Celecoxib  (Synonyms: SC 58635)

Celecoxib (GMP) is Celecoxib (HY-14398) produced by using GMP guidelines. GMP small molecules work appropriately as an auxiliary reagent for cell therapy manufacture. Celecoxib,a selective non-steroidal anti-inflammatory drug (NSAID), is a selective COX-2 inhibitor with an IC₅₀ of 40 nM.

The selective cyclooxygenase-2 (COX-2) inhibitor Celecoxib (10-75 μM) inhibits the proliferation of the NPC cell lines in a dose-dependent manner. Celecoxib (25 and 50 μM) induces apoptosis and cell-cycle arrest at the G₀/G₁ checkpoint in the NPC cell lines, which is associated with significantly reduced STAT3 phosphorylation. The genes downstream of STAT3 (ie, Survivin, Mcl-1, Bcl-2 and Cyclin D1) are significantly down-regulated after exposure to Celecoxib (25 and 50 μM)^[2].
Targeting the YAP/TAZ transcriptional target cyclooxygenase 2 (COX-2) using celecoxib inhibits cell proliferation and tumorigenesis in NF2 mutant cells^[6].
Celecoxib (5 μM, 28 d) in combination with TTNPB (HY-15682) (3 μM) converts fibroblasts into articular chondrocytes^[7].
Celecoxib (10 μM, 7-14 d) enhances trans-differentiation of Wharton’s jelly derived mesenchymal stromal cells (WJ-MSC) into endothelial progenitor cells (EPCs) ^[8].
Celecoxib (5 μM, 14 d) induces human aortic valve interstitial cells (AVICs) trans-differentiation towards a myofibroblast^[9].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Celecoxib demonstrates potent, oral anti-inflammatory activity. Celecoxib reduces acute inflammation in the carrageenan edema assay with an ED₅₀ of 7.1 mg/kg and reduces chronic inflammation in the adjuvant arthritis model with an ED₅₀ of 0.37 mg/kg/day. In addition, Celecoxib also exhibits analgesic activity in the Hargreaves hyperalgesia model with an ED₅₀ of 34.5 mg/kg. Celecoxib has potency equivalent to that of standard nonsteroidal anti-inflammatory drugs (NSAIDs), yet shows no acute GI toxicity in rats at doses up to 200 mg/kg. In addition, it displays no chronic GI toxicity in rats at doses up to 600 mg/kg/day over 10 days^[1]. In the KpB mice fed a high fat diet (obese) and treated with Celecoxib, tumor weight decreases by 66% when compare with control animals. Among KpB mice fed a low fat diet (non-obese), tumor weight decreases by 46% after treatment with Celecoxib^[3]. Rat models are orally administrated with Celecoxib (20 mg/kg) and/or intramuscularly with Fasudil (10 mg/kg) for 2 weeks. Results demonstrates that the combined use of Celecoxib and Fasudil (HY-10341A) significantly decreases COX-2 and Rho kinase II expression surrounding the lesion site in rats with spinal cord injury, improves the pathomorphology of the injured spinal cord, and promoted the recovery of motor function^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

381.37

C₁₇H₁₄F₃N₃O₂S

169590-42-5

CC1=CC=C(C=C1)C2=CC(C(F)(F)F)=NN2C3=CC=C(C=C3)S(=O)(N)=O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Pobbati AV, et al. A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy. Theranostics. 2020 Feb 18;10(8):3622-3635.  [Content Brief]

  [2]. Hou XL, et al. Combination of fasudil and celecoxib promotes the recovery of injured spinal cord in rats better than celecoxib or fasudil alone. Neural Regen Res. 2015 Nov;10(11):1836-40.  [Content Brief]

  [3]. Suri A, et al. The effect of celecoxib on tumor growth in ovarian cancer cells and a genetically engineered mouse model of serous ovarian cancer. Oncotarget. 2016 Apr 8.  [Content Brief]

  [4]. Liu DB, et al. Celecoxib induces apoptosis and cell-cycle arrest in nasopharyngeal carcinoma cell lines via inhibition of STAT3 phosphorylation. Acta Pharmacol Sin. 2012 May;33(5):682-90.  [Content Brief]

  [5]. Penning TD, et al. Synthesis and biological evaluation of the 1,5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem. 1997  [Content Brief]

  [6]. Liu C, et al. Celecoxib alleviates nonalcoholic fatty liver disease by restoring autophagic flux. Sci Rep. 2018 Mar 7;8(1):4108.  [Content Brief]

  [7]. Chen Y, Wu B, Lin J, et al. High-Resolution Dissection of Chemical Reprogramming from Mouse Embryonic Fibroblasts into Fibrocartilaginous Cells. Stem Cell Reports. 2020;14(3):478-492.  [Content Brief]

  [8]. Kaushik K, Das A. Cycloxygenase-2 inhibition potentiates trans-differentiation of Wharton's jelly-mesenchymal stromal cells into endothelial cells: Transplantation enhances neovascularization-mediated wound repair. Cytotherapy. 2019;21(2):260-273.  [Content Brief]

  [9]. Vieceli Dalla Sega F, Fortini F, Cimaglia P, et al. COX-2 Is Downregulated in Human Stenotic Aortic Valves and Its Inhibition Promotes Dystrophic Calcification. Int J Mol Sci. 2020;21(23):8917. Published 2020 Nov 24. doi:10.3390/ijms21238917  [Content Brief]