Brain-protective peptide found in injured rat brain (BINP)
A small peptide discovered in damaged brain tissue that helps nerve cells survive and shields them from toxic injury in lab studies; experimental, not yet an approved drug.
- Class
- Experimental neuropeptide
- Status
- No approved therapeutic status identified
- Best-supported effect
- Neuronal survival promotion in neonatal rat primary cell cultures (in vitro)
- Main caveat
- Evidence is limited to cell culture assays; no in vivo animal or human data are present in this card's source file
A researcher, an agent, or an algorithm wrote down the sequence and picked a target to hit.
An AI model like OpenFold3 or AlphaFold built a 3D structure and scored how well it fits the binding site.
A second contributor repeated the computation on their own hardware and the scores matched.
A chemistry service or a researcher ordered the sequence, it was manufactured, and mass spectrometry confirmed the right molecule was produced.
A binding or activity measurement confirmed that it actually does what the computer predicted — or didn't.
Snapshot
Class: Experimental neuropeptide
Evidence tier: In vitro / assay evidence
Status: No approved therapeutic status identified
Best-supported effect: Neuronal survival promotion in neonatal rat primary cell cultures (in vitro)
Main caveat: Evidence is limited to cell culture assays; no in vivo animal or human data are present
What this is
BINP (Brain Injury Derived Neurotrophic Peptide) is a synthetic 13-amino-acid peptide originally isolated from traumatized rat brain tissue. In primary cell culture experiments, it promoted the survival of septal cholinergic neurons and mesencephalic dopaminergic neurons derived from neonatal rats, and protected cultured neurons from glutamate-induced injury. No in vivo animal studies or human data are present.
Evidence map
| Evidence layer | Grade | What it supports |
|---|---|---|
| Human | None identified | No human evidence present |
| Animal | None identified | No in vivo animal evidence present |
| In vitro | Weak | Neuronal survival promotion and glutamate-injury rescue in neonatal rat primary cell cultures (one published study) |
| Computational | None identified | No computational or structural prediction data present |
| Mechanism | Plausible | Neurotrophic activity proposed based on cell culture observations; molecular target not specified in source |
Claim check
| Claim | Verdict | Evidence layer | Confidence |
|---|---|---|---|
| Promotes neuronal survival of septal cholinergic and dopaminergic neurons | Supported (in vitro) | In vitro | Low — single published study; cell culture only, no in vivo replication identified in source |
| Rescues neurons from glutamate-induced injury | Supported (in vitro) | In vitro | Low — single published study; cell culture only, no in vivo replication identified in source |
| Neuroprotective effect in living organisms | Not established | In vitro | Low — no in vivo data present in source |
| Human therapeutic or neuroprotective application | Not established | None | Low — no human evidence present in source |
Assay conditions
This section reports conditions used in cell culture assays. It does not establish in vivo animal or human exposure.
| Context | System | Assay condition | Timepoint | Endpoint | Limitation |
|---|---|---|---|---|---|
| Cell culture | Primary cultures of neonatal rat septal cholinergic neurons | Not individually extracted from source | Not individually extracted from source | Neuronal survival | Cell culture; no in vivo translation established |
| Cell culture | Primary cultures of neonatal rat mesencephalic dopaminergic neurons | Not individually extracted from source | Not individually extracted from source | Neuronal survival | Cell culture; no in vivo translation established |
| Cell culture | Primary cultures of neonatal rat neurons | Not individually extracted from source | Not individually extracted from source | Rescue from glutamate-induced injury | Cell culture; no in vivo translation established |
Assay limitations
- All reported activity data derive from primary cell culture experiments; no in vivo animal or human data are identified.
- The single published reference (Hama et al., 1996) is the sole attached evidence; independent replication is not documented.
- The molecular target mediating neurotrophic activity is not specified in available literature.
- In vitro neurotrophic activity does not establish systemic tolerability, in vivo efficacy, or clinical relevance.
Regulatory status
No approved therapeutic status identified. This card describes a research or literature-derived peptide, not an approved medicine.
| Region / body | Status | Notes |
|---|---|---|
| US | No approved status | per available sources; not independently verified in this card |
| EU | No approved status | per available sources; not independently verified in this card |
| WADA | Not checked | Status not extracted from source; not independently verified in this card |
Mechanism
BINP is proposed to act as a neurotrophic factor based on its isolated origin from traumatized rat brain tissue and its observed promotion of neuronal survival in primary cell cultures. activity toward septal cholinergic and mesencephalic dopaminergic neurons, consistent with a neurotrophic profile. The specific molecular target, receptor, or intracellular pathway has not been identified in available literature. This mechanism is inferred from cell culture observations and has not been validated in vivo.
Chemistry
| Field | Value |
|---|---|
| Sequence (single-letter) | EALELARGAIFQA |
| Full notation | H-Glu-Ala-Leu-Glu-Leu-Ala-Arg-Gly-Ala-Ile-Phe-Gln-Ala-NH2 |
| Length | 13 amino acids |
| Topology | Linear |
| C-terminal modification | Amide (–NH₂) |
| Molecular weight | Not provided in source |
| Formula | Not provided in source |
| CAS | Not provided in source |
| Sequence confidence | Needs review |
Open questions
- In vivo translation: No in vivo animal studies are documented. Whether the in vitro neurotrophic activity translates to living organisms has not been established.
- Molecular target: The receptor or molecular mechanism underlying BINP's neurotrophic activity has not been identified in available literature.
- Human relevance: No human evidence is present, whether any neuroprotective effect is translatable to human biology is unknown.
- Replication: A single published study from 1996 is the sole attached evidence; independent replication studies are not documented.
- Long-term stability and formulation: Published research provides only storage conditions; no pharmaceutical formulation or stability data beyond lyophilized form are present.
Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.
Does BINP protect only certain brain cells because those cells carry the receptor it binds, rather than because of something special in the peptide's chemical makeup?
If receptor location controls which cells BINP protects, doctors could predict which patients and which brain diseases would respond to it just by looking at receptor maps from existing brain databases. That would make clinical trial design much faster and cheaper, and could help match the right patients to the treatment.
Does BINP work by switching on a known brain signaling receptor, rather than acting through a vague or unknown mechanism?
If true, doctors and researchers would have a precise molecular handle for developing BINP-based drugs, making it far easier to design better versions and predict which patients might benefit. It would move this peptide from a mysterious lab curiosity into a real drug development pipeline.
Is the business end of BINP just its short hydrophobic tail, with the rest acting mainly as a handle?
If the active core is just six amino acids, chemists could build a much smaller, more drug-like molecule that does the same job, one that survives longer in the body and crosses into the brain more easily. Smaller peptides are generally cheaper to make and easier to turn into medicines.
Does BINP stop the chain reaction of cell death by quieting a GPCR relay, rather than physically blocking glutamate?
Current drugs that directly block glutamate can scramble perception and cognition. If BINP works through a more targeted relay, it might prevent stroke or traumatic brain injury damage without those mental side effects, a major unmet need in neurology.
Is BINP something the damaged brain already releases to protect itself, and could giving more of it improve recovery?
If BINP is a natural distress signal the brain already uses, boosting its levels after a head injury or stroke could amplify the brain's own healing response. That would be a fundamentally safer starting point than most current experimental treatments, which introduce entirely foreign chemicals.
▸full evidence table2 metrics
| metric | value | tool |
|---|---|---|
| ipTM | 0.9538408517837524 | boltz-2 |
| ranking score | 0.8833171725273132 | boltz-2 |
▸3-letter notation
▸recipeboltz-2 2.2.1
| parameter | value |
|---|---|
| model | boltz-2 2.2.1 |
| weights | — |
| hardware | vast_v100_32gb |
| mlx version | — |
| python | — |
| random seed | 1 |
| msa strategy | colabfold_local |
| runtime | — |
| predicted by | — |
| predicted at | 2026-05-22 |
▸citationbibtex
@peptide{pep10530,
sequence = {EALELARGAIFQA},
target = {npbwr1},
author = {peptidemodel},
year = {2026},
status = {computed}
}