据6月19日的《科学》杂志报道说，一种转运蛋白配体（或称结合分子）看来能够抵消在小鼠以及人类中的焦虑症和惊恐发作，而且它没有与其它的当前疗法相关的负面的副作用。 这些发现表明，这种叫做XBD173的配体可能成为一个安全及快速起效的抗焦虑症的良好的候选药物。 目前的诸如benzodiazepines的疗法常常存在有害的副作用：如镇静、耐受或在长期使用之后会出现戒断症状等。 抗忧郁症药物有时也被用来治疗焦虑症，但它们的疗效仅仅是在几个星期的治疗之后才会出现。
为了寻找新的治疗方法，Rainer Rupprecht及其同僚给实验室大鼠施用了XBD173。他们观察到，XBD173几乎能够立刻防止惊恐行为的发生，而这些大鼠不会出现耐受性或任何有害的副作用。 他们接着在70位健康男性中进行有关的研究，其中还包括一个服用安慰剂的小组。他们发现，XBD173可快速启动一种抗焦虑反应且不会在长期使用之后出现任何的戒断症状。 文章的作者说，XBD173可通过调节抑制性的神经递质GABA来促进其镇静效果。他们表示，这种配体可被考虑在未来用于临床。（生物谷Bioon.com）
生物谷推荐原始出处：
Science June 18, 2009 DOI: 10.1126/science.1175055
Translocator Protein (18 kD) as Target for Anxiolytics Without Benzodiazepine-Like Side Effects
Rainer Rupprecht 1*, Gerhard Rammes 2, Daniela Eser 3, Thomas C. Baghai 3, Cornelius Schüle 3, Caroline Nothdurfter 1, Thomas Troxler 4, Conrad Gentsch 4, Hans O. Kalkman 4, Frederique Chaperon 4, Veska Uzunov 4, Kevin H. McAllister 4, Valerie Bertaina-Anglade 5, Christophe Drieu La Rochelle 5, Dietrich Tuerck 6, Annette Floesser 4, Beate Kiese 7, Michael Schumacher 8, Rainer Landgraf 9, Florian Holsboer 9, Klaus Kucher 4
1 Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstrasse 7, Munich, 80336 Germany.; Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, Munich, 80804 Germany.
2 Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, Munich, 80804 Germany.; Department of Anaesthesiology, Technische Universit?t, Munich, Germany.
3 Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstrasse 7, Munich, 80336 Germany.
4 Novartis Institute for Biomedical Research (NIBR), Neuroscience, Basel, Switzerland.
5 Biotrial, Rennes, France.
6 DMPK, F. Hoffmann-La Roche AG, Basel, Switzerland.
7 Biostatistics, Novartis Pharma AG, Basel, Switzerland.
8 INSERM UMR 788, Paris, France.
9 Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, Munich, 80804 Germany.
Most antianxiety drugs (anxiolytics) work by modulating neurotransmitters in the brain. Benzodiazepines are fast and effective anxiolytic drugs; however, their long-term use is limited by development of tolerance and withdrawal symptoms. Ligands of the translocator protein (18 kD) may promote the synthesis of endogenous neurosteroids, which also exert anxiolytic effects in animal models. Here, we found that the translocator protein (18 kD) ligand XBD173 enhanced GABAergic neurotransmission and counteracted induced panic attacks in rodents in the absence of sedation and tolerance development. XBD173 also exerted antipanic activity in humans and, in contrast to benzodiazepines, did not cause sedation and withdrawal symptoms. Thus, translocator protein (18 kD) ligands are promising candidates for fast-acting anxiolytic drugs with less severe side effects than benzodiazepines.
