) used to reduce maternal blood pressure in participants with postpartum hypertension.Study appraisal and synthesis methodsSearch results were screened independently by 2 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.ResultsOf the 944 studies identified, 40/44 included had informative data. Certainty of evidence was low or very low. There were no safety concerns. In 7 trials (n=1113 participants) of diuretics (primarily furosemide) vs placebo/no therapy, blood pressure control was better with diuretics when administered alongside antihypertensive. In 3 trials (n=96) of antihypertensive vs placebo, data were insufficient to inform effectiveness. In 9 trials (n=865) of antihypertensive (4 types) vs another (3 types) for nonsevere hypertension, additional antihypertensive need was similar in comparisons with either nifedipine or methyldopa, but greater when amlodipine or either enalapril or lisinopril/thiazide were compared with nifedipine. In 8 trials (n=403) of antihypertensive vs another for severe hypertension, blood pressure was lower with diltiazem (vs nifedipine). In 4 trials (n=668) of uterine curettage vs usual care, observed improvements in laboratory parameters were of unclear clinical significance. In 9 trials (n=1263) of models of postnatal care (usually blood pressure self-monitoring/management, N=6) vs usual care, blood pressure was lower 8 months postpartum following blood pressure self-monitoring/management or lifestyle change.ConclusionWhile diuretics may aid in blood pressure control, they cannot be recommended as monotherapy. Evidence guiding the optimal choice of antihypertensive agents remains limited. Of greatest relevance to practice is the effectiveness of: enalapril or amlodipine (vs nifedipine) in controlling blood pressure; and blood pressure self-measurement/management or lifestyle change (vs usual care) in preventing longer-term cardiovascular outcomes.
Abstract licence: CC BY
Bambang Rahardjo, Rahajeng, Yohanes Rico Nurhaeni
Majalah Obstetri dan Ginekologi, 2026
P. Plouin, G. Bréart, F. Maillard, et al.
BJOG: An International Journal of Obstetrics & Gynaecology, 1988
M. Sprackling, J. Mitchell, A. Short, et al.
British Medical Journal (Clinical research ed.), 1981
Zahra Goudarzi, Mojtaba Nouhi, Najmeh Bordbar
Health Science Reports, 2026
M. Salama, M. Rezk, Wael Gaber, et al.
Obstetrical & Gynecological Survey, 2019
B. Djahanguiri, S. Hemmati, D. Sadeghi, et al.
Medicina et pharmacologia experimentalis. International journal of experimental medicine, 1967
F. Fouad, Yoshiyuki Nakashima, R. Tarazi, et al.
The American journal of cardiology, 1982
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
105 minutes
Mechanism
The exact mechanism of methyldopa is not fully elucidated; however, the main mec…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
25%
[A231789]
…
Half-life
105 minutes
[L32614]
Following intravenous injection, the plasma half-life of methyldopa ranges from 90 to 127 minutes.
[L32624]
…
Protein binding
15%
[A231789]
…
Volume of distribution
0.32L/kg
Metabolism
[A232224]
…
Elimination
70%
Clearance
130 mL/min
[L32614]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
First introduced in 1960 as an antihypertensive agent, methyldopa was considered to be useful in certain patient populations, such as pregnant women and patients with renal insufficiency. Since then, methyldopa was largely replaced by newer, better-tolerated antihypertensive agents;[A231784] however, it is still used as monotherapy [L32614] or in combination with [hydrochlorothiazide].[L32619] Methyldopa is also available as intravenous injection, which is used to manage hypertension when oral therapy is unfeasible and to treat hypertensive crisis.[L32624]
[L32619]
Methyldopa injection is used to manage hypertensive crises.
[L32624]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1316 interactions
[L32704]
Acute overdosage is characterized by acute hypotension and other presentations attributed to the brain and gastrointestinal dysfunction, such as excessive sedation, weakness, bradycardia, dizziness, light-headedness, constipation, distention, flatus, diarrhea, nausea, and vomiting.
Symptomatic and supportive measures should be initiated in the event of methyldopa overdose. Overdosage following recent oral ingestion can be managed by gastric lavage or emesis, as well as infusions to limit further drug absorption. Cardiac rate and output, blood volume, electrolyte balance, paralytic ileus, urinary function and cerebral activity should be closely monitored.
The use of sympathomimetic drugs such as levarterenol, epinephrine, and metaraminol bitartrate, or dialysis may be considered.
[L32614]
The L-isomer of alpha-methyldopa also reduces blood pressure by inhibiting aromatic L-amino acid decarboxylase, also known as DOPA decarboxylase, which is an enzyme responsible for the syntheses of dopamine and serotonin.[L32614] Inhibiting this enzyme leads to depletion of biogenic amines such as norepinephrine. However, inhibition of aromatic L-amino acid decarboxylase plays a minimal role in the blood-pressure‐lowering effect of methyldopa.[A1501][A1505]
Following oral administration, blood-pressure-lowering effects are observed within 12 to 24 hours in most patients, and a maximum reduction in blood pressure occurs in 4 to 6 hours. Blood pressure returns to pre-treatment levels within 24 to 48 hours following drug discontinuation.[L32614] Following intravenous administration, the blood-pressure-lowering effects of methyldopa last for about 10 to 16 hours.[A231784]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A231789]
In healthy individuals, the inactive D-isomer is less readily absorbed than the active L-isomer.
[A232224]
The mean bioavailability of methyldopa is 25%, ranging from eight to 62%.
[A231789]
Following oral administration, about 50% of the dose is absorbed and Tmax is about three to six hours.
[A232219][A231784]
[L32614]
Following intravenous injection, the plasma half-life of methyldopa ranges from 90 to 127 minutes.
[L32624]
[A231789]
Following intravenous administration, approximately 17% of the dose in normal subjects were circulating in the plasma as free methyldopa.
[L32624]
[L32614]
[A232224]
L-α-methyldopa is biotransformed to its pharmacologically active metabolite, alpha-methylnorepinephrine. Methyldopa is extensively metabolized in the liver to form the main circulating metabolite in the plasma, alpha (α)-methyldopa mono-O-sulfate. Its other metabolites also include 3-O-methyl-α-methyldopa; 3,4-dihydroxyphenylacetone; α-methyldopamine; and 3-O-methyl-α-methyldopamine.
These metabolites are further conjugated in the liver to form sulfate conjugates.
[L32614]
After intravenous administration, the most prominent metabolites are alpha-methyldopamine and the glucuronide of dihydroxyphenylacetone, along with other uncharacterized metabolites.
[A231789]
D-α-methyldopa, which is the inactive isomer of methyldopa, is also metabolized to 3-O-methyl-α-methyldopa and 3,4-dihydroxyphenylacetone to a minimal extent; however, there are no amines (α-methyldopamine and 3-O-methyl-α-methyldopamine) formed.
[A232224]
[A232219]
Unabsorbed drug is excreted in feces as the unchanged parent compound.
[A231784]
After oral doses, excretion is essentially complete in 36 hours.
[L32619]
Due to attenuated excretion in patients with renal failure, accumulation of the drug and its metabolites may occur,[A231784] possibly leading to more profound and prolonged hypotensive effects in these patients.
[A231789]
[L32614]
Proteins and enzymes this drug interacts with in the body
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:15521010 PMID:18367661 PMID:19685173 PMID:26320580 PMID:7896779 PMID:8914574 PMID:9835627
Primarily responsible for the absorption of dietary di- and tripeptides from the small intestinal lumen (By similarity). Mediates transepithelial transport of muramyl and N-formylated bacterial dipeptides contributing to recognition of pathogenic bacteria by the mucosal immune system PMID:15521010 PMID:9835627
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 C02AB01
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)
Methyldopa
Additional database identifiers
Drugs Product Database (DPD)
10295
Drugs Product Database (DPD)
20297
ChemSpider
35562
BindingDB
48449
ZINC
ZINC000000020255
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2719
GenAtlas
DDC
GeneCards
DDC
GenBank Gene Database
M76180
GenBank Protein Database
181521
UniProt Accession
DDC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2228
GenAtlas
COMT
GeneCards
COMT
GenBank Gene Database
M65212
GenBank Protein Database
180920
Guide to Pharmacology
2472
UniProt Accession
COMT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2719
GenAtlas
DDC
GeneCards
DDC
GenBank Gene Database
M76180
GenBank Protein Database
181521
UniProt Accession
DDC_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11453
GenAtlas
SULT1A1
GeneCards
SULT1A1
GenBank Gene Database
L10819
GenBank Protein Database
179042
UniProt Accession
ST1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11454
GeneCards
SULT1A2
UniProt Accession
ST1A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11455
GeneCards
SULT1A3
UniProt Accession
ST1A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:30004
GeneCards
SULT1A4
UniProt Accession
ST1A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17845
GenAtlas
SULT1B1
GeneCards
SULT1B1
GenBank Gene Database
D89479
UniProt Accession
ST1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11456
GeneCards
SULT1C2
UniProt Accession
ST1C2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:33543
GeneCards
SULT1C3
UniProt Accession
ST1C3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11457
GeneCards
SULT1C4
UniProt Accession
ST1C4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11458
GenAtlas
SULT2A1
GeneCards
SULT2A1
GenBank Gene Database
L20000
GenBank Protein Database
306702
UniProt Accession
ST2A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14903
GeneCards
SULT4A1
UniProt Accession
ST4A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:33433
GeneCards
SULT6B1
UniProt Accession
ST6B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2689
GenAtlas
DBH
GeneCards
DBH
GenBank Gene Database
X13255
GenBank Protein Database
30474
Guide to Pharmacology
2486
UniProt Accession
DOPO_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9160
GenAtlas
PNMT
GeneCards
PNMT
GenBank Gene Database
J03727
GenBank Protein Database
190142
Guide to Pharmacology
2496
UniProt Accession
PNMT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10920
GenAtlas
SLC15A1
GeneCards
SLC15A1
GenBank Gene Database
U13173
GenBank Protein Database
773588
Guide to Pharmacology
984
UniProt Accession
S15A1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72