2026 Conference Insights: ASCP

From psychopharmacology to sleep science to schizophrenia research, a look at what shaped the conversation at 3 major meetings this year.

ASCP

The 2026 American Society of Clinical Psychopharmacology (ASCP) Annual Meeting, held May 26–29, 2026, in Miami Beach, Florida, brought together researchers and clinicians at the forefront of psychiatric pharmacology. Sessions spanned safety questions around established treatments, early data on investigational agents, and a growing push to ground psychiatric care in biological markers. Throughout the conference, it became clear the field is actively moving from reactive treatments to a more predictive, precision-oriented model.

Ketamine Safety: What Psychiatrists Need to Know About Monitoring, Neurotoxicity, and Clinical Guardrails

Heidi Anne Duerr, MPH

With ketamine use expanding across psychiatric practice, a panel of experts shared suggested safety guardrails for clinicians attempting to keep pace with adoption. Benjamin Brody, MD, service chief for acute care services at Westchester Behavioral Health in White Plains and the inpatient psychiatric service at Weill Cornell Medical Center in Manhattan, New York, co-organized a session following high-profile ketamine-associated deaths that sharpened public and clinical scrutiny of the treatment. The discussion drew on recently published work examining both best monitoring practices and evidence for potential neurotoxic effects at higher or more frequent doses.^1,2

Although some of the recommendations were new, many were leveraged from the American Psychiatric Association’s 2017 consensus statement.³ Key among them are monitoring vital signs and conducting in-person observation for dissociative experiences that may become clinically problematic rather than therapeutic.

Beyond acute monitoring, the discussed emerging concerns surrounding potential neurotoxic effects associated with ketamine exposure. Current evidence suggests that ketamine’s neurological effects may depend heavily on dose and treatment frequency, Brody told Psychiatric Times.

“At low doses, with appropriate intervals between administration, ketamine probably has neurotrophic effects,” he explained. “However, if it’s dosed at higher doses and without appropriate intervals between dosing—or if it’s dosed too frequently—at some point it becomes neurotoxic.”

The conversation reflected a growing recognition that ketamine treatment should not be viewed simply as a binary question of efficacy vs inefficacy, but rather as a nuanced intervention that requires thoughtful attention to dosing schedules, cumulative exposure, and long-term outcomes.

Ultimately, Brody’s session was to provide psychiatrists with practical, evidence-informed guidance that reflects both the promise and the limitations of ketamine treatment in 2026. To do so, the panel included experts with complementary perspectives on safety, neurobiology, clinical implementation, and special populations, with Cristina Cusin, MD, of Massachusetts General Hospital and Harvard Medical School serving as discussant.

“It’s a rapidly changing and expanding environment, and we want clinicians, researchers, and the general community to have a good sense of how do we use this intervention safely, effectively, with appropriate guardrails,” Brody said.

References
1. Brody BD, Popeo DM, Smetana RW, Kanellopoulos D. How do we get ketamine safety right? three questions from a clinical service. J Clin Psychiatry. 2025;86(3):25com15946.

2. Li SW, Kumpf KT, Urrutia J, et al. Ketamine for depression, but at what cost? a review of ketamine’s neurotoxic effects from preclinical and human studies. Am J Psychiatry. 2025;182(10):903-912.

3. Sanacora G, Frye MA, McDonald W, et al; American Psychiatric Association (APA) Council of Research Task Force on Novel Biomarkers and Treatments. A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA Psychiatry. 2017;74(4):399-405.

BXCL501 At-Home Administration Resulted in Agitation Reduction in Bipolar and Schizophrenic

Jessica Walters

A new analysis from the SERENITY at-home phase 3 trial presented at the meeting demonstrated that BXCL501 (sublingual dexmedetomidine) meaningfully reduced agitation associated with bipolar disorder and schizophrenia when self-administered at home, with the most pronounced effect in severe episodes. Efficacy was observed across all severity levels (mild, moderate, and severe), and benefits persisted with repeated dosing regardless of baseline agitation severity.¹

The randomized, double-blind, placebo-controlled trial enrolled 246 patients over 12 weeks and collected data from more than 2600 agitation episodes. Over 80% of patients completed the full trial, with no discontinuations due to tolerability and no drug-related serious adverse events.²

“These new analyses from the SERENITY at-home phase 3 trial further strengthen the growing body of evidence supporting BXCL501 as a potential treatment option for acute agitation associated with bipolar disorders or schizophrenia in the at-home setting,” said Dusan Kostic, PhD, senior vice president of clinical and medical affairs at BioXcel Therapeutics.¹ “If approved, BXCL501 could become the first FDA-approved treatment for acute agitation in the at-home setting, significantly impacting the lives of patients,” Kostic highlighted in a news release.

BXCL501 is already approved as Igalmi for agitation in supervised medical settings; the new data support potential expansion to the home setting. BioXcel Therapeutics submitted a supplemental new drug application to the FDA in April 2026, with a Prescription Drug User Fee Act action date of November 14, 2026.¹

References
1. BioXcel Therapeutics presents new data from SERENITY at-home phase 3 trial for agitation associated with bipolar disorders or schizophrenia at 2026 ASCP Annual Meeting. News release. BioXcel Therapeutics. May 28, 2026. Accessed June 15, 2026. https://www.globenewswire.com/news-release/2026/05/28/3302675/0/en/bioxcel-therapeutics-presents-new-data-from-serenity-at-home-phase-3-trial-for-agitation-associated-with-bipolar-disorders-or-schizophrenia-at-2026-ascp-annual-meeting.html

2. BioXcel Therapeutics announces SERENITY at-home pivotal phase 3 safety trial met its primary endpoint in support of sNDA submission for label expansion of Igalmi. News release. BioXcel Therapeutics. August 27, 2025. Accessed June 15, 2026. https://ir.bioxceltherapeutics.com/news-releases/news-release-details/bioxcel-therapeutics-announces-serenity-home-pivotal-phase-3

Next-Generation Pharmacotherapies Emerge for Mood and Anxiety Disorders

Leah Kuntz

Positive phase 3 results from Compass Pathways’ COMP005 and COMP006 psilocybin trials headline a rapidly expanding pipeline for treatment-resistant mood and anxiety disorders, according to a poster presented at the meeting.¹ The poster surveyed emerging pharmacotherapies across 4 categories (psychedelics, glutamatergic and GABA modulators, ion channel modulators, and novel mechanisms), framing the breadth of development activity against a clinical reality that roughly 30% of patients with mood and anxiety disorders remain unresponsive to available treatments.

In the glutamatergic and GABA modulator category, results were mixed, Alana King, a research fellow at Yale’s Depression Research Program and poster presenter, told Psychiatric Times. Neurocrine reported a positive phase 2 trial for osavampator, an AMPA receptor–positive allosteric modulator, and has since advanced to 4 ongoing phase 3 trials.² Boehringer Ingelheim, by contrast, announced negative results from its NR2B subunit trial, a reminder of the mechanistic complexity in this space. Although the ion channel modulator category was small, King noted Xenon Pharmaceuticals had azetukalner, a novel Kv7 potassium channel opener, in phase 3 trials for MDD.

The novel and emerging mechanisms category was an interesting mix, she noted, and included compounds such as a Sestrin2 modulator (NV-5138) and TAAR1 agonists (eg, ulotaront). Another novel mechanism includes Vistagen’s fasedienol, which is being studied as a nasal spray for social anxiety disorder.

King noted persistent challenges across the landscape, including functional unblinding in psychedelic trials and questions about the generalizability of trial populations to real-world clinical settings. She described the poster as a snapshot of the current clinical moment defined by broadening mechanisms, several anticipated FDA decisions, and a field still working out which of these diverse approaches will translate into durable, accessible treatments for patients.

“It shows that the landscape really is broadening, and it was interesting to see how diverse the mechanisms were,” King concluded.

References

1. Kuntz L, Goodwin G. Phase 3 program investigating COMP360 psilocybin for treatment-resistant depression: breaking poster data from the 2026 ASCP Annual Meeting. Psychiatric Times. May 28, 2026. https://www.psychiatrictimes.com/view/phase-3-program-investigating-comp360-psilocybin-for-treatment-resistant-depression-breaking-poster-data-from-the-2026-ascp-annual-meeting

2. Singh JB, Ge T, Ionescu A, et al. Osavampator (NBI-1065845/TAK-653) demonstrates statistically significant and clinically meaningful improvements in depression severity and is well tolerated in adults with major depressive disorder: phase 2 SAVITRI results. Presented at: 2025 Psych Congress, September 17-21, 2025; San Diego, CA.

Could Brain Insulin Signaling Predict Depression Outcomes? Pilot MRI Study Points to a Potential Biomarker

Leah Kuntz

A small but provocative neuroimaging pilot study (N = 12) found that impaired brain insulin signaling may predict worsening depression severity in adolescents, adding to growing evidence that metabolic dysfunction and psychiatric illness may be more biologically intertwined than traditionally appreciated.¹

Kateryna Maksyutynska, PhD, a postdoctoral research fellow at the Centre for Addiction and Mental Health, and colleagues assessed insulin action in the brains of adolescents aged 14 to 18 years with depression via MRI, along with assessing depression severity, and then reassessed 6 months later.

“What we found was that individuals who had maybe more impaired, or our take on impaired, insulin action in the brain predicted worse illness severity 6 months after,” Maksyutynska told Psychiatric Times. “They actually had increased depression severity score at that follow-up assessment.”

Although preliminary, the findings raise the possibility that disrupted brain insulin signaling could serve as a predictive biomarker for depression trajectory. According to Maksyutynska, the team has since secured funding for a larger follow-up study to determine whether the signal can be replicated in a broader cohort.

“We know insulin action in the brain is related to a lot of processes that have been seen to be disrupted in depression,” she explained. “So things like regulating mood, cognitive function, metabolic function. That’s why we want to dig into it a little bit further in this project.”

For practicing psychiatrists, the work reinforces increasing calls to integrate metabolic assessment more routinely into psychiatric care. Rather than viewing psychiatric illness and metabolic dysfunction as isolated domains, Maksyutynska suggested clinicians may need to adopt a more unified framework.

“The fact that these 2 disorders, metabolic dysfunction specifically and depressive disorders, are so interlinked, it’s really difficult to look at them separately,” she said. “We have to kind of take a very holistic approach to it and move away from the more siloed health care systems.”

She added that metabolic screening may provide clinically relevant information beyond physical health monitoring alone.

“I think looking at a metabolic panel for individuals with psychiatric disorders is very important,” Maksyutynska told Psychiatric Times. “There’s been a lot of research looking at whether higher rates of metabolic dysfunction can predict worse clinical performance or worse illness severity.”

Reference
1. Maksyutynska K, Stogios N, Korran V, et al. Is brain insulin action implicated in the biology of depression? a pilot neuroimaging study in adolescents. Presented at: 2026 American Society of Clinical Psychopharmacology Annual Meeting; May 26-29, 2026; Miami, FL.

Phase 2b/3 Trial Evaluates Forvisirvat in Major Depressive Disorder

Heidi Anne Duerr, MPH

A large phase 2b/3 trial of Forvisirvat (SP-624), an oral first-in-class sirtuin 6 (SIRT6) activator, is nearing completion in major depressive disorder (MDD), according to Joel Raskin, MD, chief medical officer of Arrivo BioVentures.¹

He presented data from the trial comparing 20 mg once-daily Forvisirvat with placebo over 4 weeks, followed by a 2-week blinded off-drug phase to assess whether effects persist. “We’re doing that because we saw in our previous study and in animal models that a single dose can actually have long-term effects, probably through the epigenetic mechanism of action,” he said. This strategy allows the investigators to further explore that phenomenon.

The trial’s primary outcome measure is the Montgomery-Åsberg Depression Rating Scale in female patients, a strategy driven by a post hoc finding from the preceding phase 2 study. “We found that [the treatment in women] had a very dramatic effect, a very statistically significant effect on the Montgomery-Åsberg scale at week 3, but was already separating toward week 2,” he told Psychiatric Times. “It maintained that effect for the off-drug 1-week phase at that time, whereas placebo started returning to baseline like we would expect,” he said. In addition, 5 of the 6 outcome measures were statistically significant in women.

“The question became, as we looked at it, was the female effect a true effect?” Raskin said. “And we think so based on that widening separation over time, a low placebo response in the [women], and that maintenance of effect on the blinded phase.”

Raskin said the research team subsequently began reviewing literature on biologic sex differences in depression and treatment response. “We know that men and women are different,” he said. “However, in all research, they’re lumped together.”

Raskin said their current hypothesis centers on inflammatory and hormonal differences in depression between women and men.

“We know that women have more of a chronic inflammation pattern to depression than men,” he said, noting that Forvisirvat has demonstrated gene-silencing effects on the NF-κB inflammatory pathway. He also referenced emerging findings on the estrogen effects they have observed.

“The hypothesis that led to our current trial was that [women] will have a preferential benefit to Forvisirvat,” Raskin said. “But we have to confirm that, and we have [men] in the trial as well, and we shall see.”

Reference
1. Raskin J. Forvisirvat (SP-624), a first-in-human SIRT6 activator with an epigenetic mechanism of action, currently in a phase 2b-3 study for the treatment of major depressive disorder. Poster presented at: 2026 American Society of Clinical Psychopharmacology Annual Meeting; May 26-29, 2026; Miami, FL.