In a randomized, double‑blind, placebo‑controlled phase 3 trial of 90 patients with severe PTSD (including common comorbidities), MDMA‑assisted therapy produced a large, significant reduction in PTSD symptoms versus placebo (mean CAPS‑5 change −24.4 vs −13.9; P<0.0001, d=0.91) and improved functioning (SDS: P=0.0116, d=0.43). Treatment was well tolerated with no signals of abuse potential, increased suicidality or QT prolongation, indicating MDMA‑assisted therapy is a promising intervention warranting expedited evaluation.
Post-traumatic stress disorder (PTSD) presents a major public health problem for which currently available treatments are modestly effective. We report the findings of a randomized, double-blind, placebo-controlled, multi-site phase 3 clinical trial (NCT03537014) to test the efficacy and safety of 3,4-methylenedioxymethamphetamine (MDMA)-assisted therapy for the treatment of patients with severe PTSD, including those with common comorbidities such as dissociation, depression, a history of alcohol and substance use disorders, and childhood trauma. After psychiatric medication washout, participants ( n = 90) were randomized 1:1 to receive manualized therapy with MDMA or with placebo, combined with three preparatory and nine integrative therapy sessions. PTSD symptoms, measured with the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5, the primary endpoint), and functional impairment, measured with the Sheehan Disability Scale (SDS, the secondary endpoint) were assessed at baseline and at 2 months after the last experimental session. Adverse events and suicidality were tracked throughout the study. MDMA was found to induce significant and robust attenuation in CAPS-5 score compared with placebo ( P < 0.0001, d = 0.91) and to significantly decrease the SDS total score ( P = 0.0116, d = 0.43). The mean change in CAPS-5 scores in participants completing treatment was −24.4 (s.d. 11.6) in the MDMA group and −13.9 (s.d. 11.5) in the placebo group. MDMA did not induce adverse events of abuse potential, suicidality or QT prolongation. These data indicate that, compared with manualized therapy with inactive placebo, MDMA-assisted therapy is highly efficacious in individuals with severe PTSD, and treatment is safe and well-tolerated, even in those with comorbidities. We conclude that MDMA-assisted therapy represents a potential breakthrough treatment that merits expedited clinical evaluation.
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This was a randomised, double-blind, placebo-controlled Phase III trial testing MDMA-assisted therapy for people with moderate-to-severe PTSD. Participants were recruited via advertisements and referrals and had to meet DSM-5 criteria for current PTSD of at least 6 months’ duration and have a baseline CAPS-5 total severity score of ≥35. Key exclusions included primary psychotic disorder, bipolar I disorder, dissociative identity disorder, current alcohol or substance use disorders, pregnancy or lactation, and medical conditions that would make a sympathomimetic drug hazardous (for example uncontrolled hypertension or arrhythmia). Participants were required to discontinue many psychiatric medications before baseline according to a supervised taper schedule. Randomisation was 1:1 to MDMA-assisted therapy or therapy with an inactive placebo, stratified by site and managed centrally to maintain blinding. To limit bias in efficacy measurement, outcome assessments (CAPS-5 and SDS) were conducted by an independent, observer‑blind pool of raters who did not repeatedly see the same participant and were blind to treatment allocation and visit number. The treatment model comprised three 90‑minute preparatory sessions, three 8‑hour experimental sessions spaced approximately 4 weeks apart, and nine 90‑minute integration sessions, with independent-rater efficacy assessments after each experimental session and a primary endpoint at ~18 weeks after baseline (about 8 weeks after the third experimental session). Experimental-session dosing used a circadian-adjusted morning schedule: session 1 typically 80 mg followed by a supplemental 40 mg 1.5–2.5 h later; sessions 2 and 3 typically 120 mg followed by a supplemental 60 mg. Primary efficacy was change in CAPS-5 total severity score from baseline to 18 weeks after baseline; the secondary efficacy endpoint was change in clinician-rated functional impairment as measured by the Sheehan Disability Scale (SDS). Exploratory outcomes included depression (BDI-II), alcohol and drug use screening measures, and adverse childhood experiences. Safety monitoring emphasised treatment-emergent adverse events (TEAEs) and specified adverse events of special interest (AESIs) related to cardiac function, abuse liability and suicidality; suicidality was tracked throughout with the Columbia Suicide Severity Rating Scale (C-SSRS). Statistical analysis used mixed model repeated measures (MMRM) comparing change from baseline in CAPS-5 and SDS between groups. The statistical analysis plan implemented the use of estimands: a de jure estimand (efficacy if the drug is taken as directed) as the primary analysis and a de facto estimand (effectiveness if taken as assigned regardless of adherence) as a sensitivity analysis. The modified intent-to-treat (mITT) set included participants who completed at least one blinded experimental session and one post-treatment assessment; a per-protocol completer set comprised participants who completed all three experimental sessions and assessments. Missing outcome data were not imputed. Effect sizes were reported with Cohen’s d and two‑sided hypothesis tests controlled type I error using a hierarchical testing strategy.
The modified intent-to-treat set comprised 90 participants (46 randomised to MDMA, 44 to placebo with therapy); the de jure efficacy analysis included 89 participants after excluding one participant with no post‑dose data. The per-protocol completer set included 42 participants in the MDMA arm and 37 in the placebo arm. The primary outcome showed a significant and clinically meaningful greater reduction in CAPS-5 scores for the MDMA-assisted therapy group versus placebo with therapy. MMRM analysis of the de jure estimand reported a between-group difference of 11.9 points on the CAPS-5 from baseline to 18 weeks (95% CI = 6.3–17.4, P < 0.0001, d.f. = 71). Among completers, mean CAPS-5 change was −24.4 (s.d. 11.6; n = 42) in the MDMA group and −13.9 (s.d. 11.5; n = 37) in the placebo group. Between-group effect size was d = 0.91 (95% CI = 0.44–1.37) for the de jure estimand and d = 0.97 (95% CI = 0.51–1.42) for the de facto estimand. When considering within‑group change (which includes the effect of the supportive therapy common to both arms), the reported within‑group effect sizes were larger in the MDMA group (d = 2.1) than in the placebo group (d = 1.2). Clinician-rated functional impairment improved significantly more in the MDMA group. MMRM of the de jure estimand for SDS showed a significant between‑group difference (n = 89, P = 0.0116) with an effect size of 0.43 (95% CI = −0.01–0.88); completer mean SDS change was −3.1 (s.d. 2.6; n = 42) for MDMA and −2.0 (s.d. 2.4; n = 37) for placebo. Exploratory analysis of depressive symptoms (BDI‑II) found greater reduction in the MDMA arm: mean change −19.7 (s.d. 14.0; n = 42) versus −10.8 (s.d. 11.3; n = 39) in placebo (t = −3.11, P = 0.0026), with an effect size of 0.67 (95% CI = 0.22–1.12). Diagnostic outcomes favoured MDMA-assisted therapy. At the primary endpoint (18 weeks), 28 of 42 participants (67%) in the MDMA group no longer met criteria for PTSD versus 12 of 37 (32%) in the placebo group. Remission, defined by the study as loss of diagnosis plus CAPS-5 total score ≤11, occurred in 14 of 42 participants (33%) in the MDMA arm and 2 of 37 participants (5%) in the placebo arm. Subgroup and site analyses indicated consistency across study sites (no significant site effect, P = 0.1003). MDMA benefit was also observed in participants with comorbidities often associated with poorer outcomes. For example, participants with the dissociative subtype showed substantial reductions in CAPS-5 with MDMA (mean Δ = −30.8, s.d. 9.0) compared with placebo (mean Δ = −12.8, s.d. 12.8); reductions in non‑dissociative participants were similar (MDMA mean Δ = −23.6, s.d. 11.7; placebo mean Δ = −14.3, s.d. 11.2). The extracted text reports no obvious modulation of treatment effect by history of SSRI use, history of alcohol or substance use disorder, overnight stay, or severe childhood trauma. Safety findings: TEAEs that were more common in the MDMA arm tended to be transient and of mild–moderate severity and included muscle tightness, decreased appetite, nausea, hyperhidrosis and feeling cold. Expected transient increases in systolic and diastolic blood pressure and heart rate occurred during MDMA sessions; two MDMA participants had transient body temperature rises to 38.1 °C. Two participants in the placebo arm reported three serious adverse events (SAEs) related to suicidal behaviour or ideation; no SAEs were reported in the MDMA arm in the extracted text. AESIs of suicidality/self‑harm were reported by five participants in the placebo group and three in the MDMA group. One participant in the placebo group reported two cardiovascular AESIs where cardiac aetiology could not be ruled out. One MDMA‑randomised participant discontinued because the CAPS-5 assessments were triggering and because of depressed mood following an experimental session; this participant was classified as a non‑responder. Lifetime suicidal ideation was common (>90% reported lifetime ideation), and baseline past‑week ideation was 37% in MDMA and 32% in placebo; the prevalence of suicidal ideation during the study never exceeded baseline levels and was not exacerbated in the MDMA group. Serious suicidal ideation during the study was minimal and occurred almost entirely in the placebo arm.
Mitchell and colleagues interpret their findings as showing that three doses of MDMA administered alongside manualised supportive therapy produced significant and robust reductions in PTSD symptoms and clinician‑rated functional impairment over an 18‑week period. The investigators also report significant reduction in depressive symptoms and emphasise that MDMA did not increase suicidality in this trial. They note that the between‑group effect size (d ≈ 0.91) for CAPS-5 change exceeds effect sizes reported for FDA‑approved SSRIs in pivotal trials and that participants receiving MDMA plus supportive therapy showed larger within‑group improvement than those receiving supportive therapy with placebo, suggesting MDMA potentiated the therapeutic model used in the study. The discussion places the clinical findings in a mechanistic context, noting prior preclinical and human imaging evidence implicating serotonergic modulation of amygdala activity, brain‑derived neurotrophic factor–mediated plasticity and oxytocin‑related prosocial effects as plausible contributors to therapeutic change. The authors propose that MDMA may open a transient window of tolerance or heightened neuroplasticity that facilitates processing of traumatic memories with less overwhelming fear or dissociation and that the acute prosocial effects may improve therapeutic alliance and adherence. Safety and generalisability are discussed candidly. The authors report no major safety signals specific to MDMA in this dataset, and consider the observed transient cardiovascular effects expected based on prior studies. They acknowledge limitations: the achieved sample size was reduced by the COVID‑19 pandemic though the data retained adequate statistical power; the sample was relatively homogeneous and lacked racial and ethnic diversity; the primary outcome is a short‑term endpoint (≈8 weeks after the final experimental session) with longer‑term durability to be reported later; and blinding was challenging given the subjective effects of MDMA, which may introduce expectation effects despite the use of blinded independent raters for efficacy assessments. The authors also note that safety data collection by site therapists could have affected blinding of some safety assessments, but that efficacy data were collected by blinded raters to minimise bias. Finally, the investigators highlight clinical implications they draw from the data: MDMA-assisted therapy showed efficacy in participants with chronic, severe and comorbid PTSD presentations, including the dissociative subtype, suggesting a potential role for this model in treatment‑resistant or complex cases. They recommend further studies to replicate findings, evaluate specific comorbid populations, and ultimately consider head‑to‑head comparisons with existing pharmacotherapies and longer‑term follow‑up to establish durability and broader safety.
Statistical power calculations for the initial sample size were made by fitting an MMRM of CAPS-4 data (converted to the CAPS-5 scale and pooled from the phase 2 studies) to obtain variance and covariance parameter estimates. Using the estimated effect size and variance and covariance parameters, the sample size was calculated to achieve a power of 90% at an alpha of 0.049. The intent-to-treat (ITT) set consisted of 91 randomized participants, however, one participant declined dosing on the morning of the session and provided no additional data, and therefore it was not possible to complete this analysis. Participants were randomized in a blinded fashion with 1:1 allocation as described in the section on randomization, masking and bias minimization above. The modified intent-to-treat (mITT) set consisted of 90 randomized participants who had completed at least one blinded experimental session and at least one post-treatment assessment. The mITT set consisted of 46 participants randomized to the MDMA group and 44 participants randomized to the placebo group, with identical therapy. The per protocol set (completers) consisted of all participants who completed three experimental sessions and assessments (MDMA, n = 42; placebo, n = 37) (Fig.). The SAP was guided by the ICH E9 (R1) guidelines, which describe the use of estimands and sensitivity analyses to measure the effects of the drug if taken as directed (de jure, assessment of efficacy), and the effects of the drug if taken as assigned, regardless of adherence (de facto, assessment of effectiveness). The SAP was developed in accordance with FDA requirements and was approved by the European Medicines Agency to meet the requirements for future marketing applications. The primary and secondary efficacy analyses therefore utilized a de jure estimand of the mITT set for assessing treatment efficacy from the CAPS-5 and SDS data while on the study drug. The de jure dataset did not include outcome measurements taken after treatment discontinuation in the analysis of treatment efficacy. Missing data were not imputed. One participant in the placebo group completed only the baseline assessment, and discontinued intervention but provided CAPS data at the T4 timepoint, ~18 weeks after baseline. Given that no endpoint assessment was collected prior to treatment discontinuation, this participant is excluded from the de jure estimand (leaving n = 89) but is included in the de facto estimand sensitivity analysis (for a total of n = 90). Two additional CAPS data points at the T4 timepoint, ~18 weeks after baseline, from two participants in the placebo group who provided these data following discontinuation of treatment, were not included in the de jure estimand (Supplementary Table). The de facto estimand assessed the impact of these missing data points in the mITT set. That is, the CAPS measures at the T4 timepoint, ~18 weeks after baseline for the three placebo participants who discontinued treatment but provided off-treatment outcome assessments were included in a sensitivity analysis, which determined that inclusion of these measures in the model did not significantly alter the results. The primary and secondary efficacy analyses were carried out using an MMRM that included all outcome data from baseline and the first, second and third experimental sessions. The efficacy of treatment was tested by comparing the change from baseline to the third experimental session in CAPS-5 and SDS scores between treatment groups in two-sided tests. The fixed effects were treatment (MDMA or placebo), baseline CAPS score, dissociative subtype and investigational site, with random effect specified as study participant. A hierarchical testing strategy was used to control for type I error, such that the hypothesis for the key secondary endpoint (SDS) would be tested only if the statistical test for the primary efficacy comparison rejected the null hypothesis. An analysis of covariance (ANCOVA) to test the effects of study participation before versus after the COVID-19 pandemic declaration by the World Health Organization indicated a non-significant interaction and therefore was not included in the primary outcome model (Supplementary Table). The primary outcome analysis was replicated independently by one blinded programmer and one unblinded programmer. An independent data monitoring committee monitored adverse events for safety and conducted one administrative interim analysis, after completion of enrollment and of 60% of primary endpoints to examine the adequacy of the sample size. The data monitoring committee recommended that no additional participants should be added, based on conditional power calculations supporting 90% statistical power, but in keeping with the SAP did not provide the sponsor with any information on the conditional power or effect size. The alpha level was set to 0.05, and 2% of the alpha (0.001) was spent on the interim analysis and 98% (0.0499) was left for the final analysis. Statistics for the primary and secondary efficacy comparisons (CAPS and SDS) are reported as P values from the results of the MMRM analysis. In exploratory analyses, additional baseline covariates of age, gender, ethnicity, prior use of SSRIs, depression as measured by the BDI-II, adverse childhood experiences, and alcohol and substance use disorders were assessed in the model, with the threshold of significance set at P < 0.05 (Supplementary Table). BDI-II score was also assessed as an exploratory efficacy outcome measure with a paired, two-tailed t-test. Results are reported as mean (s.d.) throughout the text. Between-group effect size was calculated with Cohen's d, and 95% CIs are reported. SAS version 9.4 (SAS Institute) was used for analyses. The safety analysis included all participants who were given at least one dose of the study drug or placebo. The primary safety analysis evaluated TEAEs as a participant-level analysis. An association with MDMA was determined based on the relative incidence of TEAEs with at least a twofold difference between the MDMA and placebo groups.
Here, we demonstrate that three doses of MDMA given in conjunction with manualized therapy over the course of 18 weeks results in a significant and robust attenuation of PTSD symptoms and functional impairment as assessed using the CAPS-5 and SDS, respectively. MDMA also significantly mitigated depressive symptoms as assessed using the BDI-II. Of note, MDMA did not increase the occurrence of suicidality during the study. These data illustrate the potential benefit of MDMA-assisted therapy for PTSD over the FDA-approved first-line pharmacotherapies sertraline and paroxetine, which have both exhibited smaller effect sizes in pivotal studies. Previous comparison of change in CAPS score between sertraline and placebo showed effect sizes of 0.31 and 0.37 (ref.). Similarly, comparison of change in CAPS score between paroxetine and placebo showed effect sizes of 0.56, 0.45 and 0.09 (ref.). By contrast, the effect size of 0.91 demonstrated in this study between MDMA-assisted therapy and placebo with therapy was larger than that for any other previously identified PTSD pharmacotherapy. To directly assess superiority, a head-to-head comparison of MDMA-assisted therapy with SSRIs for PTSD would be needed. Although the present study tested the effects of MDMA using a model in which both treatment groups received supportive therapy, participants who received MDMA and supportive therapy (d = 2.1) had greater improvement in PTSD change scores compared with those who received placebo with supportive therapy (d = 1.2), suggesting that MDMA enhanced the effects of supportive therapy. In clinical practice, both MDMA and supportive therapy will be components of this PTSD treatment. Previous research on MDMA for PTSD has suggested that those with a recent history of SSRI treatment may not respond as robustly to MDMA. Given that 65.5% of participants in the current trial have a lifetime history of SSRI use, it is difficult to separate the ramifications of long-term SSRI treatment from the effects of treatment resistance. However, there was no obvious effect of previous SSRI use on therapeutic efficacy in this trial. Similarly, although years of PTSD diagnosis or age of onset may affect treatment efficacy, no obvious relationship was seen here between duration or onset of PTSD diagnosis and treatment efficacy. Serotonin and the serotonin transporter are of particular importance in the generation, consolidation, retrieval and reconsolidation of fear memories. Reduced serotonin transporter levels (which result in greater amounts of extracellular serotonin) have been shown to predict propensity to develop PTSD, increase fear and anxiety-related behaviors, and induce greater amygdalar blood oxygenation level-dependent (BOLD) activity in response to fearful images. There is extensive serotonergic innervation of the amygdala, and amygdalar serotonin levels have been shown to increase following exposure to stressful and fear-inducing stimuli. MDMA enhances the extinction of fear memories in mice through increased expression of brain-derived neurotrophic factor in the amygdala, and human neuroimaging studies have demonstrated that MDMA is associated with attenuated amygdalar BOLD activity during presentation of negative emotional stimuli. Together these data suggest that MDMA may exert its therapeutic effects through a well-conserved mechanism of amygdalar serotonergic function that regulates fear-based behaviors and contributes to the maintenance of PTSD. Perhaps by reopening an oxytocin-dependent critical period of neuroplasticity that typically closes after adolescence, MDMA may facilitate the processing and release of particularly intractable, potentially developmental, fear-related memories. It is intriguing to speculate that the pharmacological properties of MDMA, when combined with therapy, may produce a 'window of tolerance, ' in which participants are able to revisit and process traumatic content without becoming overwhelmed or encumbered by hyperarousal and dissociative symptoms. MDMA-assisted
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