pio
its over
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For context, I have a history of absence epilepsy and was reading this study from the January 6, 2026, press release from Bright Minds Biosciences about their Phase 2 BREAKTHROUGH trial for BMB-101, a selective 5-HT2C biased agonist being studied for drug-resistant absence seizures and developmental/encephalopathic epilepsies. The study made me curious as to whether this drug could be used to prolong total time spent in REM sleep even in people without a history if siezures, and reap the benefits.
They enrolled 24 adults in an open-label study. In the absence seizure group, there was a 73.1% median reduction in seizures (p = 0.012). In the DEE group, there was a 63.3% median reduction in major motor seizures. Overall, it was reported as generally well tolerated, with mostly mild to moderate side effects.
What stood out to me was the sleep data. Patients with absence seizures had about a 90% increase in REM sleep, going from roughly 56 minutes at baseline to about 106 minutes on BMB-101, while total sleep time stayed basically the same (around 9 hours). So it didn’t increase total sleep — it shifted sleep architecture toward more REM.
Since REM is tied to memory consolidation, emotional regulation, and cognitive processing, I’m curious what people think about this. Is that REM increase likely specific to the epilepsy population, or could it generalize? And mechanistically, could the selective 5-HT2C Gq bias be driving that shift?
Source: January 6, 2026 GlobeNewswire press release from Bright Minds Biosciences. https://www.globenewswire.com/news-...elopmental-and-encephalopathic-epilepsie.html
They enrolled 24 adults in an open-label study. In the absence seizure group, there was a 73.1% median reduction in seizures (p = 0.012). In the DEE group, there was a 63.3% median reduction in major motor seizures. Overall, it was reported as generally well tolerated, with mostly mild to moderate side effects.
What stood out to me was the sleep data. Patients with absence seizures had about a 90% increase in REM sleep, going from roughly 56 minutes at baseline to about 106 minutes on BMB-101, while total sleep time stayed basically the same (around 9 hours). So it didn’t increase total sleep — it shifted sleep architecture toward more REM.
Since REM is tied to memory consolidation, emotional regulation, and cognitive processing, I’m curious what people think about this. Is that REM increase likely specific to the epilepsy population, or could it generalize? And mechanistically, could the selective 5-HT2C Gq bias be driving that shift?
Source: January 6, 2026 GlobeNewswire press release from Bright Minds Biosciences. https://www.globenewswire.com/news-...elopmental-and-encephalopathic-epilepsie.html
