This Phase I study provides the first detailed human pharmacokinetic characterisation of intravenous DMT fumarate (SPL026), demonstrating dose‑proportional exposure across 9–21.5 mg, rapid peak plasma concentrations (~10 min), a short elimination half‑life (9–12 min), ~70% unbound fraction and good tolerability. In vitro data indicate mitochondrial MAO‑A‑mediated metabolism with modulation by CYP2D6 and CYP2C19, supporting the design of DMT infusion regimens for major depressive disorder.
Aim
N,N-dimethyltryptamine (DMT) is a psychedelic compound under development for the treatment of major depressive disorder (MDD). This study evaluated the in vitro metabolism and clinical pharmacokinetics (PK) of DMT fumarate (SPL026) in healthy subjects.
Methods
Results are from the Phase I component of an ongoing Phase I/IIa randomised, double-blind, placebo-controlled, parallel-group, dose-escalation trial. Healthy adults received escalating doses of SPL026 via a 2-phase intravenous (IV) infusion. Dosing regimens were calculated based on PK modelling and predictions, with progression to each subsequent dose level according to safety and tolerability. In vitro experiments assessed hepatic clearance and metabolism of DMT by monoamine oxidase (MAO) and cytochrome P450 enzymes.
Results
24 healthy subjects received escalating doses of SPL026 which were safe and well-tolerated. Dose-proportional increases in DMT exposure were observed over the range of 9–21.5 mg. For all doses, median time to peak plasma concentration was ~10 min and mean elimination half-life was 9–12 min. There was no relationship between peak DMT plasma concentration and body mass index, weight or age. In vitro hepatic mitochondrial fraction clearance of SPL026 was inhibited by MAO-A, but not MAO-B, inhibition. CYP2D6 and CYP2C19 modified SPL026 clearance in vitro. The unbound fraction of SPL026 was approximately 70%.
Conclusion
This is the first study to determine, in detail, the full PK profile of DMT in humans, confirming rapid attainment of peak plasma concentrations followed by accelerated clearance. These findings provide evidence which support the development of novel DMT infusion regimens for the treatment of MDD.
Papers cited by this study that are also in Blossom
Carhart-Harris, R. L., Bolstridge, &. M., Day, C. M. J. et al. · Psychopharmacology (2017)
Earlier clinical work and animal studies have suggested that psychedelic compounds can have therapeutic potential in major depressive disorder (MDD), with efficacy linked to dose-dependent receptor pharmacology and the subjective quality of the psychedelic experience. N,N-dimethyltryptamine (DMT) is the principal psychoactive constituent of ayahuasca, but prior human pharmacokinetic (PK) data have mainly come from oral ayahuasca studies in which harmala alkaloids inhibit monoamine oxidase (MAO) and thereby render DMT orally active. Injected DMT is extremely short acting owing to rapid oxidative deamination to indole-3-acetic acid (IAA), and earlier intravenous (IV) reports described very rapid peak levels and brief subjective effects but provided limited PK parameters. Good and colleagues set out to characterise, in detail, the in vitro metabolism and the clinical pharmacokinetics of DMT in healthy, psychedelic-naïve adults. The paper reports preclinical assays of physicochemical properties, MAO and cytochrome P450 (CYP) contributions to metabolism, followed by the Phase I component of a Phase I/IIa randomised, double-blind, placebo-controlled, parallel-group dose‑escalation trial (NCT04673383) in which escalating single doses of DMT fumarate (administered as a two‑phase 10‑min IV infusion) were evaluated for safety, tolerability and PK to inform later clinical development and infusion regimen design.
The preclinical work comprised a suite of validated in vitro assays using LC-MS/MS to inform metabolism and physiochemical properties. Human hepatocytes from ten donors were incubated with DMT fumarate at nominal concentrations (1–5 µM) with and without MAO‑A (clorgyline) and MAO‑B (deprenyl/selegiline) inhibitors; timepoints up to 60 min were sampled to estimate intrinsic clearance and half‑life. Human liver mitochondrial fractions (5‑donor pool) were assayed similarly to probe MAO activity specifically. CYP phenotyping used recombinant human CYP bactosomes for eight major isozymes with NADPH‑dependent incubations and time‑course sampling to derive isozyme-specific intrinsic clearance and half‑life estimates. Separate in vitro assays measured blood:plasma partitioning, plasma protein binding by rapid equilibrium dialysis, and lipophilicity (logD7.4) in octanol/buffer systems. Analytical methods and calibration ranges for DMT and IAA were reported for LC‑MS/MS instruments. The clinical study was a single‑centre, randomised, double‑blind, placebo‑controlled, parallel single ascending dose (SAD) design conducted under EMA and GCP standards. Eligible participants were aged ≥25 years, psychedelic‑naïve, BMI 18.0–30.9 kg/m2, medically and psychiatrically screened to exclude current or past DSM‑5 mental health disorders or family history of psychotic/bipolar disorder; the extraction does not report ethnic composition. The investigational product was a GMP‑manufactured fumarate salt of DMT (SPL026) formulated at 2.5 mg/ml free base; placebo matched excipients. Four sequential dose cohorts were planned, each randomised so six subjects received active and two received placebo, with sentinel dosing (1 active, 1 placebo) before dosing the remainder. Escalation depended on review of safety, tolerability and PK from prior cohorts. Study drug was delivered as a continuous 10‑min IV infusion split into two 5‑min phases via a single cannula with two syringe pumps: phase 1 (gentle rise to the fringe of psychedelic experience) and phase 2 (raise/maintain peak exposure). Dosing regimens were modelled from prior bolus IV data using a one‑compartment model fitted by iteratively reweighted non‑linear least squares; compartmental simulations were used to select four final infusion regimens intended to produce ascending peak exposures, including a target intended to elicit a 'breakthrough' experience. Pharmacokinetic blood sampling was intensive pre‑dose and up to 240 min post‑start of infusion with validated bioanalysis for DMT (calibration range down to 0.0619 ng/ml) and IAA. Noncompartmental PK parameters were calculated for evaluable subjects; dose proportionality of Cmax and AUClast was assessed with a power model fitted by REML mixed effects, and post‑hoc hierarchical regression assessed relationships of BMI and weight with dose‑normalised exposure. Missing concentrations below LLOQ were treated as zero if before Tmax or as missing otherwise; no imputation was performed.
In vitro experiments indicated different clearance behaviours across systems. In plated human hepatocytes (0.62 µM DMT), intrinsic clearance was 19.4 ± 0.8 µl/min/million cells with a half‑life of 98.9 ± 3.9 min. MAO inhibition in hepatocytes produced minimal change in intrinsic clearance at the tested concentrations. In contrast, human liver mitochondrial fractions showed high intrinsic clearance (175 µl/min/mg protein at 0.62 µM, half‑life 7.9 min) and a concentration‑dependent effect: at 3.1 µM, MAO‑A inhibition reduced intrinsic clearance by >90% and prolonged half‑life markedly, while MAO‑B inhibition had little effect. CYP phenotyping identified substantial intrinsic clearance via CYP2D6 (801 µl/min/nmol CYP, half‑life ~9 min) and a minor contribution from CYP2C19 (37 µl/min/nmol CYP, half‑life ~189 min); no appreciable turnover was detected for CYP1A2, 2B6, 2C8, 2C9, 3A4 or 3A5. Physicochemical assays returned mean logD7.4 = 0.15 (low lipophilicity), plasma unbound fraction ≈ 67.7% (i.e. most DMT unbound), and a blood:plasma ratio of 1.53 indicating notable partitioning into blood cells. Thirty‑two subjects were enrolled in the Phase I study (mean age 36.4 years, range 25–76; mean BMI 25.0 kg/m2; eight female, 25%). All subjects completed dosing; 13 subjects experienced drug‑related treatment‑emergent adverse events (drTEAEs), all categorised as mild or moderate and transient; no serious adverse events were recorded. Pharmacokinetic analyses excluded two subjects due to dosing errors and encountered missing samples in some cohorts (notably cohort 3), limiting parameter derivation for a small number of individuals. Across cohorts DMT was rapidly absorbed and eliminated. Median Tmax was approximately 10 min (near end of the 10‑min infusion). Cohort results reported were: cohort 1 (9 mg total, n=5 evaluable) mean Cmax 20.8 ng/ml (range 5.0–34.9), mean AUClast 349 ng·min/ml (range 71–705), mean t1/2 12.1 min (range 5.8–18.3); cohort 2 (12 mg, n=6) mean Cmax 30.6 ng/ml (range 12.7–62.3), AUClast 451 ng·min/ml (range 245–755), mean t1/2 9.5 min (range 6.0–17.0); cohort 3 (17 mg) sampling issues meant only Cmax (mean 72.1 ng/ml, range 16.2–126.0) and AUClast (mean 842 ng·min/ml) could be reported; cohort 4 (21.5 mg, n=6) mean Cmax 62.7 ng/ml (range approximately 29–107 reported) and AUClast 835 ng·min/ml (range 477–1052), mean t1/2 12.1 min (range 6.3–20.3). Individual concentrations at 5 min after a 6 mg administration (C5min) ranged from 3.32 to 43.0 ng/ml across cohorts and there were no significant differences between cohorts by one‑way ANOVA (F(3,20)=1.628, p=0.214). Exploratory IAA measures in eight subjects (cohorts 2 and 4) showed high baseline IAA (mean pre‑dose 316 ng/ml) and mean maximal plasma IAA concentrations of 1532.5 ng/ml (cohort 2) and 2182.5 ng/ml (cohort 4), recorded between 30–60 min after infusion start. Peak IAA concentrations exceeded DMT Cmax by roughly 30–100‑fold in the sampled subjects and IAA had not returned to baseline by 240 min in these cases. Dose proportionality assessment using a power model yielded slope (β) estimates for Cmax and AUClast of 1.58 (90% CI 0.84–2.33) and 1.35 (90% CI 0.65–2.04), respectively; sensitivity analysis excluding cohort 3 produced β estimates of 1.47 (0.74–2.20) for Cmax and 1.29 (0.59–2.00) for AUClast. As the 90% CIs encompassed 1.0, the authors report these findings as consistent with dose proportionality but caution that wide CIs and inter‑individual variability temper that conclusion. Post‑hoc hierarchical regression found no significant relationships between BMI or weight and dose‑normalised Cmax (BMI β=0.179, p=0.508; weight β=0.107, p=0.671) or C5min (BMI β=‑0.490, p=0.078; weight β=‑0.215, p=0.426) when controlling for age, sex and dose cohort.
Good and colleagues interpret the combined in vitro and clinical data as reinforcing a picture in which DMT is rapidly distributed and cleared in humans, with MAO‑A playing the primary role in systemic metabolism and CYP2D6 (and to a lesser extent CYP2C19) contributing under conditions where MAO‑A activity is limited. The contrasted behaviour between hepatocyte and mitochondrial fractions led the investigators to conclude that mitochondrial MAO‑A accounts for the high clearance seen in mitochondrial preparations and that MAO‑independent routes (CYPs) can nevertheless contribute to DMT breakdown in some physiological contexts. Low lipophilicity (logD7.4 ≈ 0.15) and a high unbound plasma fraction (>65%) corroborate the rapid availability of DMT for distribution and metabolism, while a blood:plasma ratio >1 suggests erythrocyte partitioning that should be considered in PK interpretation. Clinically, the infusion regimens produced rapid attainment of peak plasma levels near the end of the 10‑min infusion and a short terminal half‑life in the order of 9–12 min across doses. All regimens were tolerated without serious safety signals. The authors note substantial inter‑individual variability in Cmax and AUClast, consistent with prior reports, and propose that rapid clearance and sampling timing may amplify apparent differences at Tmax. Post‑hoc analyses did not identify BMI or weight as predictors of peak exposure, supporting the practicality of fixed infusion dosing rather than weight‑based dosing in this context. On metabolism, exploratory IAA data showed much higher plasma IAA concentrations than DMT and rapid increases in IAA after dosing, concordant with rapid oxidative deamination; however, the authors caution that high baseline and early fluctuations in IAA complicate interpretation. They also highlight that estimated blood clearance for the highest cohort substantially exceeded typical liver blood flow, suggesting extrahepatic clearance sites for IV DMT and a dominant role for MAO‑A expressed outside the liver. Important limitations acknowledged include missing PK samples in some cohorts, small cohort sizes typical of Phase I SAD studies, high inter‑individual variability, and limited IAA characterisation (sparse sampling, baseline fluctuations and the need for a more sensitive assay). The paper calls for larger studies and population PK/PK‑PD modelling, plus longer and more sensitive monitoring of IAA, to better define sources of variability and the full DMT‑IAA relationship. The authors suggest these data can inform design of IV infusion regimens for therapeutic development while clarifying metabolic pathways relevant to oral bioavailability and potential drug interactions.
This study provides a detailed characterisation of DMT pharmacokinetics following a slow 10‑min IV infusion in healthy adults, showing rapid attainment of peak plasma concentrations and rapid clearance largely mediated by MAO‑A. In vitro data identify CYP2D6 and CYP2C19 as potential contributors to DMT metabolism in MAO‑A‑sparse environments. The findings are presented as a basis for improved PK and metabolic models of DMT and to guide the design of IV infusion regimens for clinical development in mental health indications.
The pharmacokinetic concentration population comprised subjects who received at least one dose of study treatment and for whom a blood sample had been analysed. The pharmacokinetic parameter population comprised subjects in the pharmacokinetic concentration population for whom pharmacokinetic parameters could be derived. Actual sampling times were used to derive pharmacokinetic parameters and missing data were not imputed. Plasma concentrations of DMT below the LLOQ of the LC-MS/MS were either treated as zero (if they occurred before T max ) or considered missing. Plasma concentrations and pharmacokinetic parameters were summarised by treatment, using descriptive statistics. For log-transformed parameters, the primary measure of central tendency was the geometric mean, and for other parameters, it was the arithmetic mean or median. Dose proportional relationship between C max and AUC last dose were assessed using the power model(log pharmacokinetic parameter = α + β × log(dose) + ε), where α = intercept and β = slope. The power model was fitted by restricted maximum likelihood (REML) mixed effect model, with intercept and log(dose) as fixed effects. The dose proportionality of each PK parameter was confirmed if the 90% confidence interval (CI) of β (log pharmacokinetic parameter vs. log dose) included the value 1.0. The relationship between BMI and body weight vs. dosenormalised C max and concentration at 5 min (C 5min ) was determined by separate hierarchical regression analyses; age and sex were included as control variables. These analyses were conducted post hoc to investigate the relationship of BMI and body weight regarding pharmacokinetic variability and to confirm that fixed dosing (rather than weight-based dosing) of DMT was appropriate. Pharmacokinetic analysis was conducted by the Statistics and Data Management Department at HMR, using WinNonlin version 8.1 or higher. Descriptive statistics were derived using SAS version 9.4 or higher, including mean, standard deviation (SD), median, minimum and maximum values. Additionally, for pharmacokinetic variables percent coefficient of variation (%CV) and 95% CI of the arithmetic mean were derived. The adjusted coefficient of determination (R 2 ) measured the goodness of fit for the linear regression model (where values range from 0-1, 0 indicating that the predictor variable accounts for no variation in the dependent variable and 1 predictor variable accounts for all variation in dependent variable values). Post-hoc analyses were performed using IBM SPSS version 28.0 and tested at the p < 0.05 significance level.
DMT is a short-acting psychedelic tryptamine which is currently being developed, with supportive therapy, as a treatment for MDD. While data have previously been published on the metabolism and pharmacokinetics of DMT, data have been limited to a few pharmacokinetic parameterson studies of ayahuascaand in animals. The in vitro and in vivo data presented in this paper aim to strengthen the current understanding of DMT pharmacokinetics and metabolism, which can be used to inform future dose selection in healthy adults and patients with MDD. DMT metabolism is substantially slowed when administered with MAO inhibitors and is a known substrate for MAO-A. One study found DMT preferentially binds to MAO-B, and CYP enzymes have been suggested to play a role in DMT metabolismalthough supporting experimental data have not been published. The in vitro studies reported here demonstrate a role for MAO-A, CYP2D6 and, in part, CYP2C19 in the metabolism of DMT. Intrinsic clearance was relatively low in whole cell hepatocytes compared to mitochondrial fractions attributed to a greater proportion of MAO enzymes present in mitochondria, demonstrated by the slower clearance rate of MAO substrate controls (benzylamine and serotonin) in hepatocyte vs. mitochondrial fractions (Table). DMT clearance rate was not concentration-dependent and surprisingly was not affected by MAO inhibition in hepatocytes (Table). These results suggest that a MAO-independent route of metabolism (e.g., via CYP enzymes) can contribute to DMT breakdown at a slower rate in certain physiological environments. This hypothesis is supported by CYP phenotyping results which demonstrated a role for CYP2D6 and, to a lesser extent, CYP2C19 in the clearance of DMT. Analogously, CYP2D6 and CYP2C19 isoforms were also shown to contribute to the O-demethylation of a similar family of psychoactive N,N-dialkylated tryptaminesindicating that CYP enzymes may contribute to the demethylation of DMT and subsequent formation of N-methyltryptamine metabolite. In contrast, in the mitochondrial fractions DMT clearance rate was high and concentration dependent indicating a saturation of metabolism at the 3.1 µM concentration level which was further slowed by MAO-A inhibition, but not MAO-B inhibition (Table). To improve interpretation of pharmacokinetic and metabolism data, specific physiochemical properties were determined for DMT. The preclinical data in this paper confirm that DMT is a lipophobic molecule (logD 7.4 = 0.15) which remains largely unbound in human plasma (> 65%, Table), indicating a high proportion of drug available for distribution and metabolism, consistent with the very rapid clinical pharmacokinetic and clearance results (Table). The high) indicates that DMT is likely distributed into erythrocytes and therefore should be considered when evaluating blood and plasma pharmacokinetics. Cohort 4 (21.5 mg IV) plasma clearance was 27.9 l/min, which equates to an estimated blood clearance rate of 18.2 l/min when divided by the 1.53 blood:plasma ratio factor. This value far exceeds average liver blood flow (approximately 1.45 l/min, based on a 70-kg man), indicating that IV-administered DMT is largely cleared before reaching the human liver. CYP enzymes are mainly expressed in the liver whereas MAO enzymes are found in many tissues including the lung, brain, heart, gastrointestinal tract and liver. Therefore, while DMT is a substrate for CYP2D6 and CYP2C19 in vitro, these enzymes are unlikely to play a significant role in DMT metabolism following IV administration in humans; however, they may contribute to its poor oral bioavailability. We predict that DMT is primarily metabolised by MAO-A expressed throughout the body. The general clinical pharmacokinetic profiles obtained from administration of different doses of DMT were similar to those obtained in previous studies, demonstrating a very short plasma half-life of 10-12 min. Median T max (10-12 min) was notably different from other studies because of the longer IV infusion regimen in this study. Administration of each infusion regimen was well tolerated and there were no safety concerns: only 1 drTEAE was recorded in placebo and cohort 4 groups (Table). There was an overall statistical trend of dose-proportional increases in C max and AUC last for doses of DMT between 9 mg and 21.5 mg; however, these results should be interpreted with caution given the high level of inter-individual variability in C max and AUC last across all dosing cohorts (Table). The variability of DMT pharmacokinetics observed in this study is in broad agreement with previously published data. In the study conducted by Strassman and Qualls, reported C max for ten subjects ranged from 32 to 204 ng/ml following an IV bolus of 0.4 mg/kg DMT. It is possible that the variability may be explained, at least in part, by the rapid clearance rate causing small deviations in pharmacokinetic sampling time points to contribute to concentration differences. The most notable variability in DMT concentrations was around T max , which could be explained by first-order reaction principles, i.e., clearance rate is proportional to drug concentration. A number of post-hoc analyses explored potential sources of pharmacokinetic variability; however, no significant predictors were detected. Weight-based dosing is commonly used in pharmacological research as body weight and BMI have been shown to influence drug distribution and metabolism. Based on this, many studies using DMT and other psychedelics have applied a weight-adjusted approach to dosing with the aim of reducing subjective psychedelic response variability. However, fixed dosing of DMT, particularly when given as an IV infusion, is preferable in terms of practicality and clinical feasibility. Within this study, BMI and weight were not shown to be predictive of peak DMT exposure, measured via dose-normalised C max and C 5min parameters, demonstrating the appropriateness of fixed infusion doses of DMT. These findings support previous analyses showing no association between the subjective effects of psilocybin and weight or BMI. The preclinical and clinical data reviewed thus far suggest that, following IV administration, DMT is rapidly distributed and is primarily metabolised by MAO-A in the circulatory system and/or brain. To further explore the metabolism of DMT, additional exploratory analyses were performed to estimate potential differences in DMT metabolism through determination of IAA concentrations in a total of eight subjects from cohort 2 (12 mg) and cohort 4 (21.5 mg). Plasma IAA concentrations were substantially larger than DMT; a similar result has recently been reported following IV bolus dosing. This counterintuitive finding may be explained by DMT's rapid clearance rate and/or larger volume of distribution, relative to IAA. The high baseline and oscillating IAA concentrations within the first 7 min of pharmacokinetic sampling obscure interpretation relative to DMT breakdown. Nevertheless, by 13 min IAA levels were doubled compared to baseline for all eight analysed subjects, confirming the rapid degradation of DMT in plasma. IAA to DMT C max ratio appeared to be higher in cohort 2 (12 mg) compared to cohort 4 (21.5 mg), which supports a theory of potential saturation of metabolism, consistent with in vitro mitochondrial fraction data described above. However, dose-normalised C max and AUC last of DMT did not increase with dose (calculated from Table) and, when excluding cohort 3 (17 mg) results, were relatively consistent across cohorts 1 (9 mg), 2 (12 mg) and 4 (21.5 mg), which contradicts results expected from a system with saturated metabolism. Additionally, baseline IAA concentration and DMT C max did not correlate with maximum IAA concentration in cohort 2 or cohort 4 upon visual inspection of data (data not shown) indicating that the rate of oxidative deamination may contribute to, but is unlikely to account for, the variability in DMT pharmacokinetics. However, small sample sizes, high variability and lack of appropriate IAA AUC calculations mean that these interpretations should be treated with caution. To provide a more reliable analysis of the DMT-IAA relationship, future clinical studies should monitor the pharmacokinetic profile IAA metabolite over a longer duration and in a larger population size to determine the complete pharmacokinetic profile of IAA. In addition, efforts should be made to validate a more sensitive bioanalytical method for IAA detection prior to future studies. There were several other limitations in the clinical study that may impact the results presented here. First, missing samples from cohort 1 and 3 prevented the calculation of pharmacokinetic parameters for all subjects in these cohorts. While the sample sizes were determined in accordance with a standard phase 1 study, a larger sample size would be beneficial to better understand the variability of DMT pharmacokinetics. Population models investigating the pharmacokinetic-pharmacodynamic effects of DMT have been developed,however, have not performed covariate analysis to shed light on the driving factors leading to the rapid clearance, distribution and variability in the pharmacokinetic profile of DMT. The development of such population models would be of interest to investigate the potential within subject variability in pharmacokinetic and pharmacodynamic effects of DMT.
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Carhart-Harris, R. L., Giribaldi, B., Watts, R. et al. · New England Journal of Medicine (2021)
Sanches, R. F., Osório, F. L., Dos Santos, R. G. et al. · Journal of Clinical Psychopharmacology (2016)
Palhano-Fontes, F., Barreto, D., Onias, H. et al. · Psychological Medicine (2018)
Carhart-Harris, R. L., Muthukumaraswamy, S., Roseman, L. et al. · PNAS (2016)
Schenberg, E. E., Alexandre, J. F. M., Filev, R. et al. · PLOS ONE (2015)
Callaway, J. C., Mckenna, D. J., Grob, C. S. et al. · Journal of Ethnopharmacology (1999)
Riba, J., Valle, M., Urbano, G. et al. · Journal of Pharmacology and Experimental Therapeutics (2003)
Strassman, R. J., Qualls, C .R. · JAMA Psychiatry (1994)
Timmermann, C., Roseman, L., Schartner, M. et al. · Scientific Reports (2019)
Johnson, M. W., Richards, W. A., Griffiths, R. R. · Journal of Psychopharmacology (2008)
Timmermann, C., Roseman, L., Williams, L. et al. · Frontiers in Psychology (2018)
D’Souza, D. C., Syed, S. A., Safi-Aghdam, H. et al. · Neuropsychopharmacology (2022)
Gouzoulis-Mayfrank, E., Heekeren, K., Neukirch, A. et al. · Pharmacopsychiatry (2005)
Garcia-Romeu, A., Barrett, F. S., Carbonaro, T. M. et al. · Journal of Psychopharmacology (2021)
Studerus, E., Kometer, M., Hasler, F. et al. · Journal of Psychopharmacology (2010)
Giribaldi, B., Lyons, T., Rosas, F. E. et al. · Journal of Psychopharmacology (2022)
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