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Kirsten rat sarcoma viral oncogene homolog (KRAS) protein inhibitors are a promising class of therapeutics, but research on molecules that effectively penetrate the blood-brain barrier (BBB) remains limited, which is crucial for treating central nervous system (CNS) malignancies. Although molecular generation models have recently advanced drug discovery, they often overlook the complexity of biological and chemical factors, leaving room for improvement. In this study, we present a structure-constrained molecular generation workflow designed to optimize lead compounds for both drug efficacy and drug absorption properties. Our approach utilizes a variational autoencoder (VAE) generative model integrated with reinforcement learning for multi-objective optimization. This method specifically aims to enhance BBB permeability (BBBp) while maintaining high-affinity substructures of KRAS inhibitors. To support this, we incorporate a specialized KRAS BBB predictor based on active learning and an affinity predictor employing comparative learning models. Additionally, we introduce two novel metrics, the knowledge-integrated reproduction score (KIRS) and the composite diversity score (CDS), to assess structural performance and biological relevance. Retrospective validation with KRAS inhibitors, AMG510 and MRTX849, demonstrates the framework's effectiveness in optimizing BBBp and highlights its potential for real-world drug development applications. This study provides a robust framework for accelerating the structural enhancement of lead compounds, advancing the drug development process across diverse targets.
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http://dx.doi.org/10.1016/j.jpha.2025.101337 | DOI Listing |
Crit Rev Oncol Hematol
September 2025
Unit of Cancer Genetics, Institute of Genetic & Biomedical Research (IRGB), National Research Council (CNR), Traversa La Crucca n. 3, 07100, Sassari, Italy; Immuno-Oncology & Targeted Cancer Biotherapies, University of Sassari, Viale San Pietro 43, 07100, Sassari, Italy. Electronic address: gpalmier
Mutations in the KRAS gene are prominent oncogenic drivers in non-small cell lung cancer (NSCLC), with multiple pathophysiological, clinical and prognostic implications. Although historically considered an "undruggable" target, recent research led to the development of specific KRAS-G12C inhibitors, like sotorasib and adagrasib which are currently approved for clinical use in patients affected by advanced NSCLC. However, the clinical utility of these drugs is often limited by resistance development through several biological mechanisms, including additional KRAS mutations, activation of compensatory pathways and metabolic reprogramming.
View Article and Find Full Text PDFEur J Pharmacol
September 2025
General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, PR China. Electronic address:
We previously screened a peptide PDBAG1 that remarkably inhibited triple-negative breast cancer, and found that its target was C1QBP. Recently, C1QBP has been reported as a potential tumor marker in ovarian cancer, which of the mortality rate ranks first among malignant tumors of the female reproductive tract. However, it is unclear whether and how PDBAG1 plays a regulatory role in ovarian cancer.
View Article and Find Full Text PDFCancer Genet
August 2025
National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India. Electronic address:
Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic and epigenetic alterations that drive uncontrolled cellular proliferation and survival. This review provides a comprehensive overview of key cancer driver genes, including oncogenes such as KRAS and PIK3CA, as well as tumor suppressor genes like TP53, PTEN, and CDKN2A, highlighting their molecular mechanisms and roles across various types of cancer. Leveraging insights from large-scale cancer genome initiatives and whole-genome sequencing, we examine the landscape of somatic mutations and their association with hallmark cancer pathways, including cell cycle regulation, apoptosis, metabolic reprogramming, and immune evasion.
View Article and Find Full Text PDFFront Oncol
August 2025
Department of Radiology, Guang an District People's Hospital of Sichuan Province, Guang an, Sichuan, China.
Colorectal cancer (CRC), a highly prevalent malignant tumor in clinical practice, poses a serious threat to human health. In 2015, the relevant guidelines issued by the United States clearly stipulated that only patients with the wild-type kirsten rat sarcoma viral oncogene homologue (KRAS) gene were recommended to receive epidermal growth factor receptor (EGFR) inhibitor treatment. Therefore, accurately predicting the status of the KRAS gene plays a crucial role in formulating scientific and reasonable treatment plans and improving prognosis.
View Article and Find Full Text PDFJ Cancer Res Ther
September 2025
Center of Interventional Radiology and Vascular Surgery, Department of Radiology, Zhongda Hospital, Medical School, Southeast University, Nanjing, China.
Objective: This study examined the effect of hepatic arterial infusion chemotherapy (HAIC) plus programmed death 1 inhibitors (HAICPs) in patients with unresected colorectal cancer liver metastases (UCRLM) with and without KRAS mutations.
Materials And Methods: We retrospectively collected data from patients with UCRLM, who received HAIC with HAICP or HAIC alone (oxaliplatin plus fluorouracil), including information on KRAS status (mutated, MUT; wild-type, WT) from a multicenter institutional database. Propensity score matching (PSM) was performed.