| Bioactivity | Celecoxib,a selective non-steroidal anti-inflammatory drug (NSAID), is a selective COX-2 inhibitor with an IC50 of 40 nM. | ||||||||||||
| Invitro | 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]. | ||||||||||||
| In Vivo | 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 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]. | ||||||||||||
| Name | Celecoxib | ||||||||||||
| CAS | 169590-42-5 | ||||||||||||
| Formula | C17H14F3N3O2S | ||||||||||||
| Molar Mass | 381.37 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
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| Reference | [1]. 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 [2]. 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. [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. [4]. 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. [5]. Liu C, et al. Celecoxib alleviates nonalcoholic fatty liver disease by restoring autophagic flux. Sci Rep. 2018 Mar 7;8(1):4108. [6]. Pobbati AV, et al. A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy. Theranostics. 2020 Feb 18;10(8):3622-3635. |
Celecoxib
CAS: 169590-42-5 F: C17H14F3N3O2S W: 381.37
Celecoxib,a selective non-steroidal anti-inflammatory drug (NSAID), is a selective COX-2 inhibitor with an IC50 of 40 nM
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