Cancer persists as a global challenge necessitating continual innovation in treatment strategies. Despite significant advancements in comprehending the disease, cancer remains a leading cause of mortality worldwide, exerting substantial economic burdens on healthcare systems and societies. The emergence of drug resistance further complicates therapeutic efficacy, underscoring the urgent need for alternative approaches. Drug repurposing, characterized by the utilization of existing drugs for novel clinical applications, emerges as a promising avenue for addressing these challenges. Repurposed drugs, comprising FDA-approved (in other disease indications), generic, off-patent, and failed medications, offer distinct advantages including established safety profiles, cost-effectiveness, and expedited development timelines compared to novel drug discovery processes. Various methodologies, such as knowledge-based analyses, drug-centric strategies, and computational approaches, play pivotal roles in identifying potential candidates for repurposing. However, despite the promise of repurposed drugs, drug repositioning confronts formidable obstacles. Patenting issues, financial constraints associated with conducting extensive clinical trials, and the necessity for combination therapies to overcome the limitations of monotherapy pose significant challenges. This review provides an in-depth exploration of drug repurposing, covering a diverse array of approaches including experimental, re-engineering protein, nanotechnology, and computational methods. Each of these avenues presents distinct opportunities and obstacles in the pursuit of identifying novel clinical uses for established drugs. By examining the multifaceted landscape of drug repurposing, this review aims to offer comprehensive insights into its potential to transform cancer therapeutics.

This review article explores the fundamental role of receptor targeting in overcoming drug resistance in cancer therapy, an area of critical concern given the persistently high rates of cancer morbidity and mortality globally. We highlight how receptor biology intersects with the development of therapeutic resistance with a specific focus on anti-angiogenic agents, immune checkpoint inhibitors, and monoclonal antibodies, which directly or indirectly influence receptor pathways. We also explore how other receptor tyrosine kinases can initially suppress tumor growth, yet often lead to resistance, underscoring the need for novel combinatorial approaches that incorporate advanced receptor modulation techniques. Further, the review delves into the mechanisms by which modulation of the tumor microenvironment and immune system via receptor pathways can overcome resistance to traditional immunotherapies. Additionally, emerging technologies in receptor-targeted nanomedicine are also highlighted, showcasing their potential to revolutionize drug delivery and improve therapeutic outcomes by targeting specific receptor interactions. Ultimately, this review calls for a deeper understanding of receptor dynamics to develop more precise interventions, including insights from various healthcare settings that can prevent or circumvent drug resistance, thus enhancing patient outcomes in oncology.

This research evaluates the biological activities of three medicinal plants: Butea monosperma, Delonix regia, and Spathodea campanulata. These plants, belonging to the Fabaceae and Bignoniaceae families, were investigated for their antibacterial, antifungal, antioxidant, and cytotoxic properties. Phytochemicals were extracted from the flowers and leaves using methanol, ethanol, and acetone. The antibacterial and antifungal activities were assessed using a disc diffusion assay against pathogens S. epidermidis, B. cereus, E. coli, K. aerogenes, P. vulgaris, S. aureus, and C. albicans. The antioxidant potential was evaluated using the DPPH assay, and the cytotoxic activity was measured using the MTT assay on human lung cancer (A549) cells. Results indicated that ethanol extracts demonstrated the highest antimicrobial efficacy against both Gram-negative and Gram-positive bacteria, as well as the fungal strain Candida albicans. The extracts also demonstrated antioxidant activity, with the Butea monosperma ethanol extract showing the highest activity at an IC50 value of 61.55±1.22 μg/mL. Methanol extracts showed significant cytotoxic effects on the A549 cell line, with Butea monosperma having an IC50 value of 36.12±1.01 μg/mL. These findings suggest that the extracts from these plants have potential therapeutic applications against bacterial and fungal infections, oxidative stress, and cancer cells.

Receptor dysregulation is a hallmark of cancer and a major driver of tumor initiation, progression, and therapeutic resistance. Among the most clinically relevant receptors are the epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), estrogen receptor (ER), and androgen receptor (AR), which regulate critical processes including cell proliferation, survival, and metastasis. Genetic alterations, receptor overexpression, and aberrant signaling can lead to persistent activation of these pathways, promoting oncogenic progression. Advances in the understanding of EGFR, HER2, ER, and AR signaling have enabled the development of targeted therapies that have significantly improved clinical outcomes. However, therapeutic resistance, signaling crosstalk, and tumor heterogeneity continue to limit treatment efficacy. This review summarizes the mechanisms underlying the dysregulation of these receptor pathways, their roles in cancer development, and current and emerging therapeutic strategies targeting receptor-driven malignancies. A better understanding of these signaling networks may facilitate the development of more effective biomarkers and precision oncology approaches.