General
Preferred name
KETOROLAC
Synonyms
KETOROLAC TROMETHAMINE ()
Ketorolac tris salt ()
Toradol ()
Sprix ()
Acuvail ()
Macril ()
Acular ()
Acular LS ()
Ketorolac (tromethamine salt) ()
RS37619 tromethamine salt ()
RS37619 ()
Ketorolaco ()
Ketorolac tromethamine salt ()
Lixidol ()
NSC-758637 ()
Dolac ()
Tarasyn ()
Ketorolac (+/-)-form tromethamine salt ()
Acular preservative free ()
Ketorolac tromethamine component of omidria ()
Ketorolac trometamol ()
Ketorolac (calcium salt) ()
P&D ID
PD010012
CAS
74103-07-4
74103-06-3
66635-83-4
167105-81-9
Tags
available
drug
Approved by
FDA
First approval
1989
Drug indication
Pain
Heart disease
Postoperative inflammation
Drug Status
approved
withdrawn
Max Phase
4.0
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
PRICE 29
DESCRIPTION Ketorolac tromethamine salt (RS37619 tromethamine salt) is a non-steroidal anti-inflammatory agent, acting as a nonselective COX inhibitor, with IC50s of 20 nM for COX-1 and 120 nM for COX-2.
ROE Ketorolac is primarily renally eliminated and approximately 92% of the dose can be recovered in urine with 60% of this proportion recovered unchanged and 40% recovered as metabolites. In addition 6% of a single dose is eliminated in the feces. [F4105]
PHARMACODYNAMICS Ketorolac is a non-selective NSAID and acts by inhibiting both COX-1 and COX-2 enzymes which are normally responsible for converting arachidonic acid to prostaglandins. The COX-1 enzyme is constitutively active and can be found in platelets, gastric mucosa, and vascular endothelium. On the other hand, the COX-2 enzyme is inducible and mediates inflammation, pain and fever. As a result, inhibition of the COX-1 enzyme is linked to the increased risk of bleeding and risk of gastric ulceration associated with ketorolac, while the desired anti-inflammatory and analgesic properties are linked to inhibition of the COX-2 enzyme.[A176134]
ABSORPTION Ketorolac is rapidly, and completely absorbed after oral administration. [F4105][A76143]
MOA Ketorolac inhibits key pathways in prostaglandin synthesis which appears crucial to it's mechanism of action. [A176143] Although ketorolac is non-selective and inhibits both COX-1 and COX-2 enzymes, it's clinical efficacy is derived from it's COX-2 inhibition. The COX-2 enzyme is inducible and is responsible for converting arachidonic acid to prostaglandins that mediate inflammation and pain. By blocking this pathway, ketorolac achieves analgesia and reduces inflammation. [A176134] Ketorolac is administered as a racemic mixture; however, the "S" enantiomer is largely responsible for it's pharmacological activity. [A176246]
TOXICITY The rate of adverse effects increases with higher doses of ketorolac. The most frequently observed adverse effects in patients occurring with an incidence of greater than 10% include: abdominal pain, dyspepsia, nausea, and headaches. [F4003] 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. [F4105]
METABOLISM Ketorolac is heavily metabolized in the liver where the parent drug is hydroxylated or conjugated; however, it appears that the key metabolic pathway in humans is glucuronic acid conjugation. [F4105][A176143]
HALF-LIFE Ketorolac tromethamine is administered as a racemic mixture, therefore the half-life of each enantiomer must be considered. The half life of the S-enantiomer is ~2.5 hours, while the half life of the R-enantiomer is ~5 hours. Based on this data, the S enantiomer is cleared about twice as fast as the R enantiomer. [F4105]
PHARMACODYNAMICS Ketorolac is a non-selective NSAID and acts by inhibiting both COX-1 and COX-2 enzymes which are normally responsible for converting arachidonic acid to prostaglandins. The COX-1 enzyme is constitutively active and can be found in platelets, gastric mucosa, and vascular endothelium. On the other hand, the COX-2 enzyme is inducible and mediates inflammation, pain and fever. ; ; 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]
MOA Ketorolac inhibits key pathways in prostaglandin synthesis which is crucial to it's mechanism of action.[A176143] Although ketorolac is non-selective and inhibits both COX-1 and COX-2 enzymes, it's clinical efficacy is derived from it's COX-2 inhibition. The COX-2 enzyme is inducible and is responsible for converting arachidonic acid to prostaglandins that mediate inflammation and pain. By blocking this pathway, ketorolac achieves analgesia and reduces inflammation.[A176134] Ketorolac is administered as a racemic mixture; however, the "S" enantiomer is largely responsible for it's pharmacological activity.[A176246]
INDICATION Ketorolac is a Non-steroidal anti-inflammatory drug (NSAID) and has antipyretic, analgesic and anti-inflammatory properties. [A176131] It is indicated for short term management of acute pain that requires the caliber of pain management offered by opioids. [L6526] 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).[L6526] 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]
ROE Ketorolac is primarily renally eliminated and approximately 92% of the dose can be recovered in the urine with 60% of this proportion recovered unchanged, and 40% recovered as metabolites. In addition 6% of a single dose is eliminated in the feces. [L6526]
HALF-LIFE Ketorolac tromethamine is administered as a racemic mixture, therefore the half-life of each enantiomer must be considered. The half life of the S-enantiomer is ~2.5 hours, while the half life of the R-enantiomer is ~5 hours. Based on this data, the S enantiomer is cleared about twice as fast as the R enantiomer. [L6526]
TOXICITY The rate of adverse effects increases with higher doses of ketorolac. The most frequently observed adverse effects in patients occurring with an incidence of greater than 10% include: abdominal pain, dyspepsia, nausea, and headaches. [L6523] 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. [L6526]; ; Ketorolac is classified as Pregnancy Category C since there is a lack of evidence demonstrating safety in pregnant women.[L6532] 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.[L6532]; ; 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.[L6523][L6526] 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.[L6523][L6526]; ; Women who are trying to conceive are not advised to take ketorolac since it's effect on prostaglandin synthesis may impair fertility.[L6523]
METABOLISM Ketorolac is heavily metabolized via hydroxylation or conjugation in the liver; however, it appears that the key metabolic pathway is glucuronic acid conjugation.[L6526][A176143] Enzymes involved in phase I metabolism include CYP2C8 and CYP2C9, while phase II metabolism is carried out by UDP-glucuronosyltransferase (UGT) 2B7.[A176234]
DESCRIPTION Ketorolac is a heterocyclic acetic acid class non-steroidal anti-inflammatory drug (NSAID). It acts as a non-selective COX inhibitor. The administered drug is a racemic mixture of enantiomers. We show the chemical structure without specified stereochemistry to represent the mixture. (GtoPdb)
INDICATION Ketorolac is a Non-steroidal anti-inflammatory drug (NSAID) and has antipyretic, analgesic and anti-inflammatory properties. [A176131] It is indicated for short term management of acute pain that requires the caliber of pain management offered by opioids. [F4105] 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. [F3952] 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). [F4105] 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]
ABSORPTION Ketorolac is rapidly, and completely absorbed after oral administration with a bioavailability of 80% after oral administration.[L6526][A176143] Cmax is attained 20-60 minutes after administration, and after intramuscular administration, the area under the plasma concentration-time curve (AUC) is proportional to the dose administered.[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]
DESCRIPTION Ketorolac (RS37619) is a non-steroidal anti-inflammatory drug (NSAID), acting as a nonselective COX inhibitor, with IC50s of 20 nM for COX-1 and 120 nM for COX-2. Ketorolac tromethamine is used as 0.5% ophthalmic solution for the research of allergic conjunctivitis, cystoid macular edema, intraoperative miosis, and postoperative ocular inflammation and pain. Ketorolac tromethamine is also a DDX3 inhibitor that can be used for cancer research[1][4].
PRICE 29
DESCRIPTION Non-steroidal anti-inflammatory (NSAID) drug (LOPAC library)
DESCRIPTION Ketorolac tromethamine salt (Ketorolac tris salt) non-selective inhibits the enzymes cyclooxygenase 1 (COX-1) and COX-2with anti-inflammatory, analgesic, and antipyretic activities. (TargetMol Bioactive Compound Library)
DESCRIPTION Ketorolaco is a potent, short acting nonsteroidal antiinflammatory drug (NSAID) in the family of heterocyclic acetic acid derivatives. It is a pyrrolizine carboxylic acid derivative structurally related to indomethacin. It is used as an analgesic. It acts by inhibiting the bodily synthesis of prostaglandins. It is also used to treat eye pain and to relieve the itchiness and burning of seasonal allergies. It was developed in 1989 by Syntex Corp. (BOC Sciences Bioactive Compounds)
DESCRIPTION Ketorolac is a non-steroidal anti-inflammatory drug (NSAID) and a non-selective prostaglandin synthase (COX) inhibitor. Ketorolac has been used to manage postoperative pain and as ophthalmic solutions to treat ocular pain and inflammation. (Enamine Bioactive Compounds)
DESCRIPTION Ketorolac (Acuvail) is a non-steroidal anti-inflammatory drug (NSAID) in the family of heterocyclic acetic acid derivatives. It acts by inhibiting the bodily synthesis of prostaglandins. (TargetMol Bioactive Compound Library)
Cell lines
1
Organisms
0
Compound Sets
31
BOC Sciences Bioactive Compounds
ketorolaco-cas-66635-83-4-item-476094
Cayman Chemical Bioactives
70690
9001148
9003475
ChEMBL Approved Drugs
CHEMBL1201124
CHEMBL469
ChEMBL Drugs
CHEMBL1201124
CHEMBL469
Concise Guide to Pharmacology 2017/18
6661
Concise Guide to Pharmacology 2019/20
6661
Concise Guide to Pharmacology 2021/22
6661
Concise Guide to Pharmacology 2023/24
6661
CZ-OPENSCREEN Bioactive Library
DrugBank
DB00465
DrugBank Approved Drugs
DB00465
DrugCentral
1529
DrugCentral Approved Drugs
1529
DrugMAP
DMI4EL5
DrugMAP Approved Drugs
DMI4EL5
Enamine Bioactive Compounds
EBC-03780
Enamine BioReference Compounds
EU-OPENSCREEN Bioactive Compound Library
EOS101212
Guide to Pharmacology
6661
LOPAC library
LSP-MoA library (Laboratory of Systems Pharmacology)
CHEMBL469
MedChem Express Bioactive Compound Library
HY-B0138
HY-B0580
NCATS Inxight Approved Drugs
4EVE5946BQ
NIH Clinical Collections (NCC)
NPC Screening Collection
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
ketorolac-tromethamine-salt
Ketorolac-Tromethamine(Toradol)
TargetMol Bioactive Compound Library
T1212
T21412
The Spectrum Collection
Withdrawn 2.0
w101
External IDs
70
Properties
(calculated by RDKit )
Molecular Weight
255.09
Hydrogen Bond Acceptors
3
Hydrogen Bond Donors
1
Rotatable Bonds
3
Ring Count
3
Aromatic Ring Count
2
cLogP
2.29
TPSA
59.3
Fraction CSP3
0.2
Chiral centers
1.0
Largest ring
6.0
QED
0.86
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Selectivity
COX
Target
COX-1
COX-2
Apoptosis
ATC
M01AB15
S01BC05
Toxicity type
renal, hematological
Therapeutic Class
Analgesics
Pathway
Immunology/Inflammation
Neuroscience
Solubility
Soluble in DMSO, not in water
Source data