Bosutinib: Transforming the therapeutic landscape for HER2-positive and triple-negative breast cancer

• Bosutinib targets Src and Abl kinases, tackling HER2+ and TNBC breast cancers. • Dual inhibition mechanisms overcome therapy resistance and enhance cancer cell apoptosis. • Nanoparticle-based delivery improves bioavailability and minimizes systemic toxicity. • Combination therapies with bosutinib synergize to boost treatment efficacy. • Advances precision medicine by aligning therapies with tumor molecular profiles. Breast cancer remains one of the most prevalent and challenging malignancies, especially in aggressive subtypes such as HER2-positive and triple-negative breast cancer (TNBC). These subtypes are characterized by rapid proliferation, high metastatic potential, and resistance to conventional therapies, leading to poor prognosis. Bosutinib, a second-generation tyrosine kinase inhibitor, has emerged as a promising therapeutic candidate due to its dual inhibition of SRC family and Abl kinases, which are pivotal in cancer cell proliferation, survival, and metastasis. Preclinical and clinical studies indicate that bosutinib effectively suppresses tumor growth, induces apoptosis, and reduces metastatic potential. Moreover, its combination with existing therapies, such as trastuzumab or immune checkpoint inhibitors, enhances therapeutic efficacy, particularly in resistant cases. Innovative strategies, including nanoparticle-based delivery systems, further improve bosutinib’s bioavailability and targeted action, minimizing systemic toxicity. However, challenges such as resistance development and toxicity management require ongoing investigation. This review underscores bosutinib’s potential in addressing therapeutic resistance and highlights its role in precision medicine, advancing breast cancer treatment.