Sucralfate 1g/5ml oral suspension
Requires a prescription from a doctor or prescriber
Safety information for pregnancy and breastfeeding
Pregnancy
This drug is considered a pregnancy Category B drug.
Breastfeeding
Whether this drug is excreted in human milk is currently unknown.
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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MHRA alerts for Sucralfate
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 Sucralfate
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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 Sucralfate
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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.
1 branded products available
WHO defined daily dose (DDD)
4 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
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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: 16 · Randomised trials: 28 · 1982–2026
Showing the 50 most relevant studies, sorted by most relevant.
Andrea Messori, S. Trippoli, M. Vaiani, et al.
BMJ : British Medical Journal, 2000
M. Tryba
Critical Care Medicine, 1991
G. Lo, K. Lai, Jin‐shiung Cheng, et al.
Hepatology, 2000
M. Wells, Maureen S Macmillan, G. Raab, et al.
Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 2004
N. Agrawal, S. Roth, D. Graham, et al.
Annals of Internal Medicine, 1991
Coppini M, Caponio VCA, Mauceri R, et al.
2024
- Stomatitis
- Sucralfate
- Administration, Topical
BackgroundOral mucositis (OM) is considered one of the most common side effects of patients undergoing cancer therapy. OM prevention plays a crucial role in the effectiveness of cancer treatment and the patient's quality of life. Different preventive treatments have been proposed in clinical trials, however with inconclusive results.Materials and methodsA systematic review search was conducted in PubMed, Scopus, Web of Science, and Cochrane Database to answer the PICO question: in cancer patients, do specific topical agents compared to standard treatments or placebo reduce the onset and severity of oral mucositis? The risk of bias was assessed, and a network meta-analysis was conducted.ResultsOf 2913 results, 30 randomized clinical trials were considered suitable for inclusion. A total of 2564 patients were analyzed, of which 1284 belonged to the test group and 1280 belonged to the control group. Natural products were the most used, followed mainly by antimicrobial agents, coating agents, and basic oral care measures. Topical sucralfate resulted in the most powerful intervention for the OM prevention (OR = 0.04, 95%C.I. = 0.01-0.25, p-value = 0.001).ConclusionDue to its cytoprotective action, low cost, ease of administration, and safety, sucralfate could become a potential ally to prevent the onset of OM during cancer therapy.
Abstract licence: CC BY
Berntsson H, Thien A, Hind D, et al.
2024
- Radiation Injuries
- Pelvis
- Pelvic Neoplasms
AimsPelvic radiotherapy can induce gastrointestinal injury and symptoms, which can affect quality of life. We assessed interventions for managing these symptoms.Materials and methodsA review of randomised controlled trials published between January 1990 and June 2023 from databases including MEDLINE, EMBASE, CENTRAL, CINAHL, clinicaltrials.gov, ISRCTN and grey literature sources was conducted. Meta-analyses were carried out using the DerSimonian and Laird random effects model to produce overall treatment differences with 95% confidence intervals.ResultsTwenty-eight studies (2392 participants) of varying methodological quality were included. 4% formalin was superior to sucralfate for improving gastrointestinal symptom score (standardised mean difference [SMD] -1.07, 95% confidence interval -1.48 to -0.65). Argon plasma coagulation (APC) was inferior to sucralfate (SMD 1.22, 95% confidence interval 0.84 to 1.59). Counselling positively influenced symptom score (SMD -0.53, 95% confidence interval -0.76 to -0.29), whereas hyperbaric oxygen therapy showed conflicting results. Sucralfate combined with APC increased endoscopic markers of moderate-severe bleeding versus APC alone (risk ratio 2.26, 95% confidence interval 1.12 to 4.55). No definite conclusions on pain, incontinence, diarrhoea, tenesmus or quality of life interventions were confirmed.ConclusionsSmall study sizes, methodological quality and heterogeneity limit support of any individual intervention. APC and 4% formalin seem to be promising interventions, with further larger randomised controlled trials now warranted.
Abstract licence: CC BY
Shibli F, Mari A, Fass R
2025
Background and objectiveErosive esophagitis (EE) is the second most common phenotype of gastroesophageal reflux disease (GERD). While proton pump inhibitors (PPIs) are considered the mainstay treatment for healing and maintaining remission of EE, a significant proportion of patients, particularly those with advanced grades, fail to respond adequately. This review provides an updated overview of the current pharmacological treatment options for EE.MethodsAn extensive electronic literature search was performed using PubMed database to identify relevant articles. The search included prospective clinical trials, observational trials, case-control studies, systematic reviews with or without meta-analysis, and narrative reviews describing pharmacological therapy for adult patients with EE. Articles were limited to English language publications. Search terms encompassed various treatment modalities including PPIs, potassium-competitive acid blockers (P-CABs), histamine 2 receptor antagonists (H2RAs), sucralfate, prokinetics, rebamipide and alginates.Key content and findingsResearch has shown varying effectiveness across different treatments for EE. While randomized controlled trials found alginates, sucralfate, and histamine-2 receptor antagonists to have limited healing efficacy, PPIs remain the most effective treatment, achieving healing rates of 75-95% after 8 weeks, though symptom resolution reaches about 60-85%. Among PPIs, esomeprazole shows slightly better healing outcomes compared to others. However, PPI effectiveness decreases in advanced EE cases [Los Angeles (LA) grades C/D], with healing rates dropping to 60-70%. More recently, P-CABs have demonstrated promising results, demonstrating healing rates non-inferior to PPIS but superior in patients with advanced EE or PPI-resistent EE. Given that most patients experience relapse upon discontinuation, maintaining PPI or PCAB therapy is crucial for preventing EE recurrence.ConclusionsThe future of EE management lies in a more personalized approach that takes into account disease severity, PPI response, and patient preferences. While PPIs remain the mainstay of treatment, P-CABs represent a promising new therapeutic option, particularly for severe and PPI-resistant cases. The addition of nighttime to bedtime H2RAs or use of double PPI dose may benefit refractory cases. Further studies are needed to directly compare PPIs and P-CABs in different EE grades and evaluate the value of adjunctive therapies.
Abstract licence: CC BY-NC-ND
Briggs EE, McCray LR, Patel JJ, et al.
2025
- Sucralfate
- Tonsillectomy
- Postoperative Pain
Toews I, Hussain S, Nyirenda JLZ, et al.
2025
- Gastrointestinal Hemorrhage
- Intensive Care Units
- Cimetidine
ObjectivesTo assess the efficacy and safety of pharmacological interventions for preventing upper gastrointestinal (GI) bleeding in people admitted to intensive care units (ICUs).Design and settingSystematic review and frequentist network meta-analysis using standard methodological procedures as recommended by Cochrane for screening of records, data extraction and analysis. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach was used to assess the certainty of evidence.ParticipantsRandomised controlled trials involving patients admitted to ICUs for longer than 24 hours were included.Search methodsThe Cochrane Gut Specialised Register, Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase and Latin American and Caribbean Health Science Information database (LILACS) databases were searched from August 2017 to March 2022. The search in MEDLINE was updated in April 2023. We also searched ClinicalTrials.gov and the World Health Organization International Clinical Trials Registry Platform (WHO ICTRP).Main outcome measuresThe primary outcome was the prevention of clinically important upper GI bleeding.ResultsWe included 123 studies with 46 996 participants. Cimetidine (relative risk (RR) 0.56, 95% CI 0.40 to 0.77, moderate certainty), ranitidine (RR 0.54, 95% CI 0.38 to 0.76, moderate certainty), antacids (RR 0.48, 95% CI 0.33 to 0.68, moderate certainty), sucralfate (RR 0.54, 95% CI 0.39 to 0.75, moderate certainty) and a combination of ranitidine and antacids (RR 0.13, 95% CI 0.03 to 0.62, moderate certainty) are likely effective in preventing upper GI bleeding.The effect of any intervention on the prevention of nosocomial pneumonia, all-cause mortality in the ICU or the hospital, duration of the stay in the ICU, duration of intubation and (serious) adverse events remains unclear.ConclusionsSeveral interventions seem effective in preventing clinically important upper GI bleeding while there is limited evidence for other outcomes. Patient-relevant benefits and harms need to be assessed under consideration of the patients' underlying conditions.
Abstract licence: CC BY-NC
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
6-20 h
Mechanism
The mechanism of action of this drug in the healing duodenal ulcers is not yet c…
Food interactions
2 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
0.001%
Half-life
6-20 h
Protein binding
Volume of distribution
Metabolism
Elimination
48 hours
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Sucralfate has been shown to be a well-tolerated and safe drug. It is sold under many brands and is available in both tablet and suspension forms. It was approved by the FDA 1982 in tablet form, and in 1994 for the suspension form [L6073][L6076].
Sucralfate is also used in the prevention and/or treatment of gastro-esophageal reflux disease (GERD), gastritis, peptic ulcer disease, stress ulcer, in addition to dyspepsia [A177655][F4519].
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 861 interactions
Overdosage has never been observed with sucralfate [F4519]. It is unlikely, as administering a maximum dose of up to 12 g/kg/body weight in several animal species did not result in death. The lethal dose could not be determined in these studies [F4519].
It is likely that overdose of sucralfate in humans would result in constipation, and supportive treatment would be advised [F4519].
Use in pregnancy
This drug is considered a pregnancy Category B drug. Studies have been performed in rodents and rabbits at doses up to 50 times the recommended human dose. No harm to the fetus has been observed in the abovementioned studies. Sufficient and well-controlled clinical trials have not been performed in pregnant women.
Due to the fact that the results of animal studies are not always relevant to human response, sucralfate should be used during pregnancy only if it is deemed essential for the mother's health [FDA label].
Use in nursing
Whether this drug is excreted in human milk is currently unknown. Many drugs are excreted in breast milk, therefore, if sucralfate is administered to a lactating and nursing woman, caution should be observed [FDA label].
Carcinogenesis
24 month toxicity studies were performed in rodents, and the dose of sucralfate reached up to 1 g/kg (equivalent to 12 times the recommended human dose). No signs of sucralfate-related tumors were noted[FDA label].
Studies in both humans and animals have indicated that sucralfate forms a complex that binds to protein-rich exudate found on the surface of ulcers. It binds to albumin and fibrinogen [A11831][A177685] preventing blood clot lysis by stomach acid (hydrochloric acid). Sucralfate increases the tissue levels of fibroblast growth factors and epidermal growth factors,[A16738][A16741] leading to an increase in prostaglandins at the gastrointestinal tract lining, which promotes the healing of gastrointestinal ulcers.[A177655]
In the laboratory setting, a sucralfate-albumin film provides a barrier against the entry of hydrogen ions, which are a component of gastric acid. In humans, sucralfate, given at therapeutic doses for ulcers, decreases pepsin activity in gastric fluids by 32% [FDA label]. Pepsin has been shown to be damaging to tissues, further aggravating ulcer lesion inflammation [A177667]. Bile salts have been implicated in mucosal injury to the gastrointestinal tract [A177697][A177700]. Sucralfate has also been shown to adsorb bile salts in the laboratory, setting, which could further contribute to its beneficial effects in ulcer healing [FDA label].
How the body processes this drug — absorption, distribution, metabolism, and elimination
In dialyzed patients diagnosed with chronic renal failure, aluminum toxicity related to sucralfate has been observed and reported. The daily amount of aluminum ingestion (including sucralfate) should be carefully examined before administering sucralfate in combination with other drugs also containing aluminum, including various antacids [F4519].
Proteins and enzymes this drug interacts with in the body
PMID:8663044
Also acts as an integrin ligand which is required for FGF2 signaling .
PMID:28302677
Binds to integrin ITGAV:ITGB3 .
PMID:28302677
Plays an important role in the regulation of cell survival, cell division, cell differentiation and cell migration .
PMID:28302677 PMID:8663044
Functions as a potent mitogen in vitro .
PMID:1721615 PMID:3732516 PMID:3964259
Can induce angiogenesis .
PMID:23469107 PMID:28302677
Mediates phosphorylation of ERK1/2 and thereby promotes retinal lens fiber differentiation PMID:29501879
Was originally thought to be essential for platelet aggregation, based on in vitro studies using anticoagulated blood. However, subsequent studies have shown that it is not absolutely required for thrombus formation in vivo. Enhances expression of SELP in activated platelets via an ITGB3-dependent pathway.
Maternal fibrinogen is essential for successful pregnancy. Fibrin deposition is also associated with infection, where it protects against IFNG-mediated hemorrhage. May also facilitate the antibacterial immune response via both innate and T-cell mediated pathways
ATC A02BX02
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)
Sucralfate
Additional database identifiers
Drugs Product Database (DPD)
2023
ChemSpider
32701653
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8887
GeneCards
PGA5
Guide to Pharmacology
2390
UniProt Accession
PEPA5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3676
GenAtlas
FGF2
GeneCards
FGF2
GenBank Gene Database
X04431
GenBank Protein Database
31362
UniProt Accession
FGF2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3229
GenAtlas
EGF
GeneCards
EGF
GenBank Gene Database
X04571
GenBank Protein Database
31121
UniProt Accession
EGF_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3661
GenAtlas
FGA
GeneCards
FGA
GenBank Gene Database
AF361104
GenBank Protein Database
13591824
UniProt Accession
FIBA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3662
GenAtlas
FGB
GeneCards
FGB
GenBank Gene Database
J00129
GenBank Protein Database
182430
UniProt Accession
FIBB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3694
GenAtlas
FGG
GeneCards
FGG
GenBank Gene Database
M10014
GenBank Protein Database
182439
UniProt Accession
FIBG_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