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The present review focuses on synthetic peptide‐based vaccine strategies in the context of anticancer intervention, paying attention to critical aspects such as peptide epitope selection, adjuvant integration, and nuanced classification of synthetic peptide cancer vaccines. Within this discussion, we delve into the diverse array of synthetic peptide‐based anticancer vaccines, each derived from tumor‐associated antigens (TAAs), including melanoma antigen recognized by T cells 1 (Melan‐A or MART‐1), mucin 1 (MUC1), human epidermal growth factor receptor 2 (HER‐2), tumor protein 53 (p53), human telomerase reverse transcriptase (hTERT), survivin, folate receptor (FR), cancer‐testis antigen 1 (NY‐ESO‐1), and prostate‐specific antigen (PSA). We also describe the synthetic peptide‐based vaccines developed for cancers triggered by oncovirus, such as human papillomavirus (HPV), and hepatitis C virus (HCV). Additionally, the potential synergy of peptide‐based vaccines with common therapeutics in cancer was considered. The last part of our discussion deals with the realm of the peptide‐based vaccines delivery, highlighting its role in translating the most promising candidates into effective clinical strategies. Although this discussion does not cover all the ongoing peptide vaccine investigations, it aims at offering valuable insights into the chemical modifications and the structural complexities of anticancer peptide‐based vaccines. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC), the leading cause of cancer-related mortality worldwide, poses a formidable challenge due to its heterogeneity and the emergence of resistance to targeted therapies. While initially effective, first- and third-generation EGFR-tyrosine kinase inhibitors (TKIs) often fail to control disease progression, leaving patients with limited treatment options. To address this unmet medical need, we explored the therapeutic potential of multitargeting agents that simultaneously inhibit two key signalling pathways, the mesenchymal-epithelial transition factor (c-MET) and the G protein-coupled receptor Smoothened (SMO), frequently dysregulated in NSCLC. By employing a combination of in silico drug repurposing and structure-based structure-activity relationship (SAR) studies, we identified and developed novel c-MET/SMO-targeting agents with antiproliferative activity against first- as well as third-generation EGFR-TKI-resistant NSCLC cells suggesting a synergistic effect arising from the simultaneous inhibition of c-MET and SMO., Competing Interests: The authors affirm that there are no identifiable competing financial interests or personal relationships that could have been perceived to impact the findings presented in this paper., (This journal is © The Royal Society of Chemistry.)