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newest 2026BnH-015B is an oral compound from a Korean company, in a first-in-human trial for Alzheimer's disease. It is described by its sponsor as a positive modulator at the GluN2B site of the NMDA receptor. ⚠️ Nothing about it has ever been published. There is no structure, no CAS number, no chemistry record, no potency measurement, no pharmacokinetic data and no preclinical paper in the public record. This entry exists to say what is and is not known, because the compound appears in drug-pipeline listings in a form that reads like established pharmacology.
- A registered, recruiting first-in-human trial exists, so the programme is real rather than a paper compound
- GluN2B is a well-characterised and reasonable target for cognition
- No safety data exists; the phase 1 is the first human exposure and has not reported
Mechanism
⚠️ What follows is the sponsor's description, not established pharmacology, and no part of it has been published or independently verified.
The registry entry describes a small molecule that targets the GluN2B binding site on receptors and modulates them positively, and states that non-clinical work showed improvement in cognitive decline through effects on and signalling and on microglial IL-33 and osteopontin signalling.
⚠️ No binding, functional or electrophysiological data supporting any of that exists in any accessible source, and there is not even a published molecular structure. The positive-modulator designation is an assertion in a registry text field. An independent survey of the Alzheimer's pipeline classifies it as a symptomatic cognition enhancer rather than a disease-modifying treatment [1], which is a meaningfully more modest description than the sponsor's.
The GluN2B subunit is a reasonable place to aim. It carries a well-characterised modulatory site, it is enriched at extrasynaptic locations where excess activity is thought to be harmful, and both blockers and modulators of it have been pursued for cognitive and mood indications. That makes the stated approach plausible; plausibility is not data.
receptor fingerprint
, GluN2B subunitClaimed positive allosteric modulator
Evidencehow good the literature is
The entire public record is one trial registration and one row in a pipeline review.
The trial is a randomised, double-blind, placebo-controlled single and multiple ascending dose study, taken by mouth, in healthy Korean and Caucasian male volunteers and in patients with moderate Alzheimer's disease, also examining food effect and ethnic differences. It is sponsored by the company and runs at a Seoul hospital.
The only literature mention is an annual review of the Alzheimer's drug pipeline that lists it in a table [1]. ⚠️ That table is compiled from registry entries, so it repeats the sponsor's description rather than testing it, and it is not independent evidence.
⚠️ Searches for primary literature return nothing: no PubMed record under any spelling, no chemistry database entry, and therefore no formula, no structure and no measured property of any kind. Commercial aggregator pages describing it as a first-in-class GluN2B-selective modulator with amyloid clearance and restored cortical plasticity are marketing copy with no published basis.
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
No safety data is available. The phase 1 is the first time this compound has been given to a person, and no results have been posted or published.
Company marketing materials describe a completed phase 1 with a favourable safety profile. ⚠️ The trial registry still lists the study as recruiting, so that claim is not corroborated by the registry, by any publication, or by posted results.
History
The sponsor is a small Korean company founded out of a university physiology department whose published work concerns BDNF and TrkB signalling, silent synapses and long-term potentiation. That lineage is consistent with the stated mechanism, which is worth noting as context, though none of the group's six published papers is about this compound. The phase 1 began in October 2024.
Resources
This entry is here for reference.
Research
1 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Why is there so little here?
Because there is so little anywhere. A search of the medical literature returns no papers about this compound, and chemistry databases have no record of it. What exists is a trial registration and a pipeline table row derived from that registration. This entry records that state honestly rather than dressing a registry field up as pharmacology.
Limitations of the evidence
- Zero primary publications; no paper about this compound exists anywhere
- No structure, CAS number, formula or chemistry database record
- No binding, functional or electrophysiological data supporting the stated mechanism
- The mechanism in circulation comes from a free-text field on the trial registry
- Company claims of a completed phase 1 are not corroborated by the registry, which still lists it as recruiting
Adverse effects
- No safety data exists; the phase 1 is the first human exposure and has not reported