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Biological studies of posttraumatic stress disorder (PTSD) have found alterations of physiological stress pathways [sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis] soon after trauma in individuals who have subsequently developed PTSD, leading researchers to hypothesize that pharmacological manipulation of stress hormone levels may aid in preventing the development of post-traumatic distress. The present paper first reviews the current understanding of the neurobiology of PTSD development and then provides the rationale and evidence for early pharmacological strategies to prevent/reduce post-traumatic distress in at-risk trauma victims. Emphasis is placed on those interventions targeting the SNS and the HPA axis. Furthermore, in light of recent calls to move away from categorical diagnostic outcomes, we discuss how examining post-traumatic distress from a transdiagnostic viewpoint may inform novel chemoprophylactic approaches (intervening pharmacologically after trauma to prevent post-traumatic distress). Current evidence is suggestive for medications, such as propranolol, hydrocortisone, morphine, and oxytocin, impacting early stress hormone levels and subsequent risk for post-traumatic distress; however, future research is needed prior to adapting recommendations for widespread use of any chemoprophylactic treatments.