Triple-negative breast cancer (TNBC) is a breast cancer subtype that lacks estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression. It is highly invasive, prone to recurrence, and has a poor prognosis. Due to the absence of ER, PR, and HER2, TNBC is not sensitive to endocrine or HER2-targeted therapies, and standard treatment regimens are lacking. Therefore, developing new treatment strategies is urgent. This review summarizes existing treatment regimens, therapeutic drugs, and their efficacy for different TNBC subtypes, and reviews new preclinical studies and targeted treatment regimens for TNBC, aiming to provide new ideas for TNBC treatment. TNBC is classified into various molecular subtypes, including basal-like 1 (BL1), basal-like 2 (BL2), mesenchymal (M), mesenchymal stem-like (MSL), immunomodulatory (IM), and luminal androgen receptor (LAR). Each subtype has distinct molecular characteristics and therapeutic targets. For example, BL1 subtype is sensitive to cisplatin and PARP inhibitors, while BL2 is resistant to conventional therapies. The MSL subtype may respond to PI3K inhibitors or Src antagonists. The IM subtype is similar to medullary carcinoma and may benefit from immune checkpoint inhibitors. The LAR subtype, despite being ER-negative, has active hormonal signaling pathways and may respond to anti-androgen therapy. Chemotherapy remains the main treatment for TNBC, with regimens such as TAC, TC, AC, CMF, CAF, and CEF-T. Taxanes like paclitaxel and docetaxel are effective in BL1 and BL2 subtypes. Anthracyclines, including doxorubicin and epirubicin, are used in combination with other agents. Cyclophosphamide is used in neoadjuvant chemotherapy, showing higher pCR rates in TNBC patients. Platinum agents like cisplatin and carboplatin are effective in BL1 subtypes. Fluorouracil and capecitabine are used in advanced or metastatic TNBC. Targeted therapies, including PARP inhibitors, EGFR inhibitors, and AR inhibitors, are being explored. PARP inhibitors are effective in BRCA1/2-mutated TNBC. EGFR inhibitors show limited efficacy in clinical trials. AR inhibitors, such as bicalutamide and enzalutamide, are effective in LAR subtypes. Immunotherapy, including PD-1/PD-L1 inhibitors and CTLA-4 inhibitors, is being investigated for TNBC. CAR-T cell therapy targeting FRα or mesothelin is also being explored. In summary, TNBC is a heterogeneous disease with distinct molecular subtypes and therapeutic targets. New treatment strategies, including targeted therapies and immunotherapy, are needed to improveTriple-negative breast cancer (TNBC) is a breast cancer subtype that lacks estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression. It is highly invasive, prone to recurrence, and has a poor prognosis. Due to the absence of ER, PR, and HER2, TNBC is not sensitive to endocrine or HER2-targeted therapies, and standard treatment regimens are lacking. Therefore, developing new treatment strategies is urgent. This review summarizes existing treatment regimens, therapeutic drugs, and their efficacy for different TNBC subtypes, and reviews new preclinical studies and targeted treatment regimens for TNBC, aiming to provide new ideas for TNBC treatment. TNBC is classified into various molecular subtypes, including basal-like 1 (BL1), basal-like 2 (BL2), mesenchymal (M), mesenchymal stem-like (MSL), immunomodulatory (IM), and luminal androgen receptor (LAR). Each subtype has distinct molecular characteristics and therapeutic targets. For example, BL1 subtype is sensitive to cisplatin and PARP inhibitors, while BL2 is resistant to conventional therapies. The MSL subtype may respond to PI3K inhibitors or Src antagonists. The IM subtype is similar to medullary carcinoma and may benefit from immune checkpoint inhibitors. The LAR subtype, despite being ER-negative, has active hormonal signaling pathways and may respond to anti-androgen therapy. Chemotherapy remains the main treatment for TNBC, with regimens such as TAC, TC, AC, CMF, CAF, and CEF-T. Taxanes like paclitaxel and docetaxel are effective in BL1 and BL2 subtypes. Anthracyclines, including doxorubicin and epirubicin, are used in combination with other agents. Cyclophosphamide is used in neoadjuvant chemotherapy, showing higher pCR rates in TNBC patients. Platinum agents like cisplatin and carboplatin are effective in BL1 subtypes. Fluorouracil and capecitabine are used in advanced or metastatic TNBC. Targeted therapies, including PARP inhibitors, EGFR inhibitors, and AR inhibitors, are being explored. PARP inhibitors are effective in BRCA1/2-mutated TNBC. EGFR inhibitors show limited efficacy in clinical trials. AR inhibitors, such as bicalutamide and enzalutamide, are effective in LAR subtypes. Immunotherapy, including PD-1/PD-L1 inhibitors and CTLA-4 inhibitors, is being investigated for TNBC. CAR-T cell therapy targeting FRα or mesothelin is also being explored. In summary, TNBC is a heterogeneous disease with distinct molecular subtypes and therapeutic targets. New treatment strategies, including targeted therapies and immunotherapy, are needed to improve