Drug Information

Drug (ID: DG00615) and It's Reported Resistant Information

• Name: Celecoxib
• Synonyms: Celecoxib; 169590-42-5; Celebrex; Celebra; Onsenal; Celocoxib; Celecox; SC 58635; 4-[5-(4-METHYLPHENYL)-3-(TRIFLUOROMETHYL)-1H-PYRAZOL-1-YL]BENZENESULFONAMIDE; SC-58635; YM177; 4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide; 184007-95-2; YM 177; C17H14F3N3O2S; HSDB 7038; UNII-JCX84Q7J1L; p-(5-p-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulfonamide; MFCD00941298; SC58635; 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzene-1-sulfonamide; 4-(5-(4-Methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; YM-177; CHEMBL118; JCX84Q7J1L; 194044-54-7; CHEBI:41423; 4-(5-(p-tolyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; NSC-719627; NSC-758624; NCGC00091455-01; Xilebao; DSSTox_CID_2777; 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonamide; 4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonami de; benzenesulfonamide, 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-; DSSTox_RID_76725; DSSTox_GSID_22777; Solexa; Benzenesulfonamide, 4-(5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)-; Celebrex (TN); SMR000550473; CAS-169590-42-5; SR-01000837528; Celecoxibum; Celecoxib [USAN:INN:BAN]; CCRIS 9330; TPI-336; Celecoxib- Bio-X; Celecoxib-[d4]; Onsenal (TN); AI-525; CEP-33222; CELEBCOXIB; Spectrum_000432; 1oq5; Spectrum2_001576; Spectrum3_001996; Spectrum4_000182; Spectrum5_001324; cid_2662; SCHEMBL3708; Celecoxib (JAN/USP/INN); DFN15; BSPBio_003596; KBioGR_000723; KBioGR_002351; KBioSS_000912; KBioSS_002354; MLS001165684; MLS001195656; MLS001304708; MLS006011862; BIDD:GT0408; DivK1c_000893; SPECTRUM1503678; SPBio_001512; DFN-15; GTPL2892; Celecoxib, >=98% (HPLC); DTXSID0022777; BDBM11639; HMS502M15; KBio1_000893; KBio2_000912; KBio2_002351; KBio2_003480; KBio2_004919; KBio2_006048; KBio2_007487; KBio3_002830; KBio3_003037; EX-A175; SYN3015; cMAP_000027; NINDS_000893; BCPP000290; Elyxyb (DFN-15; oral solution); HMS1922G14; HMS2089L18; HMS2093I07; HMS2234N18; HMS3259L08; HMS3261A14; HMS3373A09; HMS3654H09; HMS3715F11; HMS3867I03; HMS3884M07; Pharmakon1600-01503678; ACT02648; ALBB-033772; BCP02156; ZINC2570895; Tox21_111135; Tox21_201964; Tox21_300599; Tox21_500406; US8741944, Comparative Compound; 4-[5-(p-tolyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide; BBL029086; CCG-39354; NSC719627; NSC758624; s1261; STL373576; Celecoxib 1.0 mg/ml in Acetonitrile; AKOS015842517; Tox21_111135_1; AC-4228; AM84588; BCP9000507; CS-0570; DB00482; KS-1041; MCULE-4750749400; NC00708; NSC 719627; NSC 758624; SB19318; IDI1_000893; NCGC00091455-02; NCGC00091455-03; NCGC00091455-04; NCGC00091455-05; NCGC00091455-06; NCGC00091455-07; NCGC00091455-08; NCGC00091455-09; NCGC00091455-13; NCGC00254540-01; NCGC00259513-01; NCGC00261091-01; BC164295; BP-30217; HY-14398; NCI60_041049; PHA-00846533; SY064976; SBI-0051875.P002; CJ-016377; CP-598107; UNM-0000305813; FT-0601628; FT-0623536; FT-0700357; SW199611-3; PF-00345549; A25046; C07589; D00567; J10035; AB00052396-07; AB00052396-08; AB00052396-09; AB00052396_10; AB00052396_11; 590C425; Q408801; J-010566; J-520011; Q-200816; SR-01000837528-2; SR-01000837528-3; BRD-K02637541-001-02-4; BRD-K02637541-001-06-5; Z2210694606; Celecoxib, European Pharmacopoeia (EP) Reference Standard; Celecoxib, United States Pharmacopeia (USP) Reference Standard; 4-[5-(p-Tolyl)-3-(trifluoromethyl)-1-pyrazolyl]benzenesulfonamide; 4-(5-p-tolyl-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide; 4-[5-(4-Methylphenyl)-3-(trifluoromethyl)-pyrazol-1-yl]benzenesulfonamide; 5-(4-Methylphenyl)-1-(4-sulfamoylphenyl)-3-(trifluoromethyl)pyrazole; Celecoxib, Pharmaceutical Secondary Standard; Certified Reference Material; 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyazol-1-yl]benezenesulfonamide; Benzenesulfonamide,4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-; 4-[5-(4-Methylphenyl)-3-(trifluoromethyl)-pyrazol-1-yl]benzenesulfonamide;4-[5-(4-Methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide
• Indication:
  In total 2 Indication(s)
  Pain [ICD-11: MG30]; Approved; [1]
  Rheumatoid arthritis [ICD-11: FA20]; Approved; [1]
• Drug Resistance Disease(s):
  Disease(s) with Clinically Reported Resistance for This Drug (2 diseases)
  Dysmenorrhea [ICD-11: GA34]; [2]
  Rheumatoid arthritis [ICD-11: FA20]; [1]
• Target: Prostaglandin G/H synthase 2 (COX-2); PGH2_HUMAN; [3]
• Formula: C17H14F3N3O2S
• IsoSMILES: CC1=CC=C(C=C1)C2=CC(=NN2C3=CC=C(C=C3)S(=O)(=O)N)C(F)(F)F
• InChI: 1S/C17H14F3N3O2S/c1-11-2-4-12(5-3-11)15-10-16(17(18,19)20)22-23(15)13-6-8-14(9-7-13)26(21,24)25/h2-10H,1H3,(H2,21,24,25)
• InChIKey: RZEKVGVHFLEQIL-UHFFFAOYSA-N
• PubChem CID: 2662
• ChEBI ID: CHEBI:41423
• TTD Drug ID: D03RTS
• VARIDT ID: DR00520
• INTEDE ID: DR0286
• DrugBank ID: DB00482

Type(s) of Resistant Mechanism of This Drug

  DISM: Drug Inactivation by Structure Modification

  IDUE: Irregularity in Drug Uptake and Drug Efflux

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

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

Brain cancer [ICD-11: 2A00]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Prostaglandin G/H synthase 2 (PTGS2) [3]

• Molecule Alteration: Expression; Down-regulation
• Sensitive Disease: Glioblastoma [ICD-11: 2A00.02]
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: Cell proliferation; Inhibition; hsa05200
• Cell Pathway Regulation: Cell apoptosis; Activation; hsa04210
• Cell Pathway Regulation: Cell autophagy; Activation; hsa04140
• In Vitro Model: MDA-175 cells; Pleural effusion; Homo sapiens (Human); CVCL_1400
• In Vitro Model: MMQ cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_2117
• Experiment for Molecule Alteration: Western blot analysis; Fluorescence microscopy assay
• Experiment for Drug Resistance: MTS assay; Crystal violet staining assay; Fluorescence-activated cell sorting (FACS) assay; Flow cytometry
• Mechanism Description: Celecoxib reverses the glioblastoma chemo-resistance to temozolomide through mitochondrial metabolism.

ICD-15: Musculoskeletal/connective-tissue diseases

Rheumatoid arthritis [ICD-11: FA20]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Irregularity in Drug Uptake and Drug Efflux (IDUE)

Key Molecule: ATP-binding cassette sub-family G2 (ABCG2) [1]

• Molecule Alteration: Expression; Up-regulation
• Resistant Disease: Rheumatoid arthritis [ICD-11: FA20.0]
• Experimental Note: Identified from the Human Clinical Data
• Mechanism Description: MTX is a substrate for eight ABC transporters. In vitro studies demonstrated that RAFLS treated with MTX had higher ABCB1 expression levels than controls, with a positive correlation between ABCB1 expression levels and RA treatment duration. In addition to MTX, other DMARDs (e.g. sulfasalazine, leflunomide, bucillamine, azathioprine), glucocorticoids (e.g. betamethasone, dexamethasone), and NSAIDs (e.g. celecoxib and indomethacin) are also substrates of ABC transporters.

ICD-16: Genitourinary system diseases

Dysmenorrhea [ICD-11: GA34]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Key Molecule: Cytochrome P450 family 2 subfamily C member 9 (CYP2C9) [2]

• Molecule Alteration: SNP; CYP2C9*2/*2
• Resistant Disease: Dysmenorrhea [ICD-11: GA34.3]
• Experimental Note: Identified from the Human Clinical Data
• Mechanism Description: For example, the CYP2C9*2/*2 polymorphism was associated with increased total clearance of celecoxib and diclofenac.48 More research is necessary to determine if other gain-of-function variants exist and alter NSAID metabolism.

References

• Ref 1: Drug-resistance in rheumatoid arthritis: the role of p53 gene mutations, ABC family transporters and personal factors .Curr Opin Pharmacol. 2020 Oct;54:59-71. doi: 10.1016/j.coph.2020.08.002. Epub 2020 Sep 14. 10.1016/j.coph.2020.08.002
• Ref 2: Nonsteroidal antiinflammatory drug resistance in dysmenorrhea: epidemiology, causes, and treatment .Am J Obstet Gynecol. 2018 Apr;218(4):390-400. doi: 10.1016/j.ajog.2017.08.108. Epub 2017 Sep 6. 10.1016/j.ajog.2017.08.108
• Ref 3: Celecoxib reverses the glioblastoma chemo-resistance to temozolomide through mitochondrial metabolism .Aging (Albany NY). 2021 Sep 8;13(17):21268-21282. doi: 10.18632/aging.203443. Epub 2021 Sep 8. 10.18632/aging.203443