BMB-101

Overview

BMB-101 is a selective serotonin 5-HT2C receptor agonist of the phenylcyclopropylmethylamine (PCPMA) family which is under development for the treatment of absence epilepsy, binge eating disorder, Dravet syndrome, Lennox–Gastaut syndrome, Pitt–Hopkins syndrome, Prader–Willi syndrome, and Rett syndrome. It is taken orally.[1–5] WP

Drug class

Serotonin 5-HT2C receptor agonist WP

From the Wikipedia article's infobox.

Pharmacology

Pharmacodynamics

BMB-101 acts as a highly selective biased agonist of the serotonin 5-HT2C receptor. It has greater that 100-fold selectivity for the serotonin 5-HT2C receptor over other serotonin receptors, including the serotonin 5-HT2A and 5-HT2B receptors. In addition, the drug shows no significant activity at other serotonin receptors. BMB-101 shows functional selectivity at the serotonin 5-HT2C receptor for activation of Gq signaling with minimal β-arrestin recruitment. This in turn appears to minimize receptor desensitization and development of tolerance. Due to its much greater selectivity for the serotonin 5-HT2C receptor, BMB-101 is not expected to possess the psychedelic effects or cardiotoxicity that have been associated with existing drugs like fenfluramine and lorcaserin at therapeutic or supratherapeutic doses. In accordance with its mechanism of action, BMB-101 produces anticonvulsant effects in animals.[1][3–7] WP

The activation of serotonin 5-HT2C receptors has been shown to reduce epileptic seizure activity by inhibiting T-type calcium channels (Caᵥ3). These calcium channels facilitate high frequency burst firing in principal neurons of the subiculum. This firing pattern is upregulated following status epilepticus, with these hyperactive neurons often serving as the initiation point for seizures.[8–11] WP

Research

Research

BMB-101 is under development by Bright Minds Biosciences. As of January 2026, it is in phase 2 clinical trials for the treatment of absence epilepsy, Dravet Syndrome, Lennox–Gastaut syndrome, Pitt–Hopkins syndrome, Prader–Willi syndrome, and Rett syndrome. It is or was also under development for the treatment of binge eating disorder and opioid use disorder, but no recent development has been reported for these indications.[1][2] WP

The drug has been found to increase REM sleep time by 90% (from 56 minutes to 107 minutes) without altering total sleep duration (9.1 hours vs. 8.9 hours) in people with absence seizures in a clinical study.[12] WP

Chemistry

Harm reduction information

No harm reduction data is on file for this compound yet. That means no dose, timing or combination data from PsychonautWiki or TripSit. Please don't guess a dose from similar compounds. If you have taken it and feel unwell, contact emergency services or a poison control center.

User reports

Pop culture

No references added yet.

Sources

1. Journal / agency BMB 101. 23 October 2024
2. Other Delving into the Latest Updates on BMB-101 with Synapse. 29 October 2024
3. Other Vasilkevich A, Duan J, Smith M, McCorvy JD, Pedersen J. BMB-101: A selective 5-HT2C agonist for the treatment of rare epilepsies. May 2024
4. Other Vasilkevich A, Lovera A, Duan J, Smith MA, McCorvy J, Pedersen JT. Selective 5-HT2C Agonists for the Treatment of Rare Epileptic Disorders. October 2024
5. Other Bright Minds Investor Deck. September 2024
6. Other Bright Minds Biosciences Launches Phase 2 Trial of BMB-101 for Epilepsy. 14 September 2024
7. Other Vasilkevich A, Duan J, McDonald I, Sourbron J, Smith M, McCorvy J, Pedersen J. BMB-101 and Biased 5-HT2C Agonism: A Novel Approach for Sustained Epilepsy Management. 7 December 2024
8. Journal / agency Petersen AV, Jensen CS, Crépel V, Falkerslev M, Perrier JF. Serotonin Regulates the Firing of Principal Cells of the Subiculum by Inhibiting a T-type Ca2+ Current. Frontiers in Cellular Neuroscience. 2017. doi:10.3389/fncel.2017.00060 · PMID 28326015 · PMC5339341
9. Journal / agency Menendez de la Prida L, Gal B. Synaptic contributions to focal and widespread spatiotemporal dynamics in the isolated rat subiculum in vitro. The Journal of Neuroscience. June 2004. doi:10.1523/JNEUROSCI.0309-04.2004 · PMID 15201325 · PMC6729319
10. Journal / agency Su H, Sochivko D, Becker A, Chen J, Jiang Y, Yaari Y, Beck H. Upregulation of a T-type Ca2+ channel causes a long-lasting modification of neuronal firing mode after status epilepticus. The Journal of Neuroscience. May 2002. doi:10.1523/JNEUROSCI.22-09-03645.2002 · PMID 11978840 · PMC6758371
11. Journal / agency Cohen I, Navarro V, Clemenceau S, Baulac M, Miles R. On the origin of interictal activity in human temporal lobe epilepsy in vitro. Science. 2002. doi:10.1126/science.1076510 · PMID 12434059
12. Other Meglio, Marco. BMB-101 Heads for Registrational Trials Following Positive Phase 2 Data in Absence Seizures, Developmental Encephalopathies. 16 January 2026

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