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BPC-157 from Epic Peptides Lab is a research-use-only compound supplied in a preloaded 3ml Disposable Self-injection Pen at 5mg/ml for laboratory study, offering consistent measured delivery and reliable handling for researchers.
Epic Peptides Lab · Research Use Only
Pentadecapeptide · VEGFR2-Akt-eNOS · 3ml at 5mg/ml
The BPC-157 Disposable Self-injection Pen is a preloaded 3ml research device containing BPC-157 in solution at 5mg/ml, giving 15mg of total peptide. BPC-157 is a fifteen-residue partial sequence of a protein identified in human gastric juice, CAS 137525-51-0, molecular weight 1419.55, and its sequence composition makes it comparatively well-supported in solution.
| Property | Value |
|---|---|
| Device format | Preloaded Disposable Self-injection Pen, glass cartridge |
| Fill volume | 3 ml |
| Concentration | 5 mg/ml |
| Total compound in device | 15 mg |
| Molar concentration | Approximately 3.5 mM |
| Compound | BPC-157 |
| Full name | Body Protection Compound 157 |
| CAS number | 137525-51-0 |
| Molecular formula | C62H98N16O22 |
| Molecular weight | 1419.55 g/mol |
| Residue count | 15 (pentadecapeptide) |
| Amino acid sequence | Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val |
| Sequence origin | Partial sequence of a protein found in human gastric juice |
| Reported molecular association | VEGFR2, with downstream Akt and eNOS activation |
| Oxidation-prone residues | None. No cysteine, methionine, tryptophan, tyrosine or histidine |
| Proline content | Four residues, at positions 3, 4, 5 and 8 |
| Reconstitution required | None. Supplied as solution |
| Excipient system | Not published on the product record |
| Solution stability | Not established over device shelf life |
| Storage | 2-8°C, protected from light |
| Purity | Per lot-specific certificate of analysis |
| Regulatory status | No approved human or veterinary formulation in any jurisdiction |
Reading Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val predicts a good deal about how this peptide behaves, and it is worth doing before considering any pharmacology.
Four prolines, three of them consecutive at positions 3, 4 and 5. Proline restricts backbone rotation severely, so a run of three imposes a rigid, extended local conformation rather than allowing the flexible chain most short peptides adopt. That rigidity contributes to proteolytic resistance, since many peptidases require the substrate to adopt a particular conformation in the active site.
No cysteine. No disulfide bonds to form, scramble or reduce, which removes the single largest source of preparation ambiguity affecting growth factors and longer peptides.
None of the five oxidation-prone residues. No methionine, tryptophan, tyrosine or histidine, so metal-catalysed and photo-oxidation routes are largely closed.
Two adjacent aspartates at positions 10 and 11, followed by alanine. Asp-Gly sequences are the classic isomerisation risk; Asp-Asp-Ala is less problematic but aspartate isomerisation remains the most plausible chemical degradation route for this sequence in solution.
Hsieh and colleagues provided the clearest mechanistic characterisation available for this compound (Hsieh et al., Journal of Molecular Medicine, 2017).
In human vascular endothelial cells they reported that BPC-157 increased both mRNA and protein expression of VEGFR2, the principal receptor mediating vascular endothelial growth factor signalling, without increasing VEGF-A itself. That distinction matters: the compound appears to act on receptor availability rather than on ligand supply.
They further reported that BPC-157 promoted VEGFR2 internalisation and produced time-dependent activation of the VEGFR2-Akt-eNOS signalling axis. Endothelial nitric oxide synthase sits at the end of that chain, which links the pathway to nitric oxide production and vascular tone.
Vessel density increased in vivo and in vitro in the same body of work, and recovery of blood flow was accelerated in a rat hind-limb ischaemia model.
What this does not establish is a receptor for BPC-157 itself. No direct binding partner has been identified, and the compound is described as acting on VEGFR2 expression and trafficking rather than as a VEGFR2 ligand. That gap is real and is worth stating.
For the BPC-157 Disposable Self-injection Pen the comparison turns on the same trade-off as every device in this catalogue, though the balance here is more favourable than most.
The device removes reconstitution and its associated failure modes: diluent measurement error, incomplete dissolution, shear from over-agitation, adsorptive loss during transfer, and variable time between preparation and use.
It accepts solution-state storage in exchange. For BPC-157 that exchange is comparatively cheap, because the sequence carries no oxidation-prone residues and no disulfides, leaving aspartate isomerisation and slow amide hydrolysis as the principal routes. Both proceed considerably more slowly at 2-8°C than oxidation would in a methionine-containing peptide.
At 5 mg/ml the solution is approximately 3.5 millimolar, which suits cell-based work with modest dilution. Published in vitro concentrations for this compound span a wide range in the literature, so the appropriate dilution depends on which body of work a design is following.
A good deal, and the gaps are worth naming because BPC-157 attracts more confident description than its evidence supports.
No receptor has been identified. The VEGFR2 association concerns expression and trafficking rather than direct binding, and no protein has been shown to bind BPC-157 with the affinity and specificity a receptor implies.
No human clinical trial has been completed and published. Sikiric and colleagues reference tolerability in early inflammatory bowel disease work, but there is no phase III dataset and no approved formulation anywhere.
Pharmacokinetics are poorly characterised. Half-life figures circulate widely without traceable primary sources, and for a fifteen-residue peptide with no protective modifications beyond its proline content, rapid clearance would be the default expectation.
Solution stability over device shelf life is unpublished for this format specifically, which is the gap most relevant to anyone using this product rather than the compound generally.
This compound attracts unusually confident description, and a page that repeats it without qualification will not survive scrutiny from anyone who has read the primary literature.
The published record is substantial in volume and narrow in provenance. A large proportion of the animal work comes from one research group in Croatia, spanning tendon, muscle, gastrointestinal and vascular models over more than two decades. The work is detailed. Independent replication by unaffiliated laboratories is thinner than the citation count suggests.
Effect sizes reported in that literature are frequently large, and large effects across many unrelated tissue systems from a single compound warrant more scepticism than they usually receive. A molecule that improves every model it is tested in is either remarkable or is being tested in a way that favours it.
None of that means the findings are wrong. It means a researcher designing around them should build in the controls that would detect a false positive: blinded assessment, pre-registered endpoints, and where possible a comparator with known activity.
The absence of an identified receptor compounds the issue, because without a molecular target there is no mechanistic prediction to test against. An effect with no mechanism is harder to falsify, which is a weakness rather than a strength.
For the BPC-157 Disposable Self-injection Pen, naming what is missing is more useful than restating what exists, and for this compound the gaps are specific.
Independent replication of the principal animal findings by laboratories with no connection to the originating group would address the provenance concentration directly. Several findings have never been reproduced outside that lineage.
Identification of a molecular target would convert a descriptive literature into a mechanistic one. Affinity chromatography, photoaffinity labelling and proteomic pulldown approaches have all been applied successfully to comparable orphan peptides.
Pharmacokinetic characterisation would give exposure figures that designs could work from rather than around. No reliable half-life exists, which makes translating between in vitro and in vivo work guesswork.
Blinded, pre-registered animal work would address the effect-size question. Where a compound reports large advantages across many unrelated models, blinding is the control that distinguishes a real broad-spectrum effect from an assessment artefact.
Inspect the solution before each draw against both light and dark backgrounds. It should be clear and free of particulate. A colourless peptide solution provides no colour cue, so clarity is the only visual signal available.
Verify delivered volume gravimetrically at least once per device. Actuate onto a tared vessel, record the mass, convert using solution density, repeat across several actuations. Run the check at the temperature of intended use, since cold solution is more viscous and viscosity affects delivery in a spring mechanism.
Discard rather than measure the first actuation after any rest period. Both air ingress and seal relaxation produce under-delivery on the first use after standing.
Keep it at 2-8°C shielded from light, and return the device to packaging whenever it is not in use. Record lot, date of first actuation, storage conditions and volume drawn per session, since the interval between first use and each later draw is an experimental variable while shelf-life data remains unpublished.
Published in vitro concentrations for the BPC-157 Disposable Self-injection Pen compound span an unusually wide range, and picking one requires knowing which body of work a design is following.
That spread is itself informative. A compound with a well-characterised target usually converges on a concentration range across laboratories. Wide dispersion suggests either genuine system dependence or insufficient standardisation, and for BPC-157 the absence of an identified receptor makes the second harder to rule out.
The practical response is to run a concentration-response curve rather than adopting a single figure from a paper using a different system.
Where a design must use one concentration, state which published work it follows and why, so a reader can locate the choice in the literature rather than treating it as arbitrary.
Validated against publisher records or primary indexes. The 2017 paper is the source for the VEGFR2 findings described in the mechanism section.
What is the BPC-157 Disposable Self-injection Pen?
A preloaded 3ml research device containing BPC-157 in solution at 5mg/ml, giving 15mg total and approximately 3.5 millimolar. CAS 137525-51-0, molecular weight 1419.55, fifteen residues. Supplied for laboratory research use only and not approved anywhere.
What does the sequence predict about stability?
Favourable behaviour. No cysteine means no disulfides to scramble. None of the five oxidation-prone residues, so metal-catalysed and photo-oxidation routes are largely closed. Four prolines, three consecutive, impose a rigid conformation contributing to proteolytic resistance.
What degradation route does remain?
Aspartate isomerisation, given the adjacent aspartates at positions 10 and 11, plus slow amide hydrolysis. Asp-Gly sequences are the classic isomerisation risk and Asp-Asp-Ala is less problematic, but it remains the most plausible chemical route for this sequence in solution.
What is the VEGFR2 association?
Published work reports BPC-157 increases VEGFR2 mRNA and protein expression in human vascular endothelial cells without increasing VEGF-A, promotes receptor internalisation, and produces time-dependent activation of the VEGFR2-Akt-eNOS axis. The compound acts on receptor availability rather than ligand supply.
Does BPC-157 bind VEGFR2 directly?
No such binding has been demonstrated. The association concerns expression and trafficking rather than direct ligand interaction, and no protein has been shown to bind BPC-157 with the affinity and specificity a receptor would imply. That gap in the literature is real.
Where does the sequence come from?
It is a partial sequence of a protein identified in human gastric juice, which is where the name Body Protection Compound originates. The fifteen-residue fragment is synthetic rather than isolated, and it corresponds to a portion of that larger natural protein.
Is there human clinical data?
No completed and published clinical trial exists. Early tolerability work in inflammatory bowel disease is referenced in review literature, but there is no phase III dataset and no approved formulation in any jurisdiction. Circulating half-life figures lack traceable primary sources.
How does the device compare with a vial?
The device removes reconstitution and its failure modes: measurement error, incomplete dissolution, shear, adsorptive loss and variable time-to-use. It accepts solution storage instead, which for this sequence is a comparatively cheap exchange given the absence of oxidation-prone residues.
How should delivered volume be verified?
Gravimetrically, at least once per device. Actuate onto a tared vessel, record delivered mass, convert using solution density, and repeat across several actuations at the temperature of intended use. Discard rather than measure the first actuation after a rest period.
What should be inspected before each draw?
Clarity, against both light and dark backgrounds. A colourless peptide solution gives no colour cue to degradation, so freedom from particulate and haze is the only visual signal available. Aggregation appears as faint opalescence before obvious turbidity.
How should BPC-157 findings be read?
With more caution than the citation count suggests. A large proportion of the animal work comes from one research group, spanning many tissue systems over two decades. The work is detailed, and independent replication by unaffiliated laboratories is thinner than the volume implies.
Why does the absence of a receptor matter?
Because without a molecular target there is no mechanistic prediction to test against. An effect with no mechanism is harder to falsify, which is a weakness rather than a strength, and it compounds the difficulty of interpreting large effects across unrelated systems.
What controls would detect a false positive?
Blinded assessment, pre-registered endpoints, and a comparator with known activity where one exists. Those are standard safeguards, and they matter more for a compound reporting large effects across many unrelated models than for one with a narrow well-replicated finding.
The BPC-157 Disposable Self-injection Pen is sold exclusively for laboratory research use. It is not a drug, food, or cosmetic product, and it is not a dietary product of any kind. It is not approved by the FDA or any comparable authority for human or veterinary use. This product is not intended to diagnose, treat, cure, or prevent any disease. It must not be given to humans or animals. Purchase is restricted to qualified researchers and institutions operating within applicable laws. All handling is the responsibility of the purchasing laboratory.
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