Archive for Brain Health

BPC 157: The Healing Miracle Molecule

What is BPC 157?

The human body has a remarkable system of self-healing and damage repair. One of the important components of this system is a protein called Body Protection Compound (BPC) 157.

BPC 157 is a peptide made up of 15 amino acids; and is produced by the body in the acidic environment of the stomach. The peptide is well-known for its ability to heal, repair and regenerate. Studies suggest that BPC 157 is useful in the treatment of ulcers in the digestive tract as well as management of inflammatory bowel disease (IBD), a group of inflammatory disorders of the digestive tract. BPC 157 also facilitates wound healing of various tissues, including skin, muscle, bone, ligament, and tendon.

BPC 157 in the Digestive Tract

Given that BPC 157 is present in the juices of the stomach, we would expect it to be involved in functioning of the digestive tract. And this is indeed the case. In fact, BPC 157 is also called “stable gastric pentadecapeptide”as it remains stable in human gastric juices for at least 24 hours.

BPC 157 has several functions in the digestive tract. It preserves the integrity of the stomach lining, improves digestion, and facilitates healing throughout the digestive tract. It is particularly helpful in [1] [2]:

  1. Inflammatory bowel disease; such as Ulcerative Colitis, Crohn’s Disease and Esophagitis
  2. Fistula and intestinal anastomosis (the latter is a process where a section of an intestine is cut and removed. The two ends are then surgically connected.)
  3. Reversing short bowel syndrome
  4. Protecting the gastro-intestinal tract from NSAID overuse

Much of the healing capacity of BPC 157 comes from its ability to:

  • Protect the endothelium – inner lining of blood vessels and the lymphatic system known as the endothelium,
  • Play an important role in the formation of new blood vessels – a process known as angiogenesis.

BPC 157 as an Anti-ulcer Agent

BPC 157 is a cytoprotective agent; meaning it can limit the damage to gastric mucosa by agents that trigger ulcer formations. Most importantly, it doesn’t prevent gastric acid secretion but strengthens the protection for gastric mucosa.

NSAID’s or non-steroidal anti-inflammatory drugs are commonly used to relieve pain and inflammation. Overuse of NSAIDs is known to cause ulcers and even bleeding in the digestive tract. BPC 157 possesses the ability to heal these ulcers and a study published in 2013 noted that BPC 157 has clear antidote activity against NSAIDS side effects; and that the “variety of the beneficial effects portrayed by BPC 157 may well be a foundation for establishing BPC 157 as a NSAIDs antidote since no other single agent has portrayed a similar array of effects.” [3]

In addition, BPC 157 can heal lesions in the liver developed due to overuse of alcohol. These lesions can lead to liver tissue damage. Thus, BPC 157 can protect the liver from further deteriorating.

BPC 157 in Inflammatory Bowel Disease

BPC 157 shows great potential in reducing the symptoms of advanced inflammatory bowel disease (IBD). The peptide combines its anti-inflammatory and healing properties to manage the following conditions:

  • Crohn’s disease: chronic inflammation affecting the digestive tract. It causes abdominal pain, diarrhea, and poor absorption of nutrients leading to fatigue and malnutrition.
  • Ulcerative colitis: formation of ulcers and open sores in the colon
  • Esophagitis: inflammation of the esophagus (food pipe) making it extremely painful and difficult swallow.

BPC 157 in Wound Healing

Wound healing is a complex process involving a sequential, cascade of events; which are critical for maintaining the integrity of the body.

BPC 157 holds tremendous potential in wound healing of many tissues such as skin, muscle, bone, ligaments, and tendons. It reduces inflammation at the wound site and allows faster healing of bone ligaments, damaged muscle, Achilles tendons and skin wounds [4] [5].

There are three major processes by which BPC 157 plays a vital role in wound healing; angiogenesis, granulation tissue formation, and production of collagen. All of these mechanisms are central to any healing process occurring within the body.

Angiogenesis is a process where new blood vessels are formed around the site of injury. It allows new blood vessels to send oxygen, nutrients, and inflammatory cells to the healing and regenerating tissues. BPC 157 increases the expression of vascular endothelial growth factor (VEGF) that promotes angiogenesis [6].

A quick primer on VEGF

VEGF is a protein that signals the growth of new blood vessels when a tissue is damaged. It is a very important process that serves to reinstate the blood supply; and with it oxygen and nutrition, to the tissues at the time of reduced blood circulation. In other words, during an injury, the growth factor triggers the sprouting of new blood vessels – an action that increases the influx of nutrients to the damaged tissue.

BPC 157 exerts a particularly effective role in tendon healing. Muscles have a remarkable process of healing; owing to a highly-evolved system of blood vessels and also stem cells. However, tendons lack this blood vessel network and as a result there is a reduced flow of oxygen and nutrients to the recuperating tendon. This leads to impaired healing.

BPC 157, by up-regulating VEGF, triggers an adequate and controlled angiogenic response that allows tendons to heal faster. Controlled angiogenesis is important, as prolonged instances interferes in healing, eventually leading to chronic tendon disease.

BPC 157 achieves effective muscle and tendon healing by regulating certain underlying complex processes, “In tendon and muscle healing its functional, biomechanical, and pathohistological beneficial effect is accompanied by angiogenic action. BPC 157 may directly protect endothelium, influence the NO-system, counteract the effect of both NOS-inhibitor and NO-precursor as well as over expression of endothelin.”

The anti-inflammatory properties of BPC 157 further contribute to its healing benefits. The peptide decreases the concentration of inflammatory mediators in the injured or damaged tissues – promoting the wound healing process and allowing the tissue to heal faster.

BPC Influences the NO system

BPC 157 interacts with, and modulates the nitric oxide (NO) system; an important property responsible for many of its wound healing and tissue repair outcomes.

NO is a gas naturally produced by the body and is implicated in many aspects of repair, healing and regeneration processes – involving angiogenesis, inflammation, cell proliferation, matrix deposition, and remodeling to name a few. Nitric oxide plays a particularly important role in mediating a number of inflammatory responses and promoting angiogenesis (growth of new blood vessels).

Furthermore, a study showed that the protein’s ability to influence the NO system may be helpful in many conditions [7]:

  1. Protects the gastric mucosa following alcoholic lesions
  2. Alcohol intoxication and withdrawal
  3. Cardiovascular problems, including chronic heart failure, irregular heart beat and elevated blood pressure in the arteries of the lungs
  4. Changes in blood potassium levels that can lead to dysfunction of the cell membranes
  5. Complications with fistula healing; both of colon and esophagus.

BPC 157 is safe with no side effects

BPC 157 is naturally produced by the body in small amounts. There are no reported side effects associated with its use. With no Lethal Dose 1 achieved for BPC 157, it enjoys quite a high safety profile. Lethal Dose 1 of any substance is the dose at which 1 % of the test population is killed.

BPC 157 Benefits in a Nutshell

Miraculous healing protein

  1. Anti-ulcer and provides protection to the gastric mucosa
  2. Provides relief in inflammatory bowel disease; including Ulcerative Colitis and Crohn’s Disease
  3. Promotes healing in intestinal surgery and fistula
  4. Promotes faster healing of damaged muscle and tendons.
  5. Improved healing of superficial cuts, skin wounds and abrasions



  1. Cesarec V, Becejac T, Misic M, Djakovic Z, Olujic D, Drmic D, Brcic L, Rokotov DS, Seiwerth S, Sikiric P. Pentadecapeptide BPC 157 and the esophagocutaneous fistula healing therapy. European Journal of Pharmacology. 2013
  2. Stable gastric pentadecapeptide BPC 157: novel therapy in gastrointestinal tract.  Current Pharmaceutical Design. 2011
  3. P Sikiric et al. Toxicity by NSAIDs. Counteraction by stable gastric pentadecapeptide BPC 157. Current Pharmaceutical Design. 2013
  4. Chang CH, Tsai WC, Hsu YH, Pang JH. BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts. Molecules. 2014
  5. Krivic, A., Anic, T., Seiwerth, S., Huljev, D. and Sikiric, P. Achilles Detachment in Rat and Stable Gastric Pentadecapeptide BPC 157: Promoted Tendon-to-Bone Healing and Opposed Corticosteroid Aggravation. . J. Orthop. 2006
  6. L. Brcic et al. Modulatory Effect Of Gastric Pentadecapeptide Bpc 157 On Angiogenesis In Muscle And Tendon Healing. Journal of Physiology And Pharmacology 2009
  7. P Sikiric et al. Stable gastric pentadecapeptide BPC 157-NO-system relation. Current Pharmaceutical Design. 2014


BPC157 counteracts brain damages and convulsions

The Department of Pharmacology and Pathology,

Medical Faculty University of Zagreb, Zagreb, Croatia published this paper in 2010


To demonstrate possible BPC 157 therapy capability as a paracetamol antidote in early and advanced stage of paracetamol toxicity, BPC 157 was applied intraperitoneally or intragastrically (12, 13) (i) prophylactically, immediately after paracetamol or (ii) therapeutically, after 3 hours elapsed.

Presenting the generally known significance of paracetamol toxicity (1-3, 6, 11), this may reveal the role of BPC 157 (i.e., a free radical scavenger (17, 29)) against the early paracetamol lesions development, and even more importantly, when the original damaging process induced by an extreme paracetamol over-dose was highly advanced.

Discussion extracts:

“However, we shown that pentadecapeptide BPC 157, as an antiulcer peptide (12-15), may consistently counteract all paracetamol disturbances. This may also indicate that these disturbances are also interconnected throughout BPC 157 background. Moreover, considering the used paracetamol (5 g/kg i.p.)/BPC 157 (10 µg, 10 ng, 10 pg/kg i.p. or i.g., and effectiveness within µg-ng range) ratio (12, 13), it may be reasonably to assume that these therapy effects may indicate a likely role of BPC 157 in controlling, and then, counteracting one or more causative process(es).”

“What’s more, the premise that when given peripherally, BPC 157 may have a particular beneficial effect on CNS (i.e., markedly less damaged neurons in most severely injuried areas) is in accord with: its neuroprotective properties (22, 34), consistent antagonization of different central disturbances (16-23, 34),…”

“Also, BPC 157 was found to have anti-convulsive properties (16, 17, 21).

Also very recently, with the respect of K+-ATP channels in the substantia nigra as a predisposing factor for seizure development, BPC 157 inhibits K+ conductance in WT HEK293 cells (36).

Besides, after an induced traumatic brain injury in mice, BPC 157 regimens (corresponding to those used in the present study) demonstrated a marked attenuation of damage with an improved early outcome and a minimal postponed mortality throughout a 24 h 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 (22).”


“In conclusion, we showed the progressive hepatic encephalopathy, accompanied by severe seizures with a very early onset, in paracetamol-rats (i.e., the full threatening circuit in paracetamol’s acute hepatic toxicity).

This was consistently counteracted by the stable gastric pentadecapeptide BPC 157, showing this peptide as an effective antidote therapy (i.e., given in µg- and ng-dose regimens in either stage of paracetamol intoxication).

Also, when given parenterally or per-orally (i.e., stable in human gastric juice for more than 24 h (12, 13)), in the same dose-regimens, BPC 157 protected against various agents or procedures that would otherwise have lead to severe liver lesions (29-31) or CNS disturbances (16-23).”


“Finally, BPC 157 counteracted a particular overdose toxicity that excided regular paracetamol regimens (i.e., 1, 2, 6, 11), at either of the assessed intervals (i.e., 25 min, 3 hours and 24 hours). On the other hand, the demonstration of paracetamol’s progressive hepatic encephalopathy with severe seizures at least partly overruled the general discordance of NSAIDs’ adverse effects and therapeutic application, paracetamol in particular as previously mentioned (1-10).

Also, the significance of this peptide’s therapeutic benefit against amplified and advanced paracetamol toxicity remains to be further postulated, particularly considering the extensive investigation of gastrointestinal peptides in gastrointestinal and liver physiology (38), physiological mediators in NSAIDs-induced impairment of gastric mucosal defense and adaptation (39), and brain-gut peptide regulation (40). However, very recent novel evidence suggested that just the stable gastric pentadecapeptide BPC 157 may have possible significance and implications for novel mediator of both Robert’s cytoprotection and adaptive cytoprotection (41), and thereby potential to counteract paracetamol and other NSAIDs (over)-toxicity.”


Source of the paper:


Useful Cited References:

  • 12- Sikiric P, Petek M, Rucman R, et al. A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. J Physiol (Paris) 1993; 87: 313-327.
  • 13- Sikiric P, Seiwerth S, Brcic L, et al. Stable gastric pentadecapeptide BPC 157 in trials for inflammatory bowel disease (PL-10, PLD-116, PL 14736, Pliva, Croatia). Full and distended stomach, and vascular response. Inflammopharmacology 2006; 14: 214-221.
  • 15- Sikiric P, Seiwerth, S, Grabarevic Z, et al. The influence of a novel pentadecapeptide, BPC 157, on N(G)-nitro-L-arginine methylester and L-arginine effects on stomach mucosa integrity and blood pressure. Eur J Pharmacol 1997; 332: 23-33.
  • 16- Boban Blagaic A, Blagaic V, Mirt M, et al. Gastric pentadecapeptide BPC 157 effective against serotonin syndrome in rats. Eur J Pharmacol 2005; 512: 173-179.
  • 17- Sikiric P, Marovic A, Matoz W, et al. A behavioural study of the effect of pentadecapeptide BPC 157 in Parkinson’s disease models in mice and gastric lesions induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydrophyridine. J Physiol (Paris) 1999; 93: 505-512.
  • 21- Blagaic AB, Blagaic V, Romic Z, Sikiric P. The influence of gastric pentadecapeptide BPC 157 on acute and chronic ethanol administration in mice. Eur J Pharmacol 2004; 499: 285-290.
  • 22- Tudor M, Jandric I, Marovic A, et al. Traumatic brain injury in mice and pentadecapeptide BPC 157 effect. Regul Pept 2010; 160: 26-32.
  • 23-  Boban Blagaic A, Turcic P, Blagaic V, et al. Gastric pentadecapeptide BPC 157 counteracts morphine-induced analgesia in mice. J Physiol Pharmacol 2009; 60(Suppl. 7): 177-181.
  • 29- Sikiric P, Seiwerth S, Grabarevic Z, et al. Hepatoprotective effect of BPC 157, a 15-amino acid peptide, on liver lesions induced by either restraint stress or bile duct and hepatic artery ligation or CCl4 administration. A comparative study with dopamine agonists and somatostatin. Life Sci 1993; 53: PL291-PL296.
  • 31- Ilic S, Brcic I, Mester M, et al. Over-dose insulin and stable gastric pentadecapeptide BPC 157. Attenuated gastric ulcers, seizures, brain lesions, hepatomegaly, fatty liver, breakdown of liver glycogen, profound hypoglycemia and calcification in rats. J Physiol Pharmacol 2009; 60(Suppl 7): 107-114.
  • 34- Gjurasin M, Miklic P, Zupancic B, et al. Peptide therapy with pentadecapeptide BPC 157 in traumatic nerve injury. Regul Pept 2010; 160: 33-41.
  • 36- Barisic I, Seiwerth S, Sikiric P, Sindic A. BPC 157 inhibits K+ conductance in WT HEK293 cells J Physiol Pharmacol 2009; 60(Suppl. 2): 10.
  • 38- Konturek SJ, Brzozowski T. Gastrointestinal and liver physiology. Preface. J Physiol Pharmacol 2008; 59(Suppl 2): 3-5.
  • 39- Brzozowski T, Konturek PC, Pajdo R, et al. Physiological mediators in nonsteroidal anti-inflammatory drugs (NSAIDs)-induced impairment of gastric mucosal defense and adaptation. Focus on nitric oxide and lipoxins. J Physiol Pharmacol 2008; 59(Suppl 2): 89-102.
  • 40- Konturek SJ, Brzozowski T, Konturek PC, et al. Brain-gut and appetite regulating hormones in the control of gastric secretion and mucosal protection. J Physiol Pharmacol 2008; 59(Suppl 2): 7-31.
  • 41- Sikiric P, Seiwerth S, Brcic L, et al. Revised Robert’s cytoprotection and stable gastric pentadecapeptide BPC 157. Possible significance and implications. Curr Pharm Des 2010; in press.


This trial shows the effectiveness of BPC157 on damages caused by insulin over dosage, which can be very useful for diabetics who inject themselves too much insulin… extracts:



The general significance of insulin induced ulcers remains not determined. We focused on hyperinsulinemia, deliberate injection of excessive insulin, and possibility that an anti-ulcer therapy with anti-ulcer peptide may be more successful counteracting therapy.

Insulin induced ulcers were long ago described, and related to gastric acid hypersecretion (1, 2).

Thus, to provide some novel intriguing insights, we focused on insulin induced gastric ulcers (1, 2) and then on other disturbances that may be concomitantly induced by insulin application (3-5).


We focused on a peptide therapy, using a small, orally active, anti-ulcer peptide (7-11) stable gastric pentadecapeptide BPC 157 (MW 1419) with very safe profile (LD1 could be not achieved, no side effects in clinical trials (12, 13) stable in human gastric juice (14), effective in trials for inflammatory bowel disease therapy (12, 13) and wound healing (15-18) also in diabetic rats (18, 19).

Importantly, pentadecapeptide BPC 157 was more active than recombinant human platelet-derived growth factor (PDGF-BB), stimulating both expression of early growth response 1 (egr-1) gene and its repressor nerve growth factor 1- A binding protein-2 (NAB2) (18).

Thereby, it may be important for cytokine induction, growth factor generation, early extracellular matrix (collagen) formation (18), but also for gluconeogenesis regulation (20).

Finally, alloxan-gastric ulcers in rats and mice may be inhibited by stable gastric pentadecapeptide BPC 157 (21).



Thus, when given to insulin-rats, BPC 157 would be confronted with the all processes simultaneously occurring that eventually lead to stomach ulcer (1, 2), hypoglycemia and all mentioned disturbances and death in insulin over-dose-rats (3-5). However, we shown that pentadecapeptide BPC 157, as an antiulcer peptide (7-11), may besides stomach ulcer consistently counteract all insulin disturbances and fatal outcome. This may also indicate that these disturbances are also interconnected throughout BPC 157 background. Moreover, considering the used insulin (250 IU/kg i.p.) /BPC 157 (10 µg, 10 ng/kg i.p. or i.g.) ratio (7, 8), it may be reasonably to assume that these therapy effects may indicate a likely role of BPC 157 in insulin controlling and influence on one or more causative process(es).


In conclusion, these findings demonstrate that when one application of very high dose of insulin may induce together stomach ulcer, seizures, severely damaged neurons in cerebral cortex and hippocampus, hepatomegaly, fatty liver, breakdown of liver glycogen with profound hypoglycemia, along with calcium deposition, and finally fatal outcome in rats, all damages were markedly attenuated when BPC 157 was applied.

The same effectiveness when given intraperitoneally or intragastrically (i.e., stable in human gastric juice (14)) may be suggestive that BPC 157 may have also an incretin role in controlling insulin effects (7, 8, 11).

Intriguingly, further studies may show whether standard anti-ulcer agents that prevent insulin-stomach ulcer (1, 2) may also have a broader beneficial effect on other disturbances presented in insulin-rats.

Previously, BPC 157 was shown to counteract toxic effects of other insulin preparations (43).


Source for this article:


Useful References:

  • 7. Sikiric P, Petek M, Rucman R, et al. A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. J Physiol (Paris) 1993; 87: 313-327.
  • 8. Sikiric P, Seiwerth S, Brcic L, et al. Stable gastric pentadecapeptide BPC 157 in trials for inflammatory bowel disease (PL-10, PLD-116, PL 14736, Pliva, Croatia). Full and distended stomach, and vascular response. Inflammopharmacology 2006; 14: 214-221.
  • 9. Sikiric P, Siwerth S, Grabarevic Z, et al. The beneficial effect of BPC 157, a 15 amino acid peptide BPC fragment, on gastric and duodenal lesion induced by restraint stress, cysteamine and 96% ethanol in rats. A comparative study with H2 receptor antagonists, dopamine promoters and gut peptides. Life Sci 1994; 54: 63-68.
  • 10. Sikiric P, Seiwerth, S, Grabarevic Z, et al. The influence of a novel pentadecapeptide, BPC 157, on N(G)-nitro-L-arginine methylester and L-arginine effects on stomach mucosa integrity and blood pressure. Eur J Pharmacol 1997; 332: 23-33.
  • 11. Sikiric P, Seiwerth S, Grabarevic Z, et al. Salutary and prophylactic effect of pentadecapeptide BPC 157 on acute pancreatitis and concomitant gastroduodenal lesions in rats. Dig Dis Sci 1996; 41: 1518-1526.
  • 12. Veljaca M, Pavic-Sladoljev D, Mildner B, et al. Safety, tolerability and pharmacokinetics of PL 14736, a novel agent for treatment of ulcerative colitis, in healthy male volunteers. Gut 2003; 51: A309.
  • 13. Ruenzi M, Stolte M, Veljaca M, Oreskovic K, Peterson J. A multicenter, randomized, double blind, placebo-controlled phase II study of PL 14736 enema in the treatment of mild-to-moderate ulcerative colitis. Gastroenterology 2005; 128: A584.
  • 14. Veljaca M, Chan K, Guglietta A. Digestion of h-EGF, h-TGF alpha and BPC 157 in human gastric juice. Gastroenterology 1995; 108: 761.
  • 15. Sikiric P, Seiwerth S, Mise S, et al. Corticosteroid-impairment of healing and gastric pentadecapeptide BPC-157 creams in burned mice. Burns 2003; 29: 323-334.
  • 16. Novinscak T, Brcic L, Staresinic M, et al. Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat. Surg Today 2008; 38: 716-725.
  • 17. Staresinic M, Petrovic I, Novinscak T, et al. Effective therapy of transected quadriceps muscle in rat: gastric pentadecapeptide BPC 157. J Orthop Res 2006; 24: 1109-1117.
  • 18. Tkalcevic VI, Cuzic S, Brajsa K, et al. Enhancement by PL 14736 of granulation and collagen organization in healing wounds and the potential role of egr-1 expression. Eur J Pharmacol 2007; 570(1-3): 212-221.
  • 20. Berasi SP, Huard C, Li D, et al. Inhibition of gluconeogenesis through transcriptional activation of EGR1 and DUSP4 by AMP-activated kinase. J Biol Chem 2006; 281: 27167-27177.
  • 21. Petek M, Sikiric P, Anic T, et al. Pentadecapeptide BPC 157 attenuates gatric lesions induced by alloxan in rats and mice. J Physiol (Paris) 1999; 93: 501-504.
  • 43. Ilic S, Mester M, Filipovic M, et al. Stable gastric pentadecapeptide BPC 157 and insulin induced gastric lesions in rats. J Physiol Pharmacol 2009; 60(Suppl 2): 40.

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