Drug Information

Drug (ID: DG00762) and It's Reported Resistant Information

• Name: Ketorolac
• Synonyms: Ketorolac; 74103-06-3; 5-Benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; Ketorolaco; Ketorolacum [Latin]; Ketorolaco [Spanish]; Ketoralac; Ketorolacum; Macril; (+-)-Ketorolac; 66635-83-4; Acular; rac-ketorolac; RS 37619; (+)-Ketorolac; Toradol (TN); (+-)-5-Benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; CHEBI:76223; Acuvail; MFCD00864281; RS37619; 1H-Pyrrolizine-1-carboxylic acid, 2,3-dihydro-5-benzoyl-, (+-)-; 5-(phenylcarbonyl)-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; Ketorolac [INN:BAN]; SPRIX; RS-37619; Ketorolac (INN); rac Ketorolac-[d4]; 1H-Pyrrolizine-1-carboxylic acid, 5-benzoyl-2,3-dihydro-; NCGC00185990-01; CHEMBL469; SCHEMBL14891; MLS006011844; CHEBI:6129; GTPL6661; DTXSID8023189; BDBM85511; HMS3604J05; HMS3884M04; HY-B0580; AC-545; HTS001246; s1646; STL018674; AKOS005657203; AC-1121; CCG-204762; DB00465; KS-5175; SDCCGSBI-0050655.P004; NCGC00185990-02; NCGC00185990-05; NCGC00185990-15; K262; SMR001550090; SY107530; SBI-0050655.P003; CAS_74103-07-4; DB-011403; AB00053682; FT-0653523; FT-0670664; FT-0670665; FT-0670666; C07062; D08104; F16555; J10261; AB00053682-12; AB00053682-14; AB00053682_15; AB00053682_16; 635K834; A934549; Q2014797; BRD-A40639672-234-05-7; BRD-A40639672-234-09-9; KETOROLAC, ketorolactromethamine, Ketorolac Tromethamine; 5-(benzoyl)-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; 5-Benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid #; rac-5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; (1RS)-5-Benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; (.+/-.)-2,3-Dihydro-5-benzoyl-1H-pyrrolizine-1-carboxylic acid; (.+/-.)-5-Benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid; 5-benzoyl-1,2-dihydro-3H-pyrrolo[1,2-a]pyrrole-1-carboxylic acid; 1H-Pyrrolizine-1-carboxylic acid, 2,3-dihydro-5-benzoyl-, (.+/-.)-; 5-BENZOYL-2,3-DIHYDRO-1H-PYRROLO[1,2-A]PYRROLE-1-CARBOXYLIC ACID
• Indication:
  In total 1 Indication(s)
  Postoperative inflammation [ICD-11: 1A00-CA43]; Approved; [1]
• Target: Prostaglandin G/H synthase (COX); PGH1_HUMAN PGH2_HUMAN; [1]
• Formula: C15H13NO3
• IsoSMILES: C1CN2C(=CC=C2C(=O)C3=CC=CC=C3)C1C(=O)O
• InChI: 1S/C15H13NO3/c17-14(10-4-2-1-3-5-10)13-7-6-12-11(15(18)19)8-9-16(12)13/h1-7,11H,8-9H2,(H,18,19)
• InChIKey: OZWKMVRBQXNZKK-UHFFFAOYSA-N
• PubChem CID: 3826
• ChEBI ID: CHEBI:76223
• TTD Drug ID: D0D9JW
• INTEDE ID: DR0908
• DrugBank ID: DB00465

Type(s) of Resistant Mechanism of This Drug

  EADR: Epigenetic Alteration of DNA, RNA or Protein

  IDUE: Irregularity in Drug Uptake and Drug Efflux

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-02: Benign/in-situ/malignant neoplasm

Acute myeloid leukemia [ICD-11: 2A60]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Epigenetic Alteration of DNA, RNA or Protein (EADR)

Key Molecule: hsa_circ_0001946 [1]

• Molecule Alteration: Expression; Up-regulation
• Sensitive Disease: Acute myeloid leukemia [ICD-11: 2A60.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• Experiment for Molecule Alteration: Efflux pump genes expression analysis
• Mechanism Description: Ketorolac-fluconazole in vitro combination would be a promising strategy for further clinical in vivo trials to overcome fluconazole resistance in AML patients on induction chemotherapy. To our knowledge, the current study is the first in vitro report on the use of ketorolac in reverting fluconazole resistance in C. albicans isolated from AML patients. Resistance of C. albicans to azole antifungals is associated with overexpression of efflux pump genes especially CDR1 and MDR1.

Irregularity in Drug Uptake and Drug Efflux (IDUE)

Key Molecule: Multidrug resistance protein 1 (ABCB1) [1]

• Molecule Alteration: Expression; Up-regulation
• Sensitive Disease: Acute myeloid leukemia [ICD-11: 2A60.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• Experiment for Molecule Alteration: Efflux pump genes expression analysis
• Mechanism Description: Ketorolac-fluconazole in vitro combination would be a promising strategy for further clinical in vivo trials to overcome fluconazole resistance in AML patients on induction chemotherapy. To our knowledge, the current study is the first in vitro report on the use of ketorolac in reverting fluconazole resistance in C. albicans isolated from AML patients. Resistance of C. albicans to azole antifungals is associated with overexpression of efflux pump genes especially CDR1 and MDR1.

References

• Ref 1: Ketorolac-fluconazole: A New Combination Reverting Resistance in Candida albicans from Acute Myeloid Leukemia Patients on Induction Chemotherapy: In vitro Study .J Blood Med. 2021 Jun 15;12:465-474. doi: 10.2147/JBM.S302158. eCollection 2021. 10.2147/JBM.S302158