Triple-negative breast cancer (TNBC) is characterized by a lack of expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) and unfortunately is not associated with good prognosis. Treatment of breast cancer mainly depends on chemotherapy, due to the lack of specifically approved targeted therapies for TNBC. It is of paramount importance to find new therapeutic approaches, as resistance to chemotherapy frequently occurs. Herein, we present clinical studies published within the last five years, in order to reveal possible targeted therapies against TNBC. We aimed to discuss factors against TNBC, such as tyrosine kinase inhibitors, anti-androgens, poly ADP-ribose polymerase-1 (PARP-1) inhibitors, anti-angiogenic factors, immune checkpoints and histone deacetylase inhibitors (HDACI). Furthermore, the PI3K/AKT/mTOR pathway seems to be a promising field for the development of new anti-TNBC targeted therapies. Data from 18 clinical trials with patients suffering from TNBC were summarized and presented descriptively. Breast cancer is one of the most common cancers in females, comprising heterogeneous tumors with a variety of biological features, clinical course, prognosis and response to therapy (1, 2). In 2017, triple-negative breast cancer (TNBC) accounted for about 15% of all the new cases of breast cancer in the United States (3-7). Many different epidemiological studies have revealed that TNBC was more likely to arise among females characterized by early menarche, higher waist to hip ratio, higher parity, shorter duration of breast feeding, higher body mass index, and was more common among pre-menopausal patients (8). TNBC is a disease defined by the absence of human epidermal growth factor receptor 2 (HER2) and hormone receptors (HR), specifically the progesterone (PR) and the estrogen receptor (ER) (9) (Figure 1). There are at least 6 different subtypes, which demonstrate different biological behavior, including the basal-like 1 and 2 (BL-1 and BL-2), mesenchymal (M), mesenchymal stem-like (MSL), immunomodulatory (IM), luminal androgen receptor (LAR) and unstable subtype (7, 10).