Aminophylline 360mg suppositories
Requires a prescription from a doctor or prescriber
Aminophylline is a drug combination that contains theophylline and ethylenediamine in a 2:1 ratio.
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Aminophylline
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.
View Drug Analysis Profile
Suspected adverse reactions reported for Aminophylline
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
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.
View EudraVigilance report
Suspected adverse reactions reported for Aminophylline
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
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)
600 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 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
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 & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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. 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: 15 · Randomised trials: 19 · 1950–2026
Showing the 50 most relevant studies, sorted by most relevant.
R. Barati‐Boldaji, S. Shojaei‐Zarghani, M. Mehrabi, et al.
Anesthesia and Pain Medicine, 2023
G. Bhatt, Priya Gogia, M. Bitzan, et al.
Archives of Disease in Childhood, 2019
Alatni RI, Alsamani R, Alqefari A
2024
Post-dural puncture headache (PDPH) is occasionally an inevitable side effect of neuraxial anesthesia, which can happen after spinal anesthesia or if an accidental dural puncture (ADP) happens during epidural anesthesia. The treatment and prevention options for PDPH differ widely from one institution to another. The management of PDPH is heterogeneous in many institutions because of the absence of clear guidelines and protocols for the management of PDPH. This study aimed to summarize all articles published during the past decade that discussed the treatment or prevention of PDPH. From 2013 to 2023, 345 publications were filtered for all treatment and prevention approaches used for PDPH patients. The Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) 2020 guidelines were followed for conducting this systematic review, and 38 articles were included for analysis and review. Existing data come from small randomized clinical trials and retrospective or prospective cohort studies. This review supports the effect of oral pregabalin and intravenous aminophylline in both treatment and prevention. Intravenous mannitol, intravenous hydrocortisone, triple prophylactic regimen, and neostigmine plus atropine combination showed effective and beneficial outcomes. On the other hand, neither neuraxial morphine nor epidural dexamethasone showed promising results. Consequently, the use of neuraxial morphine or epidural dexamethasone for the prevention of PDPH remains questionable. Regarding the posture of the patient and its consequences on the incidence of the headache, lateral decubitus is better than a sitting position, and a prone position is better than a supine position. Smaller non-cutting needles play a role in avoiding PDPH. Minimally invasive nerve blocks, including sphenopalatine ganglion or greater occipital nerves, are satisfyingly effective. Epidural blood patches remain the more invasive but the gold standard and ultimate solution in patients resisting medical therapy. This study highlights the need for larger research to define the best approach to prevent and treat PDPH.
Abstract licence: CC BY
Mudawi K, Hamud A, Powell C, et al.
2025
- Asthma
- Aminophylline
- Bronchodilator Agents
Neamțu AV, Zlatian OM, Manda CV, et al.
2025
Background: Apnea of prematurity affects at least 85% of infants born before 34 weeks' gestation and represents a significant clinical challenge in neonatal intensive care. Methylxanthines, including caffeine, theophylline, and aminophylline, have emerged as the primary pharmacological intervention for this condition. Objective: To conduct a comprehensive systematic review of the use of methylxanthine in the treatment and prevention of apnea episodes in preterm infants, evaluating efficacy, safety, and long-term outcomes. Methods: We searched multiple databases including PubMed, Embase, Web of Science for randomized controlled trials, retrospective studies, or case-control studies of methylxanthine effects in preterm apnea. Risk of bias was assessed using the Cochrane Risk of Bias tool. Results were summarized narratively and grouped by methylxanthine type, study design, and primary outcomes (reduction in frequency and severity of apnea episodes, success of extubation, risk of bronchopulmonary dysplasia). Results: Twenty-five studies (n = 4599 preterm infants) were included. The landmark Caffeine for Apnea of Prematurity (CAP) trial (n = 2006) demonstrated that caffeine therapy significantly reduced bronchopulmonary dysplasia (36.3% vs. 46.9%, adjusted OR 0.63) and facilitated the earlier discontinuation of positive airway pressure (median 1 week earlier). Studies with a smaller number of cases have consistently demonstrated the efficacy of methylxanthines in reducing the incidence of bronchopulmonary dysplasia and apneic episodes and in supporting successful extubation. Long-term follow-up at 11 years showed improved pulmonary function (FEV1 z-score -1.00 vs. -1.53). Discussion: Limitations of this review include heterogeneity in outcome definitions, small sample sizes in early studies, and the dominance of evidence from the CAP trial. Methylxanthines, particularly caffeine, are an evidence-based intervention used for apnea of prematurity, with demonstrated benefits that extend beyond reducing the frequency and severity of apnea episodes, including decreasing the risk of bronchopulmonary dysplasia as well as reducing the need for mechanical ventilation. No external funding was received for this review. No registration record exists for this systematic review.
Abstract licence: CC BY
Abu-Sultaneh S, Miller AG, Basnet S, et al.
2025
- Asthma
- Bronchodilator Agents
- Critical Illness
IntroductionPediatric critical asthma is one of the most common pediatric illnesses in children admitted to the pediatric ward and pediatric intensive care unit (PICU). Adjunct intravenous (IV) bronchodilators are often used when initial management with systemic corticosteroids and inhaled short-acting beta agonists (SABA) fail to provide improvement in a patient's clinical condition. While the recent guidelines gave recommendations for the use of different IV bronchodilators compared to placebo, it did not include ranking on which one should be used as first-line or second-line agent. The aim of this network meta-analysis is to determine the effect of IV bronchodilators on patient-centered outcomes and rank medications based on their effectiveness in these outcomes.MethodsA systematic review was conducted using three databases MEDLINE, Embase, and CINAHL to identify randomized control trials examining the use of IV magnesium sulfate (MgSO4), IV methylxanthines (aminophylline or theophylline), IV SABA (salbutamol, terbutaline) in pediatric critical asthma patients. Bayesian network metanalytic framework was used to compare the interventions. Results are reported as odds ratio (OR) or mean difference (MD) and 95% Credible Interval (CrI).ResultsTwelve trials (n = 852) were included in the network meta-analysis. Largest reduction in hospital length of stay (LOS), PICU admission, and PICU LOS were noted with IV MgSO4; (MD: -3.1 days, 95% CrI: -6.9 days to 0.13 days), (OR 0.21; 95% CrI 0.02, 1.3), and (MD: -4.0 days, 95% CrI: -7.1 days to -1.2 days) respectively. IV MgSO4 was ranked first in three outcomes of interest with Surface Under the Cumulative Ranking curve (SUCRA) of 0.884 for hospital LOS, 0.919 for PICU admission, and 0.957 for PICU LOS. For preventing intubation, IV SABA was ranked the highest (SUCRA 0.995), but the only study with IV SABA had zero intubation events. In a sensitivity analysis that excluded studies with zero events, the intubation rate was lowest with IV MgSO4 (OR 0.10; 95% CrI 0.003, 0.88) and it was ranked the best treatment (SUCRA 0.921).ConclusionsIn this network meta-analysis comparing different IV adjunct bronchodilators, IV MgSO4 was ranked first followed by IV SABA, and then IV methylxanthines. Given these findings and the favorable safety profile, ease of use, and low cost, IV MgSO4 appears most promising the first adjunct IV bronchodilator, however, further large high-quality trials are still needed before it can be endorsed as routine first-line agent.
Abstract licence: CC BY-NC-ND
Alnazari M, Badawi A, Alamri O, et al.
2026
M. Yung, M. South
Archives of Disease in Childhood, 1998
Yiqun Miao, Yun Zhou, Shuliang Zhao, et al.
PLoS ONE, 2022
B. Littenberg
JAMA, 1988
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
7-9 hours
Mechanism
Aminophylline is the ethylenediamine salt of theophylline.
Food interactions
6 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
7-9 hours
Protein binding
60%
Volume of distribution
0.3 to 0.7 L/kg
Clearance
0.29 mL
* 0.64 mL/kg/min [postnatal age 25-57 days]
* 1.7…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 924 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
* 0.64 mL/kg/min [postnatal age 25-57 days]
* 1.7 mL/kg/min [ 1-4 years]
* 1.6 mL/kg/min [4-12 years]
* 0.9 mL/kg/min [13-15 years]
* 1.4 mL/kg/min [16-17 years]
* 0.65 mL/kg/min [Adults (16-60 years), non-smoking asthmatics]
* 0.41 mL/kg/min [Elderly (>60 years). liver, and renal function]
* 0.33 mL/kg/min [Acute pulmonary edema]
* 0.54 mL/kg/min [COPD->60 years, stable non-smoker >1 year]
* 0.48 mL/kg/min [COPD with cor pulmonale]
* 1.25 mL/kg/min [Cystic fibrosis (14-28 years)]
* 0.31 mL/kg/min [Liver disease -cholestasis]
* 0.35 mL/kg/min [cirrhosis]
* 0.65 mL/kg/min [acute hepatitis]
* 0.47 mL/kg/min [Sepsis with multi-organ failure]
* 0.38 mL/kg/min [hypothyroid]
* 0.8 mL/kg/min [hyperthyroid]
Proteins and enzymes this drug interacts with in the body
PMID:1315035 PMID:25961942 PMID:8155697 PMID:8695850
Also has activity toward cUMP .
PMID:27975297
Independently of its catalytic activity it is part of an E2/17beta-estradiol-induced pro-apoptotic signaling pathway. E2 stabilizes the PDE3A/SLFN12 complex in the cytosol, promoting the dephosphorylation of SLFN12 and activating its pro-apoptotic ribosomal RNA/rRNA ribonuclease activity. This apoptotic pathway might be relevant in tissues with high concentration of E2 and be for instance involved in placenta remodeling PMID:31420216 PMID:34707099
PMID:28497810
Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression and developmental events (By similarity). Histone deacetylases act via the formation of large multiprotein complexes (By similarity). Forms transcriptional repressor complexes by associating with MAD, SIN3, YY1 and N-COR .
PMID:12724404
Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development (By similarity).
Acts as a component of the histone deacetylase NuRD complex which participates in the remodeling of chromatin .
PMID:16428440 PMID:28977666
Component of the SIN3B complex that represses transcription and counteracts the histone acetyltransferase activity of EP300 through the recognition H3K27ac marks by PHF12 and the activity of the histone deacetylase HDAC2 .
PMID:37137925
Also deacetylates non-histone targets: deacetylates TSHZ3, thereby regulating its transcriptional repressor activity .
PMID:19343227
May be involved in the transcriptional repression of circadian target genes, such as PER1, mediated by CRY1 through histone deacetylation (By similarity). Involved in MTA1-mediated transcriptional corepression of TFF1 and CDKN1A .
PMID:21965678
In addition to protein deacetylase activity, also acts as a protein-lysine deacylase by recognizing other acyl groups: catalyzes removal of (2E)-butenoyl (crotonyl), lactoyl (lactyl) and 2-hydroxyisobutanoyl (2-hydroxyisobutyryl) acyl groups from lysine residues, leading to protein decrotonylation, delactylation and de-2-hydroxyisobutyrylation, respectively PMID:28497810 PMID:29192674 PMID:35044827
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC R03DA55
ATC R03DA05
ATC R03DA20
ATC R03DB05
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Aminophylline
Additional database identifiers
Drugs Product Database (DPD)
9963
ChemSpider
9062
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8778
GenAtlas
PDE3A
GeneCards
PDE3A
GenBank Gene Database
M91667
GenBank Protein Database
38201493
Guide to Pharmacology
1298
UniProt Accession
PDE3A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:262
GenAtlas
ADORA1
GeneCards
ADORA1
GenBank Gene Database
S45235
GenBank Protein Database
256155
Guide to Pharmacology
18
UniProt Accession
AA1R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:268
GenAtlas
ADORA3
GeneCards
ADORA3
GenBank Gene Database
L20463
GenBank Protein Database
349449
Guide to Pharmacology
21
UniProt Accession
AA3R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4853
GenAtlas
HDAC2
GeneCards
HDAC2
GenBank Gene Database
U31814
GenBank Protein Database
1667394
Guide to Pharmacology
2616
UniProt Accession
HDAC2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_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:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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