Ketorolac 30mg/1ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
Safety information for pregnancy and breastfeeding
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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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 Ketorolac
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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 Ketorolac
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5 branded products available
MHRA licensed products
View all licensed products for Ketorolac on the MHRA register
Toradol 30mg/1ml solution for injection ampoules
Ketorolac 30mg/1ml solution for injection ampoules
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)
30 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 BNF/ATC 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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Supply & safety information
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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
Browse tools
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: 17 · Randomised trials: 31 · 2012–2026
Showing the 50 most relevant studies, sorted by most relevant.
Gildàsio S. de Oliveira, D. Agarwal, H. Benzon
Anesthesia & Analgesia, 2012
R. Gobble, Han Hoang, Bartlomiej Kachniarz, et al.
Plastic and Reconstructive Surgery, 2014
Shehata MM, Reinert JP
2026
- Pain
- Ketamine
- Ketorolac
Ping R, Kang X, Fang R, et al.
2026
- Ketorolac
- Anti-Inflammatory Agents, Non-Steroidal
- Root Canal Therapy
Ononogbu-Uche FC, Ahmed R, Giarola Í, et al.
2026
- Ketorolac
- Anti-Inflammatory Agents, Non-Steroidal
- Spinal Fusion
Hari Babu R, Gautam SS, Pal Singh S, et al.
2026
Almeida VFA, Donato G, Dantas M, et al.
2026
- Hematoma
- Ketorolac
- Anti-Inflammatory Agents, Non-Steroidal
Bahreini M, Rashnavandi H, Rasooli F, et al.
2025
- Ketorolac
- Anti-Inflammatory Agents, Non-Steroidal
- Postoperative Pain
Tessitore A, Zupin L, Celsi F, et al.
2025
Alsabri M, Adel Diab R, Alqeeq BF
2025
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
160 found
Half-life
2.5 hours
Mechanism
Ketorolac inhibits key pathways in prostaglandin synthesis which is crucial to it's mechanism of action.
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
80%
Half-life
2.5 hours
Protein binding
99%
[A175966]
Volume of distribution
0.25 L/kg
[A176143]
Metabolism
[L3674][A176143]…
Elimination
92%
Clearance
0.021 to 0.037 L/h
[A176143]
Further, studies have illustrated that clearance of oral, IM and IV doses…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
It's analgesic properties make it a useful pain management tool across many settings including postoperative pain, rheumatoid arthritis, osteoarthritis, menstrual disorders, headaches, spinal and soft tissue pain, and ankylosing spondylitis.[L6520] Impressively, ketorolac has a similar efficacy to standard doses of morphine and meperidine making it a useful opioid sparing agent.[L6511]
[A176131]
It is indicated for short term management of acute pain that requires the calibre of pain management offered by opioids.
[L3674]
Clinicians may choose to initiate ketorolac to manage post-operative pain, spinal and soft tissue pain, rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, menstrual disorders and headaches among other ailments.
[L6520]
Regardless of the etiology of pain, patients should use the lowest possible dose, and avoid using ketorolac for an extended period of time (ideally ≤ 5 days).
[L3674]
A benefit of choosing ketorolac over other analgesics with similar potency is that that there does not appear to be a risk of dependence or tolerance with ketorolac use.
[A176131]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1642 interactions
[L11055]
Most adverse effects associated with short term use are mild in nature, related to the gastrointestinal tract and nervous system, and occur in roughly 39% of patients.
[A176131]
Common symptoms of ketorolac overdose include nausea, vomiting, epigastric pain, gastrointestinal bleeding, lethargy and drowsiness. More rare symptoms of overdose include acute renal failure, hypertension, respiratory depression, and coma.
[L3674]
Ketorolac is classified as Pregnancy Category C since there is a lack of evidence demonstrating safety in pregnant women.
[L11070]
NSAIDs including ketorolac increase the risk of premature closure of the fetal ductus arteriosus in the 3rd trimester; therefore, beginning at 30 weeks gestation, pregnant women should avoid ketorolac.
[L11070]
Ketorolac has been shown to be excreted in breast milk, and although available data has not demonstrated any adverse effects in nursing infants, practitioners should proceed with caution when suggesting ketorolac for nursing mothers.
[L11055][L3674]
The benefits should outweigh the risks and the mother should be counselled to monitor the infant closely and to contact the infant's healthcare provider should any adverse effects arise.
[L11055][L3674]
Women who are trying to conceive are not advised to take ketorolac since it's effect on prostaglandin synthesis may impair fertility.[L11055L11055]
As a result, inhibition of the COX-1 enzyme is linked to an increased risk of bleeding and risk of gastric ulceration, while the desired anti-inflammatory and analgesic properties are linked to inhibition of the COX-2 enzyme.[A176134] Therefore, despite it's effectiveness in pain management, ketorolac should not be used long-term since this increases the risk of serious adverse effects such as gastrointestinal bleeding, peptic ulcers, and perforations.[A178678]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A175966]
After intramuscular administration, ketorolac demonstrates a time to maximal plasma concentration (tmax) of approximately 45-50 minutes, and a tmax of 30-40 minutes after oral administration.
[A176143]
The rate of absorption may be reduced by food; however, the extent of absorption remains unaffected.
[A176143]
[L3674]
[A175966]
[A176143]
[L3674][A176143]
Enzymes involved in phase I metabolism include CYP2C8 and CYP2C9, while phase II metabolism is carried out by UDP-glucuronosyltransferase (UGT) 2B7.
[A176234]
[L3674]
[A176143]
Further, studies have illustrated that clearance of oral, IM and IV doses of ketorolac are comparable which suggests linear kinetics.
[L3674]
It should also be noted that clearance in children is about double the clearance found in adults.
[A176231]
Proteins and enzymes this drug interacts with in the body
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:7947975
Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells (Probable).
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC M01AB15
ATC S01FB51
ATC S01BC05
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)
Ketorolac
Additional database identifiers
Drugs Product Database (DPD)
1241
ChemSpider
3694
BindingDB
85511
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9604
GenAtlas
PTGS1
GeneCards
PTGS1
GenBank Gene Database
M31822
GenBank Protein Database
387018
Guide to Pharmacology
1375
UniProt Accession
PGH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
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