Psychedelics and the Brain: The Neuroscience of Psilocybin

Psilocybin, the active ingredient of "magic mushrooms," went from a banned Schedule I substance to the subject of phase 3 clinical trials in about fifty years. The neuroscience behind that turnaround is specific: a single serotonin receptor, a set of brain regions tied to self-focused thought, and a burst of structural change in neurons. This article explains what researchers have measured, what the major trials found, and where the evidence is thin. It is general education, not medical advice, and it does not recommend any substance or treatment.

From mushroom ceremonies to a Swiss laboratory

Indigenous peoples in Mesoamerica used psilocybin-containing mushrooms in healing and religious ceremonies long before Western science took an interest. The outside world learned of the practice in 1955, when the American ethnomycologist R. Gordon Wasson took part in a mushroom ceremony, a velada, led by the Mazatec healer María Sabina in Huautla de Jiménez, Oaxaca. Wasson brought spores back to Paris, and Swiss chemist Albert Hofmann isolated psilocybin in the laboratory in 1958 (Wikipedia: María Sabina). For Sabina the outside attention was costly. Police suspected her of dealing drugs, her community ostracized her, and her house was burned (Wikipedia: María Sabina).

Hofmann had already made his name with a different compound. He first synthesized LSD on November 16, 1938, set it aside, and then accidentally discovered its effects on April 16, 1943. Three days later, on April 19, he deliberately took 250 micrograms, a dose he thought was small but was in fact strong, and the bicycle ride home that followed gave the date its nickname, Bicycle Day (Wikipedia: Albert Hofmann).

Research then grew fast. By the mid-1960s more than 1,000 peer-reviewed clinical papers had been published, covering about 40,000 patients, although many of those trials would not meet current methodological standards (Wikipedia: Psychedelic therapy). Sandoz stopped producing LSD in 1965 under government pressure, and in 1970 the U.S. Controlled Substances Act placed LSD and other psychedelics in Schedule I, the category for drugs with no accepted medical use and a high potential for abuse. Psilocybin and psilocin were listed on October 27, 1970 (Wikipedia: Legality of psilocybin mushrooms). Authorized therapeutic research had been discontinued worldwide by the 1980s, and it restarted in the early 2000s with the help of PET and MRI imaging (Wikipedia: Psychedelic therapy).

By the mid-1960s, researchers had published more than 1,000 clinical papers on psychedelics covering about 40,000 patients. Then funding stopped for roughly three decades.

MDMA has a separate history. Merck first synthesized it in 1912 as an intermediate in making a potential blood-clotting drug, and its psychoactive effects were not described until 1976 by Alexander Shulgin, David Nichols, and colleagues. The DEA placed MDMA in Schedule I in 1986 (Wikipedia: MDMA-assisted psychotherapy). MDMA works differently from psilocybin, as the comparison table below shows, but the two are often discussed together because they share a regulatory history and a therapy-plus-drug treatment model.

How psilocybin works at the receptor level

Psilocybin itself is a prodrug, meaning it has to be converted into the active molecule. The body removes a phosphate group, a step called dephosphorylation, to make psilocin, and psilocin is what acts on the brain. After oral dosing, effects begin in about 30 to 50 minutes on average, peak after roughly one to two hours, and last about four to six hours (Wikipedia: Psilocybin).

Psilocin binds to the 5-HT2A receptor, one of the receptors that serotonin normally activates. The receptor is especially dense on the apical dendrites (the long branching input fibers) of layer V pyramidal cells in the cortex, the large neurons that send signals out of cortical columns. Like all 5-HT2 receptors it couples to a signaling pathway called Gq, which triggers a cascade ending in calcium release inside the cell. Activation of this receptor is described as necessary for the effects of classic psychedelics, a group that includes LSD, psilocin, and mescaline (Wikipedia: 5-HT2A receptor). Ketanserin, a drug that blocks the receptor, has been used as a "trip killer," which is a useful sign that this receptor really does drive the experience (Wikipedia: 5-HT2A receptor).

An analogy helps here. Serotonin is a key that fits many locks across the brain, and the 5-HT2A lock sits in a particularly influential place: the cortical neurons that integrate information from many other regions. Psilocin is a key that fits that lock more tightly than serotonin does, turning it for longer and harder than normal. For more on how chemical messengers and their receptors work in general, see how neurotransmitters work.

Why this differs from an SSRI

Selective serotonin reuptake inhibitors (SSRIs) keep more serotonin available in the synapse by slowing its recycling. They act on the whole serotonin system gradually and are usually taken daily for weeks before benefits show. Psilocin instead directly stimulates a particular receptor subtype, and the key effects of a single session appear within hours. That difference in mechanism is one reason researchers study psilocybin as a separate class of treatment rather than as a faster SSRI.

What brain scans show: the default mode network

In 2012, Robin Carhart-Harris and colleagues at Imperial College London published a PNAS study that scanned healthy volunteers who had been given psilocybin. Using task-free fMRI, they expected to see increased brain activity because the experience is so intense. Instead, they saw only decreases in cerebral blood flow and in the BOLD signal (a measure of blood oxygenation that tracks neural activity), strongest in hub regions such as the thalamus and the anterior and posterior cingulate cortex. Lower activity in the anterior cingulate and medial prefrontal cortex tracked with the intensity of the subjective effects, and the coupling between the medial prefrontal cortex and the posterior cingulate cortex weakened (Europe PMC record: Carhart-Harris et al., PNAS 2012).

The medial prefrontal and posterior cingulate cortices are central nodes of the default mode network (DMN), a large-scale network that also includes the precuneus and the angular gyrus. The DMN is most active when a person is awake but not focused on the outside world, for example while daydreaming. It supports self-referential processing, autobiographical memory, and imagining the future. The term "default mode" was coined by Marcus Raichle in 2001, and the network was mapped with resting-state fMRI in 2003 (Wikipedia: Default mode network). A deeper look at this network is in the default mode network at rest.

Rumination, the repetitive negative self-focused thinking that is a core feature of major depression, has been linked to increased DMN connectivity and dominance at rest (Wikipedia: Default mode network). That link is why the DMN became a candidate explanation for how psilocybin might help. It is still a hypothesis. A brain scan showing reduced DMN activity during the drug experience does not show that the reduction causes later relief from depression. Readers who want the background on depression circuits can start with the neuroscience of depression.

A common oversimplification

Popular accounts say psilocybin "switches off the ego" or "silences the narrator." The measurements support something narrower: reduced activity and weaker coupling in specific hub regions while the drug is active, which correlates with reports of altered self-experience. Calling that an "ego switch" goes beyond the data. Neuroscience still has no agreed account of how brain activity produces the sense of self, which is the territory of the hard problem of consciousness.

The REBUS model: loosening the brain's priors

In 2019 Carhart-Harris and Karl Friston proposed the REBUS model, short for "relaxed beliefs under psychedelics," in the journal Pharmacological Reviews (Carhart-Harris and Friston, 2019, Pharmacological Reviews 71(3): 316-344). It draws on predictive processing, the idea that the brain is a prediction machine that constantly generates expectations about what its senses will report and updates them when they are wrong.

In this framework, high-level predictions, which the authors call priors, normally dominate lower-level sensory input. REBUS proposes that psychedelics weaken those priors by acting on 5-HT2A receptors in the cortical hierarchy, so that sensory and emotional information carries more weight than usual. In people with depression, OCD, or addiction, the argument goes, some priors are rigid and unhelpful, and relaxing them could create an opening for change.

A useful picture is a footpath worn into a field. After years of walking, everyone takes the same line, and the grass on either side never gets stepped on. REBUS says the drug temporarily makes the whole field feel like open ground, so a new route becomes possible. The model is influential, but it is a theory that fits the observations, not a mechanism confirmed in a trial. The authors present it as a unifying framework, and testing it is ongoing work.

Neuroplasticity: spines, synapses, and mice

A second line of research asks whether psychedelics physically change neurons. In 2018 David Olson's laboratory at UC Davis reported in Cell Reports that serotonergic psychedelics, like ketamine, increase neurite growth and the formation of new dendritic spines in cultured cells and living animals, with more synapses and stronger synaptic function. The effects appeared to depend on TrkB, mTOR, and 5-HT2A signaling (Ly et al., 2018, Cell Reports 23(11): 3170-3182). Dendritic spines are the small protrusions on a neuron where it receives synaptic input, so more spines suggest more potential connections. The authors suggested that psychedelics could serve as starting points for developing fast-acting, plasticity-promoting antidepressants.

For psilocybin in particular, Alex Kwan's group at Yale published a 2021 study in Neuron. In mice, a single dose of psilocybin increased the size and density of dendritic spines by about 10% on the apical dendrites of layer 5 pyramidal neurons in the medial frontal cortex. The change appeared within 24 hours and lasted about one month, and the treatment also reduced a stress-related behavioral deficit (Shao et al., 2021, Neuron 109(16): 2535-2544).

These results fit a theory that some depression involves loss of connectivity in prefrontal circuits and that psychedelics could help rebuild it. They remain animal and cell-culture findings, though. A 10% change in spine density in a mouse is not a measurement in a human patient, and the link between spine growth and symptom relief in people has not been demonstrated. For general background on how brains change with experience, see neuroplasticity.

Psychedelic compounds compared

The word "psychedelic" covers drugs with different mechanisms. The table summarizes the main ones discussed in clinical research. It lists the mechanism and the regulatory position as described in the sources cited in this article, and it deliberately leaves out dose and duration figures that vary widely between sources.

Compound	Main mechanism	Regulatory position
Psilocybin (via psilocin)	5-HT2A receptor agonist	U.S. federal Schedule I since 1970; in late-stage trials; approved for prescription in Australia for treatment-resistant depression since July 2023
LSD	5-HT2A receptor agonist	Schedule I since 1970
Mescaline	5-HT2A receptor agonist	Schedule I
DMT (in ayahuasca brews)	5-HT2A receptor agonist	Schedule I
MDMA	Releases serotonin and other monoamines; not a classic 5-HT2A agonist	Schedule I since 1986; FDA declined to approve in August 2024; allowed in Australia since July 2023
Ketamine and esketamine	NMDA receptor blockade	Intranasal esketamine approved by the FDA in 2019 for treatment-resistant depression

Sources: Wikipedia: 5-HT2A receptor, Wikipedia: MDMA-assisted psychotherapy, Wikipedia: Legality of psilocybin mushrooms, Wikipedia: Psychedelic therapy.

Clinical trials: what the evidence shows

The studies below are the ones most often cited. They differ a lot in size and design, so a table helps keep them apart.

Study	Condition	Design and size	Main result	Key limit
COMPASS phase 2b (Goodwin et al., NEJM 2022)	Treatment-resistant depression	Double-blind, 233 adults, 25, 10, or 1 mg	25 mg beat 1 mg on MADRS at week 3 (difference about 6.6 points)	10 mg did not separate from control; durability beyond week 3 less certain
Johns Hopkins (Davis et al., JAMA Psychiatry 2021)	Major depression	Waitlist-controlled, 27 adults	71% response at weeks 1 and 4; 54% remission at week 4	Small; waitlist control, not placebo
Imperial College (Carhart-Harris et al., NEJM 2021)	Major depression	Psilocybin vs escitalopram, 59 adults	No significant difference on the primary scale	Small; secondary outcomes not corrected
Bogenschutz et al., JAMA Psychiatry 2022	Alcohol use disorder	Double-blind, 95 randomized	Heavy drinking days 9.7% vs 23.6%	Two U.S. academic centers; moderate sample
Johnson et al., J Psychopharmacol 2014	Tobacco dependence	Open-label pilot, 15 smokers	12 of 15 abstinent at six months	No control group
Mitchell et al., Nature Medicine 2021 (MDMA)	PTSD	Double-blind phase 3, 90 randomized	67% of completers no longer met PTSD criteria vs 32% with placebo	Functional unblinding; completer analysis

Depression

The largest peer-reviewed psilocybin trial so far is the phase 2b study led by Guy Goodwin and funded by COMPASS Pathways, published in the New England Journal of Medicine in 2022. It enrolled 233 adults with treatment-resistant depression at multiple sites and randomly assigned them to a single dose of 25 mg, 10 mg, or 1 mg of synthetic psilocybin with psychological support. At week 3, depression scores on the MADRS scale fell by 12.0 points with 25 mg, 7.9 with 10 mg, and 5.4 with 1 mg. Only the 25 mg versus 1 mg difference (6.6 points) was statistically significant (Goodwin et al., NEJM 2022).

About 37% of the 25 mg group had responded at week 3. Adverse events occurred in 77% of participants, most often dizziness, headache, and nausea, and suicidal ideation or behavior or self-injury was reported in all dose groups (Pharmacy Times summary of Goodwin et al.). Whether the week 3 advantage lasts is a recurring question in this literature.

The Johns Hopkins trial, published in JAMA Psychiatry in 2021, randomized 27 adults with major depressive disorder to immediate treatment (15 people) or a delayed-treatment waitlist (12 people). Participants received two psilocybin sessions with supportive psychotherapy. About 71% responded at both weeks 1 and 4, and remission was 58% at week 1 and 54% at week 4 (Davis et al., 2021). A follow-up of 24 participants reported response in 75% and remission in 58% at 12 months, though by then the study had no untreated comparison group (Gukasyan et al., 2022, Journal of Psychopharmacology).

The comparison with a standard antidepressant is more sobering. In a 2021 NEJM trial of 59 patients, psilocybin lowered a self-reported depression score (QIDS-SR-16) by 8.0 points and the SSRI escitalopram by 6.0 points. The 2.0-point difference was not statistically significant (95% confidence interval -5.0 to 0.9, P = 0.17). Response and remission rates favored psilocybin (70% vs 48% and 57% vs 28%), but those were secondary outcomes that were not corrected for multiple comparisons (Carhart-Harris et al., NEJM 2021). The authors concluded that larger and longer trials are needed.

The phase 3 picture in 2026

COMPASS Pathways has since reported results from two phase 3 trials of COMP360, its synthetic psilocybin formulation. COMP005 tested a single 25 mg dose against placebo in 258 dosed participants. COMP006 dosed 581 participants across 25 mg (296), 10 mg (142), and 1 mg (143) arms. The company reported that COMP006 met its primary endpoint at week 6, that 39% of the 25 mg arm reached a clinically meaningful reduction (at least 25% on the MADRS) with benefits maintained on average through week 26, and that about 30% of week 6 responders reached remission after retreatment. It also reported serious adverse events over 26 weeks of 5.7% in the 25 mg arm and 6.3% in the 1 mg arm (Compass Pathways press release, July 7, 2026).

Two cautions apply. These are company-reported results, and full phase 3 datasets had not been published in a peer-reviewed journal at the time of the sources reviewed. Regulators also have not yet ruled. The company reports a rolling new drug application with the FDA, with final submission expected in the fourth quarter of 2026, and it anticipates a launch in the first half of 2027 only if the FDA approves and the DEA reschedules psilocybin (Compass Pathways press release). The FDA issued a National Priority Voucher for psilocybin in April 2026 (Wikipedia: Psilocybin). The FDA had earlier granted breakthrough therapy status to psilocybin for treatment-resistant depression and major depressive disorder (Wikipedia: Psychedelic therapy). That designation speeds review but does not predict approval.

Addiction

For alcohol use disorder, a double-blind trial at two U.S. academic centers randomized 95 people (93 analyzed) to psilocybin or the active placebo diphenhydramine, both alongside 12 weeks of psychotherapy. Over 32 weeks, heavy drinking days made up 9.7% of days in the psilocybin group and 23.6% in the control group, a 13.9 percentage point difference (95% confidence interval 3.0 to 24.7, P = .01) (Bogenschutz et al., JAMA Psychiatry 2022).

For smoking, a 2014 pilot study gave 15 nicotine-dependent adults psilocybin as an add-on to a 15-week cessation program. Twelve of the 15 (80%) were abstinent at six months. Because the study was open-label and had no control group, it cannot show that psilocybin caused the result (Johnson et al., 2014). A larger controlled trial is needed, and the 80% figure should not be read as a success rate for the treatment. For background on why addiction is hard to treat, see the psychology of addiction and the dopamine system.

MDMA and PTSD

MDMA acts mainly by releasing serotonin and related neurotransmitters instead of directly stimulating the 5-HT2A receptor, so it is not a classic psychedelic. Its phase 3 trial, published in Nature Medicine in 2021, randomized 90 people with severe PTSD (46 to MDMA and 44 to placebo), each with manualized therapy. At the 18-week primary endpoint, 28 of 42 completers (67%) in the MDMA group no longer met criteria for PTSD, compared with 12 of 37 completers (32%) on placebo, with an effect size of d = 0.91 (Mitchell et al., 2021, via PMC). Those percentages use completers as the denominator, which tends to flatter a treatment.

The FDA's Psychopharmacologic Drugs Advisory Committee met on June 4, 2024. It voted 9 to 2 that the data did not show MDMA was effective for PTSD and 10 to 1 that its benefits did not outweigh its risks, citing selection bias and functional unblinding, because participants could tell whether they had received the drug. On August 9, 2024, the FDA issued a complete response letter asking sponsor Lykos Therapeutics to run another phase 3 trial (BioSpace report). The sources reviewed for this article report no approval since that letter.

Ketamine: the approved comparison

Ketamine acts on a different receptor system (NMDA receptors) and is not a classic psychedelic, but it is the nearest regulatory precedent. The FDA approved intranasal esketamine for treatment-resistant depression in 2019, to be used together with an oral antidepressant (Wikipedia: Psychedelic therapy). The Olson laboratory has argued that ketamine and psychedelics share downstream plasticity pathways, which is why the two are often studied together.

Why psychedelic trials are hard to interpret

Randomized trials depend on blinding, meaning that participants and staff should not know who got the active drug. With a strong psychedelic, almost everyone can tell. This functional unblinding inflates the apparent benefit of the drug, because people who know they got it expect to improve, and expectation alone can change symptom ratings. The Wikipedia summary of the field states that because blinding is so difficult in psychedelic and MDMA-assisted trials, the results are likely overestimated (Wikipedia: Psychedelic therapy). The placebo effect is a real biological and psychological phenomenon, as covered in how placebos change real symptoms.

Several other problems stack on top.

• Bundled treatment. In most trials the drug is given with preparation and integration sessions. It is hard to separate what the compound does from what the therapy does, and the therapy is expensive and difficult to scale.
• Set and setting. The mindset of the participant and the physical environment of the session influence the experience, so results from carefully supervised trials may not transfer to other settings.
• Short follow-up and drift. Many benefits are measured over weeks or months, and the later COMPASS phase 3 program tested repeat dosing and longer follow-up.
• Selection. Trials often exclude people with psychosis risk, unstable medical conditions, and some medications, so the participants differ from the broader population with depression.
• Industry funding. Several of the largest trials are sponsored by companies with a commercial stake in the outcome. That does not invalidate them, but it is a reason to wait for independent replication.

Safety and who is excluded from trials

The safety profile of psilocybin in carefully screened trial participants has been described as acceptable, but "acceptable in a supervised trial" and "safe for the general public" are different claims. In the COMPASS phase 2b trial, 77% of participants reported adverse events, and suicidal ideation or behavior was reported in all arms. Dizziness, headache, and nausea were the most commonly reported events in that trial.

Trial protocols commonly exclude people with a personal or family history of primary psychotic disorders or bipolar I disorder, and the contraindications listed in the Wikipedia overview include SSRI or MAOI use, pregnancy, epilepsy or other seizure disorders, and severe cardiovascular disease (Wikipedia: Psychedelic therapy). The exact interaction between antidepressants and psilocybin is still being studied, and anyone taking psychiatric medication should not change it on the basis of reading about trials. Questions about personal use belong with a licensed clinician.

Legal status

In the United States, psilocybin and psilocin remain Schedule I under federal law. State and local rules vary. Oregon voters approved a ballot initiative on November 3, 2020 that made psilocybin legal for mental health treatment in supervised settings. Colorado passed Proposition 122, the Natural Medicine Health Act, on November 8, 2022, which decriminalized psilocybin and some other substances for adults 21 and over and allowed licensed healing centers. Washington, D.C. passed an initiative in November 2020 that took effect on March 15, 2021, and Seattle's City Council voted for decriminalization in 2021 (Wikipedia: Legality of psilocybin mushrooms).

Decriminalization means that enforcement is deprioritized or penalties are removed locally. It is not the same as FDA approval, and it does not make a product tested or standardized. Internationally, Australia approved prescription psilocybin and MDMA for PTSD and treatment-resistant depression, effective July 1, 2023, when authorized psychiatrists could start prescribing psilocybin (Wikipedia: Legality of psilocybin mushrooms).

Common misconceptions

"Psilocybin permanently rewires the brain." The evidence is for structural changes in mouse neurons that lasted about a month. Human data on lasting structural change are limited, and "rewiring" is a metaphor, not a finding.

"The trials prove it beats antidepressants." The one direct comparison with an SSRI found no significant difference on its primary outcome. Several secondary measures favored psilocybin, but those were not corrected for multiple comparisons.

"Reduced default mode network activity is the cure." The scans show reduced activity during the acute experience. Whether that reduction explains later improvements is untested. Some other drugs and states also change DMN activity.

"It is not addictive, so it must be harmless." Classic psychedelics have a different dependence profile from stimulants and opioids, but they can cause distressing experiences, and people with a vulnerability to psychosis face particular risk. Different risks are not the same as no risks.

"The 80% smoking cessation result shows it works." That figure came from 15 people in an open-label pilot. It is an encouraging signal that justified larger trials, not an efficacy estimate.

Frequently asked questions

Q: What does psilocybin do in the brain? A: The body converts psilocybin to psilocin, which activates 5-HT2A serotonin receptors, especially on layer V pyramidal neurons in the cortex. Brain imaging shows reduced blood flow and activity in hub regions such as the medial prefrontal and posterior cingulate cortices, and weaker coupling between them, while the drug is active.

Q: How long do the effects of psilocybin last? A: After oral dosing, effects begin in about 30 to 50 minutes on average, peak after one to two hours, and last roughly four to six hours. Trial results measure symptom changes over weeks to months, and the duration of those benefits varies between studies and participants.

Q: Is psilocybin approved to treat depression? A: Not by the U.S. FDA as of the latest sources reviewed. Australia has allowed authorized psychiatrists to prescribe it for treatment-resistant depression since July 1, 2023. COMPASS Pathways reported a rolling U.S. application with final submission expected in the fourth quarter of 2026.

Q: How is psilocybin different from an SSRI? A: SSRIs raise the amount of serotonin available in synapses and are taken daily, with benefits usually emerging over weeks. Psilocin directly activates the 5-HT2A receptor, and trials give one or a few supervised sessions. In the only head-to-head trial reported here, the primary outcome did not differ significantly between psilocybin and escitalopram.

Q: Why did the FDA decline to approve MDMA for PTSD? A: An advisory committee voted in June 2024 that the data did not show effectiveness and that benefits did not outweigh risks, citing functional unblinding and selection bias. The FDA's August 9, 2024 letter asked for another phase 3 trial.

Q: What is the REBUS model? A: REBUS stands for relaxed beliefs under psychedelics. Proposed by Robin Carhart-Harris and Karl Friston in 2019, it suggests that psychedelics weaken the high-level predictions the brain uses to interpret experience, making the brain more open to sensory and emotional information. It is a theoretical framework, not a proven mechanism.

Q: Does microdosing work? A: Controlled evidence is weak. A 2021 self-blinding citizen science study in eLife with 191 participants found that psychological outcomes improved in the microdose group, but the placebo group improved too, and no significant differences emerged between them. The authors concluded that the placebo effect may explain the anecdotal benefits (Szigeti et al., eLife 2021).

The takeaway

The neuroscience of psilocybin rests on three observations. Psilocin activates a specific serotonin receptor that is concentrated in cortical neurons. Brain scans show reduced activity in hub regions of the network tied to self-referential thought. And animal work shows that a single dose can increase dendritic spines for about a month. The REBUS model connects these into a story about loosened brain priors, and the story is plausible, but it is still a story.

The clinical evidence is promising and uneven. Phase 2 trials show real separation from low-dose controls, and company-reported phase 3 data point the same way, yet small samples, functional unblinding, bundled therapy, and short follow-up make the size of the benefit hard to pin down. The most useful habit for a reader is to ask of each headline what the control group received, how many people were studied, and who funded the work.

Sources

• Wikipedia: Psilocybin, pharmacology and 2026 regulatory status.
• Wikipedia: Psychedelic therapy, research history, contraindications, blinding.
• Wikipedia: 5-HT2A receptor and Wikipedia: Default mode network.
• Wikipedia: María Sabina and Wikipedia: Albert Hofmann, history.
• Wikipedia: Legality of psilocybin mushrooms and Wikipedia: MDMA-assisted psychotherapy.
• Europe PMC: Carhart-Harris et al., PNAS 2012, psilocybin fMRI study.
• Goodwin et al., NEJM 2022, Carhart-Harris et al., NEJM 2021, and Mitchell et al., Nature Medicine 2021.
• Compass Pathways, July 7, 2026 release and BioSpace on the FDA MDMA decision.

This article is educational and does not provide medical advice. Anyone considering mental health treatment should speak with a licensed clinician.

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