来自慕尼黑马克斯·普朗克精神病学研究所的Mathias Schmidt和斯德哥尔摩卡罗林斯卡学院的Juan Pablo Lopez联合领导的研究团队发现，一种名为SAFit2的化合物能够阻断FKBP51蛋白，可能预防童年逆境对压力反应的长期影响[1]。该研究于2026年6月发表[1]。
在小鼠实验中，研究人员在母鼠经历压力期间给予SAFit2，该药物通过母乳传递给后代[1]。接受药物的小鼠在社会等级中的表现与未经历压力逆境的小鼠相同[1]。同时，该药物在内侧前额皮质和伏隔核两个脑区最明显地逆转了基因活动变化[1]。
目前，这项研究仅在雄性小鼠身上进行了测试[1]，且SAFit2仍是研究化合物，尚未进行人体安全测试[1]。研究证明的是预防机制，而非对已有创伤的修复[1]。Schmidt预测，该化合物的临床应用可在未来十年内实现[1]。
Researchers from Munich and Stockholm have identified a compound called SAFit2 that may prevent the lasting impact of early adversity on stress responses.[1] The compound works by blocking the FKBP51 protein, and when administered to pregnant mice during periods of stress, it is transmitted to offspring through breast milk, according to findings led by Mathias Schmidt of the Max Planck Institute of Psychiatry and Juan Pablo Lopez of the Karolinska Institute.[1]
In laboratory experiments, mice that received the treatment showed social outcomes comparable to animals that had not experienced adverse conditions.[1] The drug reversed gene activity changes in two key brain regions—the medial prefrontal cortex and the nucleus accumbens—that are typically altered by early stress exposure.[1] Schmidt suggests that clinical applications could be feasible within the next decade, though SAFit2 remains an experimental compound and has not yet undergone human safety testing.[1] The research demonstrates a preventive mechanism rather than a treatment for trauma already experienced, with studies so far limited to male mice.[1]