Non-Steroidal Anti-Inflammatory Drugs

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used to alleviate pain, inflammation, swelling, and fever through inhibition of cyclooxygenase enzymes COX-1 and COX-2. Beyond their well-established analgesic, anti-inflammatory, and antipyretic actions, certain NSAIDs—including Acetylsalicylic Acid (Aspirin, A118582 suitable for plant cell culture ≥99%, A104180 ≥99%) and Piroxicam (P129294 ≥98%, P407766 10mM in DMSO)—have demonstrated chemopreventive properties, reducing the risk of several cancers such as colorectal, breast, intestinal, and prostate cancers. These protective effects are mediated by both COX-dependent and COX-independent pathways.


Mechanisms of Chemoprevention: Inhibition of COX enzymes increases intracellular levels of arachidonic acid, a prostaglandin precursor. In colon cancer cells, elevated arachidonic acid promotes the conversion of sphingomyelin to ceramide, leading to apoptosis. Animal studies of colorectal cancer corroborate this mechanism; administration of Sulindac (S125148 ≥98%, S408587 10mM in DMSO) induces apoptosis and suppresses the development of aberrant crypt foci.


NSAIDs also exert chemopreventive effects by targeting phosphodiesterase 5 (PDE5). Inhibition of PDE5 raises intracellular cGMP, which activates protein kinase G (PKG). This cascade subsequently triggers JNK1 activation and downregulation of β-catenin–mediated transcription, culminating in cell cycle arrest, apoptosis induction, and reduced angiogenesis. Compounds such as Sulindac and Flurbiprofen (F134483 ≥98%, F408049 10mM in DMSO) act via this pathway, effectively suppressing cancer development in cellular models.


Aladdin provides an extensive portfolio of NSAIDs for research, including:

· Non-selective COX inhibitors

· COX-2 selective inhibitors such as Etoricoxib (E126660 ≥98%, E422460 10mM in DMSO), Meloxicam (M129228 ≥98%, M408223 10mM in DMSO), and Celecoxib (C129279 ≥99%, C408187 10mM in DMSO,  C1372189-GMP)

· And many additional compounds supporting cancer, inflammation, and cell signaling studies.



References:

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2. Schmitz-Drager BJ, Schoffski O, Marberger M, et al. Recent Results Cancer Res. 2014;202:79-91.

3. Harris RE, Kasbari S, Farrar WB. Oncol Rep. 1999 JanFeb;6(1):71-3.

4. Ritland SR, Gendler SJ. Carcinogenesis. 1999 Jan;20(1):51-8.

5. Chan TA, Morin PJ, Vogelstein B, et al. Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):681-6.

6. Martin JE, Le Leu RK, Hu Y, et al. Am J Physiol Gastrointest Liver Physiol. 2010 Jun;298(6):G860-4.

7. Gurpinar E, Grizzle WE, Piazza GA. Front Oncol. 2013 Jul 11;3:181.

8. Nath N, Liu X, Jacobs L, et al. Drug Des Devel Ther. 2013 May 6;7:389-96.

 

Aladdin: https://www.aladdinsci.com/

Categories: Technical articles

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