Celecoxib (GMP)_product_DataBase

Bioactivity	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.
Invitro	选择性环氧合酶-2 (COX-2) 抑制剂Celecoxib (10-75 μM) 以剂量依赖性方式抑制鼻咽癌细胞系的增殖。Celecoxib（25 和 50 μM）在 NPC 细胞系的 G0/G1 检查点处诱导细胞凋亡和细胞周期停滞，这与 STAT3 磷酸化显着降低有关。暴露于Celecoxib （25 和 50 μM）后，STAT3 下游基因（即 Survivin、Mcl-1、Bcl-2 和 Cyclin D1）显着下调[2]。使用Celecoxib 靶向 YAP/TAZ 转录靶点环氧合酶 2 (COX-2) 可抑制 NF2 突变细胞的细胞增殖和肿瘤发生[6]。Celecoxib (5 μM, 28 天) 联合TTNPB (HY-15682) (3 μM) 可将成纤维细胞转化为关节软骨细胞[7]。Celecoxib (10 μM, 7-14 天) 促进Wharton’s jelly 来源的间充质细胞向内皮祖细胞的转分化[8]。Celecoxib (5 μM, 14 天) 诱导人主动脉瓣间质细胞向肌成纤维细胞转分化[9]。 0 --> Celecoxib (GMP) 相关抗体:
In Vivo	Celecoxib 具有有效的口服抗炎活性。 Celecoxib 在角叉菜胶水肿测定中减少急性炎症，ED50 为 7.1 mg/kg，在佐剂关节炎模型中减少慢性炎症，ED50 为 0.37 mg/kg /天。此外，Celecoxib 在 Hargreaves 痛觉过敏模型中也表现出镇痛活性，ED50 为 34.5 mg/kg。 Celecoxib 的效力与标准非甾体类抗炎药 (NSAID) 相当，但在剂量高达 200 mg/kg 时，对大鼠没有显示急性胃肠道毒性。此外，在大鼠中，剂量高达 600 mg/kg/天、持续 10 天后，并未表现出慢性胃肠道毒性[1]。在喂食高脂肪饮食（肥胖）并接受Celecoxib 治疗的 KpB 小鼠中，与对照动物相比，肿瘤重量减少了 66%。在喂食低脂饮食（非肥胖）的 KpB 小鼠中，Celecoxib 治疗后肿瘤重量减少了 46%[3]。给大鼠模型口服 Celecoxib (20 mg/kg) 和/或肌肉注射 Fasudil (HY-10341A) (10 mg/kg)，持续 2 周。结果表明，Celecoxib 与 Fasudil 联用可显着降低脊髓损伤大鼠病变部位周围COX-2 和 Rho 激酶 II 的表达，改善损伤脊髓的病理形态，促进运动功能的恢复[4].
Name	Celecoxib (GMP)
CAS	169590-42-5
Formula	C17H14F3N3O2S
Molar Mass	381.37
Transport	Room temperature in continental US; may vary elsewhere.
Storage	Please store the product under the recommended conditions in the Certificate of Analysis.
Reference	[1]. Pobbati AV, et al. A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy. Theranostics. 2020 Feb 18;10(8):3622-3635. [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. [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]. 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. [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 [6]. Liu C, et al. Celecoxib alleviates nonalcoholic fatty liver disease by restoring autophagic flux. Sci Rep. 2018 Mar 7;8(1):4108. [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. [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. [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

PeptideDB

Celecoxib (GMP)

CAS: 169590-42-5 F: C17H14F3N3O2S W: 381.37