Dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase, has anti-tumor properties in various carcinoma models. Diisopropylamine dichloroacetate (DADA), an over-the-counter drug for chronic liver disease, is a derivative of DCA. To date, few studies have evaluated the anticancer potential of DADA in breast cancer. In this study, MDA-MB-231 cells, a breast adenocarcinoma cell line, were used in in vitro and in vivo experiments to evaluate the anti-tumor efficacy of DADA and DCA. The half maximal inhibitory concentration (IC50) of DADA (7.1 ± 1.1 mmol/L) against MDA-MB-231 cells was significantly lower than that of DCA (15.6 ± 2.0 mmol/L); 100 mg/kg (0.0004 mol/kg) DADA was better than 100 mg/kg (0.0008 mol/kg) DCA at suppressing the growth of subcutaneous transplantation breast tumor at the same dose after 24 days intervention. Histological examination showed that both DCA and DADA interventions led to necrosis, inflammation, and fibrosis of tumor tissue in a mouse subcutaneous transplantation breast tumor model. DADA treatment inhibited Ki67 expression in tumor tissue. In vitro experiments showed that DADA could inhibit lactic acid production and glucose uptake in MDA-MB-231 cells at 10 mmol/L and these effects were stronger than DCA. DADA administration also induced complete autophagy during early treatment stages and incomplete autophagy and cell death at later treatment stages. In conclusion, DADA showed better anti-tumor efficacy than DCA in a breast cancer model. 

二氯乙酸酯（DCA）是丙酮酸脱氢酶激酶抑制剂，在多种肿瘤模型中具有抗肿瘤作用。Diisopropylamine dichloroacetate（DADA）是一种慢性肝病的非处方药，是DCA的衍生物。迄今为止，很少有研究评估乳腺癌中DADA的抗癌潜力。本研究将MDA-MB-231细胞作为一种乳腺癌细胞株，在体外和体内实验中评价DADA和DCA的抗肿瘤作用。DADA（7.1±1.1 mmol/L）对MDA-MB-231细胞的半数最大抑制浓度（IC50）显著低于DCA（15.6±2 mmol/L）；100 mg/kg（0.0004 mol/kg）DADA抑制皮下移植的生长优于100 mg/kg（0.0008 mol/kg）DCA。

乳腺肿瘤在相同剂量后24天干预。组织学检查显示，DCA和DADA干预导致小鼠皮下移植乳腺肿瘤模型中肿瘤组织坏死、炎症和纤维化。DADA治疗抑制肿瘤组织Ki67表达。体外实验表明，DADA能抑制MDA-MB-231细胞在10 mmol/L时的乳酸生成和葡萄糖摄取，其作用强于DCA。达达管理还导致了早期治疗阶段完全自噬和后期治疗过程中的不完全自噬和细胞死亡。总之，DADA在乳腺癌模型中比DCA具有更好的抗肿瘤作用。