Endocrine therapy is the main treatment mode for patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) advanced breast cancer, but primary or secondary endocrine resistance can lead to treatment failure and affect patient survival. Studies have shown that abnormalities in the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway (PAM pathway) account for more than 50% of endocrine-resistant patients. The PAM pathway is not only the main mechanism of endocrine therapy resistance in breast cancer, but also mediates resistance to chemotherapy and targeted therapy. AKT is one of the core kinases of the PAM pathway, and inhibiting its activity can inhibit the aberrant activation of the pathway. Capivasertib is the first AKT kinase inhibitor, and in the phase Ⅲ CAPItello-291 clinical study, compared with fulvestrant alone, the combination of capivasertib and fulvestrant significantly increased PFS in the overall population and the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha/protein kinase B/phosphatase and tensin homolog (PIK3CA/AKT/PTEN)mutant population. In addition, capivasertib has a good safety profile, and the common adverse reactions are elevated blood glucose, diarrhea, and skin adverse reactions, which are mostly grade 1-2 and can be well tolerated. Breast cancer treatment guidelines all recommend it for post-line selection in people with PIK3CA/AKT/PTEN mutations who have failed endocrine therapy. This article mainly introduces the pharmacological mechanism, pharmacodynamics, pharmacokinetics, clinical trials and safety information of capivasertib, in order to facilitate the clinical application of the drug.