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BPC-157

Body Protection Compound-157, PL-14736, Pentadecapeptide BPC 157

Quick Stats
Studies 196
Trials 1
Score 3
2009 pubmed 40 citations

Traumatic brain injury in mice and pentadecapeptide BPC 157 effect.

Tudor. Mario M; Jandric. Ivan I; Marovic. Anton A; Gjurasin. Miroslav M; Perovic. Darko D; Radic. Bozo B; Blagaic. Alenka Boban AB; Kolenc. Danijela D; Brcic. Luka L; Zarkovic. Kamelija K; Seiwerth. Sven S; Sikiric. Predrag P

Key Findings

  • BPC‑157 (10 µg or 10 ng/kg i.p.) markedly reduced brain bleeding, lacerations and swelling after a traumatic brain injury in mice.
  • Both micro‑dose and nano‑dose regimens improved the ratio of conscious vs. unconscious vs. dead mice across a range of impact forces.
  • The protective effect depended on timing: giving the peptide 5–30 minutes before the impact was effective, with longer delays needed for stronger blows.

Practical Outcomes

  • This study shows that BPC‑157 has strong neuroprotective properties in animals, but it has never been tested for head injury in humans. For biohackers, the data suggest a potential experimental avenue for concussion prevention, yet the lack of human safety and dosing information means it should not be used clinically at this stage. The main takeaway is that BPC‑157 could be a candidate for future research on brain‑injury protection, not a ready‑to‑use protocol.

Summary

In a mouse study, giving the peptide BPC‑157 before a head blow made the brain injury less severe and helped more mice stay awake and survive for at least a day. Even tiny doses (nanograms per kilogram) worked, and the sooner the peptide was given before the impact, the better the protection.

Abstract

Gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, an anti-ulcer peptide, efficient in inflammatory bowel disease trials (PL 14736), no toxicity reported, improved muscle crush injury. After an induced traumatic brain injury (TBI) in mice by a falling weight, BPC 157 regimens (10.0microg, 10.0ng/kgi.p.) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24h post-injury period. Ultimately, the traumatic lesions (subarachnoidal and intraventricular haemorrhage, brain laceration, haemorrhagic laceration) were less intense and consecutive brain edema had considerably improved. Given prophylactically (30 min before TBI) the improved conscious/unconscious/death ratio in TBI-mice was after force impulses of 0.068 Ns, 0.093 Ns, 0.113 Ns, 0.130 Ns, 0.145 Ns, and 0.159 Ns. Counteraction (with a reduction of unconsciousness, lower mortality) with both microg- and ng-regimens included the force impulses of 0.068-0.145 Ns. A higher regimen presented effectiveness also against the maximal force impulse (0.159 Ns). Furthermore, BPC 157 application immediately prior to injury was beneficial in mice subjected to force impulses of 0.093 Ns-TBI. For a more severe force impulse (0.130 Ns, 0.145 Ns, or 0159 Ns), the time-relation to improve the conscious/unconscious/death ratio was: 5 min (0.130 Ns-TBI), 20 min (0.145 Ns-TBI) or 30 min (0.159 Ns-TBI).

Study Information

Provider

pubmed

Year

2009

Date

2009-11-18T00:00:00.000Z

DOI

10.1016/j.regpep.2009.11.012

Citations

40

References

55