RAC1 GTPase plays a key role in the regulation of multiple essential cellular processes. Aberrant activation of RAC1 is associated with tumorigenesis, invasion and metastasis in several tumor types, including breast cancer (BC). In triple-negative breast cancer (TNBC), RAC1 overexpression has been shown to lead to cancer metastasis and recurrence as well as to regulate chemosensitivity to cytotoxic agents by influencing DNA damage repair. 1-A116 is a small molecule previously developed by our team that inhibits RAC1 interaction with various GEFs, preventing its activation and showing interesting antitumor effects in several preclinical settings. Since there is a pressing need to identify novel, efficacious therapies for TNBC due to its aggressive nature, high recurrence rates, and limited treatment options, we sought to evaluate 1A-116 RAC1 inhibitor as a potential novel treatment for TNBC. First we performed a comprehensive analysis of RAC1 expression in BC using several bioinformatic platforms. RAC1 was upregulated in primary BC tissue in all stages compared with normal tissue, and was also associated to shorter overall survival. Furthermore, strong correlations between RAC1 expression and signature gene subsets associated with migration, metastasis and immuneevasion were found. These results highlight that RAC1 may have a relevant impact on BC clinical outcome. We further evaluated the RAC1 inhibitor 1A-116 in a syngeneic murine TNBC model to assess its efficacy. Daily i.p treatment with 10 mg/kg 1A-116 significantly reduced tumor volume and similar results were observed when mice were treated once a week with 1 mg/kg i.v. Notably, 1A-116 treatment was well-tolerated in mice at the tested doses, with no observed toxicity, suggesting a favorable safety profile. These findings underscore the therapeutic potential of 1A-116 in targeting RAC1, a key target in TNBC, and support its further development in combination with chemoimmunotherapy to improve patient outcomes