慕尼黑马克斯·普朗克精神病学研究所和斯德哥尔摩卡罗琳医学院的研究人员联合发表的一项研究表明，药物SAFit2可能有助于在创伤形成之前进行预防。[1]该研究在小鼠身上测试了这一药物的效果，发现在幼鼠经历困难期间给予SAFit2可以阻断FKBP51蛋白的过度表达，从而使压力反应正常化。[1]实验中，研究人员在压力期间向母鼠给予该药物，通过母乳将其传递给幼鼠，结果显示受治疗的幼鼠在社会等级中的表现与未经历逆境的对照组相同，同时预防了长期社会地位下降和大脑相关区域的改变。[1]
SAFit2的作用机制在于阻断FKBP51蛋白，使皮质醇受体更容易被触发，从而恢复身体的应激反应关闭机制。[1]研究小组负责人Mathias Schmidt表示，该药物的临床应用需要至少十年时间，且必须在创伤发生之前给予而非之后。[1]目前，创伤后应激障碍的治疗主要依赖选择性血清素再摄取抑制剂（SSRIs），但对部分患者无效。[1]
需要注意的是，本研究仅在雄性小鼠上进行，SAFit2目前仍为研究化合物，尚未进行人类安全测试。[1]
Researchers from Munich's Max Planck Institute of Psychiatry and Stockholm's Karolinska Institute have demonstrated that a drug compound called SAFit2 may prevent trauma from developing when administered before stress exposure occurs.[1] The study, published in June 2026, tested whether the medication could block excessive expression of the FKBP51 protein in young mice during periods of adversity, thereby normalizing stress responses and preventing long-term social decline and associated brain changes.[1]
The drug works by blocking FKBP51, which makes cortisol receptors more readily activated and restores the body's mechanism for shutting down stress responses.[1] When nursing mothers were given SAFit2, the compound was transmitted to their offspring through breast milk.[1] Treated male mice subsequently performed in social hierarchies identically to control animals that had never experienced adversity, whereas untreated mice exposed to stress showed lasting social impairment.[1] However, the research has significant limitations: the study involved only male mice, and SAFit2 remains an experimental compound that has not undergone human safety testing.[1]
Lead researcher Mathias Schmidt emphasized that clinical application would require at least a decade of additional development and that the drug must be administered before trauma occurs rather than after.[1] Current treatments for post-traumatic stress disorder rely primarily on selective serotonin reuptake inhibitors (SSRIs), which prove ineffective for some patients.[1]