NSAIDS

Thienopyridines consist of fused heterocyclic structures that incorporate thiophene and pyridine rings. They are important in medicinal chemistry because different substituents can be introduced into their structure to modify their biological and pharmacological properties. Thienopyridine derivatives have been reported to show several activities, including anti-inflammatory, analgesic, antiplatelet, antimicrobial and anticancer effects. Tinoridine hydrochloride is an important example of a thienopyridine with anti-inflammatory activity and can be used as a reference compound in the development of new derivatives. Some newly studied thienopyridine derivatives have shown anti-inflammatory and antiarthritic activity, with certain compounds showing lower ulcerogenic effects than indomethacin. Cyclooxygenase-2 (COX-2) is an important target for the development of anti-inflammatory drugs. Molecular docking can be used to study the possible binding of thienopyridine derivatives with COX-2, while structure–activity relationship (SAR) studies can help identify structural features related to activity. ADMET prediction can also provide information about the pharmacokinetic and toxicity properties of the compounds. Therefore, combining SAR, molecular docking and ADMET studies may help in the design of new and potentially safer thienopyridine-based anti-inflammatory agents. (1,4,6,11) Keywords: Thienopyridine; COX-2; Molecular Docking; SAR; Nsaids; Tinoridine Hydrochloride.

Wnt /β-catenin signaling plays an important role in tumor cell dedifferentiation and proliferation. Wnt proteins are a family of secreted glycoproteins. Abnormal activation of wnt signaling results in tumor progression. Wnt proteins binds to the frizzled receptors and LRP5/6 co-receptors and through the stabilization of β-catenin a critical mediator, initiates a complex signaling cascade that plays an important role in regulating cell proliferation and differentiations. The elevated levels of oncogenic protein-β-catenin have been observed in many of the human cancers, indicating that this pathway plays an important role in tumor development. The wnt signaling can be inhibited at the extracellular level, at regulatory protein level and also by targeting the expressions of β-catenin by protein knockdown and by targeting the downstream mediators of β-catenin signaling such as c-myc, cyclin D1, PPARS and COX-2. In this review we discuss the effects of  NSAIDS and flavanoids that are being used or explored to target the β-catenin signaling in the treatment of cancers.