Mycobacterium tuberculosis is the major etiological agent for tuberculosis (TB), which is the leading cause of single pathogen infection-related deaths worldwide. The End TB Strategy of the World Health Organization aimed to decrease the incidence of TB by 20% between 2015 and 2020, which was not achieved. Here, the growth-inhibitory effects of tris-(1,10-phenanthroline) iron (II) complex ([Fe(phen)₃]²⁺), a known commercially available cheap chemical substance, were examined. The best in vitro results showed great activity with MIC ranging from 0.77 to 3.06 μM against clinical strains and at low pH (mimicking the granuloma) with MIC of 0.21 μM. Preliminary safety analysis revealed that the complex did not exhibit cytotoxic activity against different cell lines or mutagenic activity in vitro. The complex was orally bioavailable after 2 h of administration in vivo. Additionally, the results of the acute toxicity test revealed that the complex did not exert toxic effects in female BALB/c mice. The mechanism of action was performed using D29 mycobacteriophages where the treatment with different concentrations of the complex inhibited viral protein synthesis, which indicated that the anti-TB mechanisms of the complex involve protein synthesis inhibition. These findings suggested that [Fe(phen)₃]²⁺ is a potential novel therapeutic for TB.

结核分枝杆菌是结核病（TB）的主要病原体，而结核病是全世界单一病原体感染相关死亡的主要原因。世界卫生组织的《终止结核病战略》旨在2015年至2020年将结核病发病率降低20%，但这一目标并未实现。这里，检查了已知的市售廉价化学物质三-(1,10-菲咯啉)铁(II)络合物([Fe(phen) ₃ ] ²⁺ )的生长抑制作用。最佳体外结果显示，对临床菌株具有良好的活性，MIC 范围为 0.77 至 3.06 μM，在低 pH（模拟肉芽肿）下，MIC 为 0.21 μM。初步安全性分析显示，该复合物不表现出针对不同细胞系的细胞毒活性或体外诱变活性。该复合物在体内给药2小时后即可口服生物利用。此外，急性毒性试验结果表明，该复合物对雌性 BALB/c 小鼠没有产生毒性作用。作用机制是使用D29分枝杆菌噬菌体进行的，其中不同浓度的复合物处理抑制病毒蛋白质合成，这表明该复合物的抗结核机制涉及蛋白质合成抑制。这些发现表明[Fe(phen) ₃ ] ²⁺是一种潜在的新型结核病治疗方法。