Celecoxib塞来昔布,169590-42-5

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Celecoxib

CAS No. : 169590-42-5

MCE 国际站：Celecoxib

产品活性：Celecoxib 是一种选择性的 COX-2 抑制剂，IC₅₀ 为 40 nM。

研究领域：Immunology/Inflammation

作用靶点：COX

In Vitro: 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).
Targeting the YAP/TAZ transcriptional target cyclooxygenase 2 (COX-2) using celecoxib inhibits cell proliferation and tumorigenesis in NF2 mutant cells.

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. 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. 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.

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