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Ibuprofen sodium

MCE China：Ibuprofen sodium

Brand：MedChemExpress (MCE)

Cat. No.HY-78131C

CAS：31121-93-4

Synonyms：(±)-Ibuprofen sodium

Purity：99.98%

Storage：4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Ibuprofen ((±)-Ibuprofen) sodium is an orally active, selective COX-1 inhibitor with an IC50 value of 13 μM. Ibuprofen sodium inhibits cell proliferation, angiogenesis, and induces cell apoptosis. Ibuprofen sodium is a nonsteroidal anti-inflammatory agent and a nitric oxide (NO) donor. Ibuprofen sodium can be used in the research of pain, swelling, inflammation, infection, immunology, cancers.

In Vitro：Ibuprofen sodium (24 h) inhibits COX-1 and COX-2 activity with IC50 values of 13 μM and 370 μM[1]. Ibuprofen sodium (500 μM, 48 h) inhibits cell proliferation and angiogenesis, and induces apoptosis in AGS cells (Adenocarcinoma gastric cell line)[2]. Ibuprofen sodium (500 μM, 48 h) downregulates transcription of Akt, VEGF-A, PCNA, Bcl2, OCT3/4 and CD44 genes, but upregulates RNA levels of wild type P53 and Bax genes in AGS cell[2]. Ibuprofen sodium (500 μM, 24 h) restores microtubule reformation, microtubule-dependent intracellular cholesterol transport, and induces extension of microtubules to the cell periphery in both cystic fibrosis (CF) cell models and primary CF nasal epithelial cells[3]. Ibuprofen sodium (500 μM, 24 h) enhances UV-induced cell death in MCF-7 cells and MDA-MB-231 cells by a photosensitization process[4].

In Vivo：Ibuprofen sodium (fed in animal feedings, 300 mg/kg, 14 days) reduces overall tumor growth and enhances anti-tumor immune characteristics without adverse autoimmune reactions in a model of postpartum breast cancer[5]. Ibuprofen sodium (subcutaneous injection, 60 mg/kg, every second day for 15 days) reduces the risk of neuropathy in a rat model of chronic Oxaliplatin?induced peripheral neuropathy[6]. Ibuprofen sodium (oral administration, 20 mg/kg, every 12 hours, 5 doses total) decreases muscle growth (average muscle fiber cross-sectional area) without affecting regulation of supraspinatus tendon adaptions to exercise[7]. Ibuprofen sodium (oral administration, 35 mg/kg, twice daily) attenuates the Inflammatory response to pseudomonas aeruginosa in a rat model of chronic pulmonary infection[8].

IC50 & Target：COX-1 13 μM (IC50) COX-2 370 μM (IC50)

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References：

[1]. Noreen Y, et al. Development of a radiochemical cyclooxygenase-1 and -2 in vitro assay for identification of natural products as inhibitors of prostaglandin biosynthesis. J Nat Prod. 1998 Jan;61(1):2-7.  [Content Brief]

[2]. Hassan Akrami, et al. Inhibitory effect of ibuprofen on tumor survival and angiogenesis in gastric cancer cell. Tumour Biol. 2015 May;36(5):3237-43.  [Content Brief]

[3]. Sharon M Rymut, et al. Ibuprofen regulation of microtubule dynamics in cystic fibrosis epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2016 Aug 1;311(2):L317-27.  [Content Brief]

[4]. Emmanuelle Bignon, et al. Ibuprofen and ketoprofen potentiate UVA-induced cell death by a photosensitization process. Sci Rep. 2017 Aug 21;7(1):8885.  [Content Brief]

[5]. Nathan D Pennock, et al. Ibuprofen supports macrophage differentiation, T cell recruitment, and tumor suppression in a model of postpartum breast cancer. J Immunother Cancer. 2018 Oct 1;6(1):98.  [Content Brief]

[6]. Thomas Krøigård, et al. Protective effect of ibuprofen in a rat model of chronic oxaliplatin-induced peripheral neuropathy. Exp Brain Res. 2019 Oct;237(10):2645-2651.  [Content Brief]

[7]. Sarah Ilkhanipour Rooney, et al. Ibuprofen Differentially Affects Supraspinatus Muscle and Tendon Adaptations to Exercise in a Rat Model. Am J Sports Med. 2016 Sep;44(9):2237-45.  [Content Brief]

[8]. M W Konstan, et al. Ibuprofen attenuates the inflammatory response to Pseudomonas aeruginosa in a rat model of chronic pulmonary infection. Implications for antiinflammatory therapy in cystic fibrosis. Am Rev Respir Dis. 1990 Jan;141(1):186-92.  [Content Brief]