Nicorandil 10mg tablets
Requires a prescription from a doctor or prescriber
Nicorandil is an orally efficacious vasodilatory drug and antianginal agent marketed in the UK, Australia, most of Europe, India, Philippines, Japan, South Korea, and Taiwan.
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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 Nicorandil
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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.
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Suspected adverse reactions reported for Nicorandil
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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.
21 branded products available
MHRA licensed products
View all licensed products for Nicorandil on the MHRA register
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg tablets
Nicorandil 10mg 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)
40 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Stable angina (QS21)
Stable angina: management (CG126)
Acute coronary syndromes (NG185)
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
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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: 31 · Randomised trials: 17 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
The Lancet, 2002
Li S, Li W, Cheng M, et al.
2025
BackgroundAnthracyclines are cornerstone chemotherapeutics, but cardiotoxicity limits their use.ObjectiveThis study aims to evaluate the efficacy of various drugs in preventing and treating anthracycline-induced cardiotoxicity (AIC).MethodsWe conducted an extensive search across seven databases to identify randomized controlled trials (RCTs) pertinent to the prevention and treatment of AIC with medications. Subsequently, a Bayesian Model-based network meta-analysis was performed in the R 4.4.0.ResultsA total of 128 RCTs involving 10,431 cancer patients treated with anthracyclines and 78 drug regimens were included in this study. The network meta-analysis results showed that, compared with patients who did not receive cardioprotective drugs, those treated with Calcium Dibutyryladenosine Cyclophosphate (Mean Difference [95% Credible Interval], 8.760 [0.5917, 16.92]), Carvedilol (4.024 [0.5372, 7.656]), Carvedilol + Candesartan (7.934 [3.159, 12.91]), Compound Salvia Miltiorrhiza + Levocarnitine (9.087 [0.9160, 17.25]), Dexrazoxane (5.066 [2.589, 7.540]), Dexrazoxane + Cinobufacini (11.61 [4.590, 18.70]), Dexrazoxane + Shenqi Fuzheng (13.05 [4.640, 21.40]), Nicorandil (14.24 [5.122, 23.31]), Qiliqiangxin (11.38 [2.826, 19.91]), and Xinmai Long (6.371 [1.735, 11.02]) experienced less decrease in LVEF after chemotherapy. The SUCRA ranking results indicated that the most effective treatment option for preserving LVEF was Nicorandil (SUCRA 91.76%).ConclusionApart from Dexrazoxane, Carvedilol, a β-blocker, also appears to show significant potential in preventing AIC. Furthermore, our results indicate that there is insufficient evidence to support the beneficial effects of statins, Sildenafil, Ivabradine, Levocarnitine, N-acetylcysteine, Glutathione, Coenzyme Q10, Vitamin E, and Vitamin C in preventing LVEF decline and exerting a positive effect on the prevention of AIC.
Abstract licence: CC BY
Khan AA, Tahir MZ, Maryam KUE, et al.
2025
- Kidney Diseases
- Nicorandil
- Contrast Media
Butt AI, Afzal F, Raza S, et al.
2025
- Kidney Diseases
- Nicorandil
- Contrast Media
Waseem R, Kumar A, Kumari S, et al.
2025
BackgroundContrast-induced nephropathy (CIN) remains a significant complication in patients undergoing coronary angiography (CAG) and percutaneous coronary intervention (PCI).MethodsA comprehensive literature search was conducted across PubMed, MEDLINE, Embase, Google Scholar, and Web of Science up to May 2024 to identify randomized controlled trials (RCTs) evaluating the efficacy and safety of nicorandil in patients undergoing CAG or PCI. The primary outcome was CIN incidence, while secondary outcomes included, changes in serum creatinine, serum cystatin C, blood urea nitrogen (BUN), and estimated glomerular filtration rate (eGFR). Risk ratios (RRs) and standardized mean differences (SMDs) with corresponding 95% confidence intervals (CIs) were pooled using a random-effects model. Heterogeneity was assessed using the I2 statistic.ResultsEleven RCTs and one prospective cohort study involving 2910 patients were included. Nicorandil administration was associated with a significant reduction in CIN incidence (RR: 0.40 [0.31-0.52], P P P = 0.02) demonstrating efficacy (p-interaction = 0.22). Patients receiving nicorandil exhibited significantly lower serum creatinine levels at 48 hours (SMD: -0.34 [-0.52, -0.16], P = 0.0002) and 72 hours (SMD: -0.24 [-0.40, -0.08], P = 0.003) post-procedure. Serum cystatin C was also significantly reduced at 48 hours (SMD: -0.48 [-0.81, -0.15], P = 0.004). However, nicorandil did not produce a significant change in eGFR at 24 hours (SMD: 0.17 [-0.07, 0.41], P = 0.17), 48 hours (SMD: 0.13 [-0.10, 0.37], P = 0.26), or 72 hours (SMD: 0.19 [-0.07, 0.45], P = 0.36).ConclusionNicorandil administration reduces CIN incidence and improves renal biomarker profiles in patients undergoing CAG and PCI. Further large-scale trials are necessary to validate its renoprotective properties.
Abstract licence: CC BY
Tariq H, Ahmed S, Ahmed S, et al.
2024
Percutaneous coronary intervention (PCI) is a common procedure for treating coronary artery disease, but it carries a risk of periprocedural myocardial injury (PMI). This meta-analysis evaluated the efficacy of nicorandil, a hybrid compound with nitrate-like and potassium channel-opening properties, in preventing PMI during PCI. A comprehensive literature search identified 14 studies involving 1,762 patients, with 882 receiving nicorandil and 880 in the control group. The analysis revealed that nicorandil significantly reduced the incidence of PMI (RR: 0.73, 95% CI: 0.61-0.86) and major adverse cardiovascular events (MACE) (RR: 0.76, 95% CI: 0.58-0.99) compared to the control group. Nicorandil's cardioprotective effects are attributed to its ability to improve coronary blood flow, precondition the myocardium, and reduce oxidative stress and inflammation. These findings suggest that nicorandil could be a valuable adjunctive therapy during PCI, potentially improving patient outcomes. However, the study had limitations, including variations in drug administration methods and a lack of individual-level data for subgroup analysis. Future research should focus on optimizing dosing regimens and administration timing and comparing nicorandil's effectiveness with other cardioprotective agents.
Abstract licence: CC BY
Aizaz MAR, Aziz U, Jaber Amin MH
2026
Abo Elnaga AA, Alawadi IS, Elettreby AM, et al.
2025
- Kidney Diseases
- Nicorandil
- Contrast Media
Ferreira NL, Aguiar DR, Nair SG, et al.
2025
Laborante R, Bianchini E, Ciliberti G, et al.
2026
- Cardiovascular Agents
- Angioplasty, Balloon, Coronary
- Percutaneous Coronary Intervention
AimsThis network meta-analysis of randomized controlled trials (RCTs) evaluates the comparative safety and efficacy of intra-coronary (IC) pharmacological and procedural treatments-on top of balloon angioplasty and stent placement-on clinical outcomes and surrogate endpoints of coronary microvascular obstruction (CMVO) in patients with ST-elevation myocardial infarction (STEMI).Methods and resultsTwo electronic databases were searched for eligible studies. Primary efficacy endpoints included all-cause mortality, non-fatal myocardial infarction (MI), and heart failure (HF) hospitalization. Primary safety endpoints included peri-procedural arrhythmias including atrioventricular blocks (AVBs) and ventricular fibrillation/sustained ventricular tachycardia (VF/SVT), any bleeding, and stroke. Secondary efficacy endpoints included the occurrence of post-procedural thrombolysis in myocardial infarction (TIMI) flow grade 0-2 and ST-segment resolution. A total of 64 RCTs involving 27 243 patients were included. In mixed comparisons, no treatment significantly reduced the incidence of primary efficacy endpoints compared to conventional primary PCI during a mean follow-up of 8 months. Several treatments significantly reduced the occurrence of post-PCI TIMI 0-2 flow grade [adenosine: 0.40 (odds ratio), (95% Confidence Interval 0.24-0.68); verapamil: 0.22 (0.07-0.69); tirofiban: 0.43 (0.27-0.71); manual thrombus aspiration (TA): 0.61 (0.45-0.82); fibrinolytic + manual TA: 0.24 (0.12-0.48); tirofiban + manual TA: 0.32 (0.14-0.75)], compared to conventional primary PCI. IC administration of tirofiban increased the risk of any bleeding [incidence rate ratio: 1.65 (1.11-2.45)], while IC adenosine increased the risk of peri-procedural AVBs [OR: 2.80 (1.14-6.84)]. Nicorandil reduced the incidence of peri-procedural VF/SVT [OR: 0.31 (0.12-0.81)].ConclusionAdjunctive IC treatments during primary PCI do not influence hard clinical outcomes compared to conventional therapy within a mean 8-month follow-up, although several of them lead to an improvement in surrogate endpoints of CMVO.Study registration numberCRD42023468559.
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
8 found
Half-life
1 hour
Mechanism
Nicorandil mediates its therapeutic efficacy via two main mechanisms.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
75%
Half-life
1 hour
[A20328]
Protein binding
25%
[A20328]
Volume of distribution
1.0-1.4 L/kg
[A20328]
Metabolism
[L887]
The main biotransformation pathways of nicorandil are denitration, followed by subsequent nicotinamide metabolism.…
Elimination
60%
[L887]
…
Clearance
1.15 L
[A20328]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1320 interactions
Headaches may arise from vasodilation. Other common side effects include myalgia, bronchitis, dyspnoea, and respiratory disorder .
[L887]
Nicorandil does not affect fertility of male or female rats, and shows no potential in carcinogenic, mutagenic or genotoxic studies .
[L887]
Oral LD50 values in mouse, rat and dog are 626 mg/kg, 1220 mg/kg and 62.5 mg/kg, respectively MSDS.
Nicorandil contain a nitrate moiety in its structure, making it a good dilator of vascular smooth muscle like other nitroglycerin esters [A20323]. Direct relaxation of venous vascular system arises from NO-donor mediated stimulation of guanylyl cyclase and increased levels of intracellular cyclic GMP (cGMP). Elevated levels of cGMP contributes to the total relaxing effect of nicorandil at higher concentrations of the drug [A7839].
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A20328]
Steady-state plasma concentrations of nicorandil usually are reached within approximately 96-120 h after twice daily dosing (10 or 20mg) .
[L887]
[A20328]
[A20328]
[A20328]
[L887]
The main biotransformation pathways of nicorandil are denitration, followed by subsequent nicotinamide metabolism. The main pharmacologically inactive denitrated metabolite 2-nicotinamidoethanol can be detected in the urine. The derivatives formed from the nicotinamide metabolism of denitrated products are nicotinuric acid, nicotinamide, N-methylnicotinamide and nicotinic acid .
[L887]
[L887]
Only approximately 1% of nicorandil is excreted unchanged in the urine, and the remaining compounds are mainly the denitrated metabolite (9%) and its derivatives (e.g. nicotinuric acid 6%, nicotinamide 1%, N-methylnicotinamide < 1% and nicotinic acid < 1%) .
[L887]
Less than 2% of administered dose is excreted through the biliary system .
[A20328]
[A20328]
Proteins and enzymes this drug interacts with in the body
PMID:9831708
Can form a sulfonylurea-sensitive but ATP-insensitive potassium channel with KCNJ8 (By similarity)
ATC C01DX16
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)
Nicorandil
Additional database identifiers
ChemSpider
43240
BindingDB
50247908
ZINC
ZINC000001533102
HUGO Gene Nomenclature Committee (HGNC)
HGNC:60
GenAtlas
ABCC9
GeneCards
ABCC9
GenBank Gene Database
AF061323
GenBank Protein Database
3127176
Guide to Pharmacology
2746
UniProt Accession
ABCC9_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