Background: Epidermal growth factor receptor-tyrosine kinase (EGFR-TK) is a well-known hallmark of oral and oropharyngeal cancers, as its overexpression leads to poor prognosis and malignancy. The activating EGFR mutations (particularly T790M and L858R double mutant) are a major challenge causing drug resistance, especially in the treatment of oral cancers. Methodology: This paper is an effort to exploit both structure-based and ligand-based pharmacophore modeling to discover EGFR-TK inhibitors, which show inhibition of proliferation of erlotinib-resistant FaDu and Cal27 oral cancer cells. Interestingly, the hit compound H2 also showed an effect on the downstream glucose and lactate metabolism pathways. Conclusion: The results indicate the potential of H2 to be developed as an EGFR-based metabolic inhibitor for oral cancer treatment.

Solid state organic fluorogens (SSOF-gens) with aggregation-induced (enhanced) emission (AIEE/AIE) property are currently defining their insistence as the transpiring tool in biological and biomedical applications. This work focuses on designing...

Malaria, where the causative agent Plasmodium is rapidly gaining resistance to practically all the antimalarial drugs in clinical use, requires the identification of new drug targets to enable the discovery of novel, more effective and safer drugs to treat the disease. Advancements in molecular techniques have provided the proof of existence of autophagy in Plasmodium; however, its role(s) in malaria is only becoming to be understood. Nevertheless, some of the recently explored dimensions of autophagy in Plasmodium have indicated its fairly larger role in parasite survival and growth. But then, autophagy is also essential for host cell survival and defence. There is thus need to explore chemotherapeutic strategies to specifically target autophagy in both the parasite and host. This review focuses on autophagy pathways in Plasmodium and in host with a view to identify autophagy-related new drug targets for the discovery of novel antimalarial drugs.