BPC-157 is a “Pentadeca Peptide” which was derived from a naturally occurring peptide found in gastric secretions. In other words, a healthy stomach produces, in very small amounts, this unique peptide, which helps keep the lining of the stomach intact. Researchers figured out a way to make a stable version of this peptide, and BPC-157 was born.
There are few peptides out there that have such a far-reaching effect on so many aspects of health. Most peptides are releasers of Growth Hormone, and have very little effect outside of the reach of benefits found from increased GH release. What makes BPC-157 so special to me, is that it positively affects every aspect of health. It can heal stomach ulcers, it can repair nerves, and soft tissue (aka ligaments and tendons). It also has been shown to reduce depressive behaviours as well as protect against addiction mechanisms (via its effect on GABA transmission as well as Dopamine and serotononin transmission, etc.)
Here’s a quick break-down of the top 5 benefits of BPC-157.
BPC-157 was originally developed because it was found in gastric acid, and promotes healing of gastric ulcers, as well as intestinal health. What’s more, this is one of the few peptides that has an effect when taken orally. Something that other peptides can’t promise.
“particularly, it has a prominent effect on alcohol-lesions (i.e. acute, chronic) and naiads lesions (interestingly, bpc 157 both prevents and reverses adjuvant arthritis). In rat esophagitis and failed function of both lower esophageal sphincter (les) and pyloric sphincters (ps), bpc 157 increased pressure in both sphincters till normal and reduced esophagitis.”
BPC-157 has far-reaching anti-inflammatory benefits, and has been studied for its effect on gingivitis and periodontitis (inflammation of the gums and oral-tissue).
“The pentadecapeptide bpc 157 has been shown to have anti-inflammatory and wound healing effects on multiple target tissues and organs. The purpose of the present study was to investigate the effect of bpc 157 on inflammation and bone resorption in experimental periodontitis in rats. First the acute effect of bpc was tested on gingival blood flow by laser doppler flowmetry. Then periodontitis was produced by a silk ligature placed around the lower left first molar. Rats were treated with bpc 157 (once daily for 12 days) or vehicle. At day 13, the gingivomucosal tissues encircling the molars were removed on both sides. Inflammation was assessed by evans blue plasma extravasation technique and by histology. Alveolar bone loss was analyzed by microct. Bpc 157 had no effect on gingivomucosal blood flow. Twelve day ligature caused a significantly increased evans blue extravasation in the gingivomucosal tissue, histological signs of inflammation, and alveolar bone destruction. Bpc 157 treatment significantly reduced both plasma extravasation, histological alterations and alveolar bone resorption. In conclusion, systemic application of bpc 157 does not alter blood circulation in healthy gingiva. Chronic application of the peptide has potent antiinflammatory effects on periodontal tissues in ligature induced periodontitis in rats. Taken together, this proof of concept study suggests that bpc 157 may represent a new peptide candidate in the treatment of periodontal disease.”
One of the most important effects of BPC-157, even though I don’t focus on it as much, is that it positively impacts the healing of soft tissue. Ligament and tendon healing is very difficult to pull off. There is very little blood-flow to this tissue in the body. Most peptides that affect GH levels have very little effect on soft tissue, and this makes BPC-157 unique in its own right.
“We improved medial collateral ligament (mcl) healing throughout 90 days after surgical transection. We introduced intraperitoneal, per-oral (in drinking water) and topical (thin cream layer) peptide therapy always given alone, without a carrier. Previously, as an effective peptide therapy, stable gastric pentadecapeptide bpc 157 (gepppgkpaddaglv, an anti-ulcer peptide effective in inflammatory bowel disease therapy (pl 14736)) particularly improved healing of transected tendon and muscle and wound healing effect including the expression of the early growth response 1 (egr-1) gene. After mcl transaction bpc 157 was effective in rats when given once daily intraperitoneally (10 microg or 10 ng/kg) or locally as a thin layer (1.0 microg dissolved in distilled water/g commercial neutral cream) at the site of injury, first application 30 min after surgery and the final application 24 h before sacrifice. Likewise, bpc 157 was effective given per-orally (0.16 microg/ml in the drinking water (12 ml/day/rat)) until sacrifice. Commonly, bpc 157 microg-ng-rats exhibited consistent functional, biomechanical, macroscopic and histological healing improvements. Thus, we suggest bpc 157 improved healing of acute ligament injuries in further ligament therapy.”
BPC-157 is one of the only peptides I’ve ever researched that has a dramatic effect on mood and wellbeing. Sure, the benefits of increased GH output from peptides like Ipamorelin can have an effect on mood and wellbeing. But when it comes to a specific effect on mood and mental health, BPC-157 stands alone.
“Various antidepressants have antiulcer activity. Likewise, the models currently used in ulcers and depression disorders research have a considerable degree of similarity. Therefore, the possibility that depression disorders could be effectively influenced by a primary antiulcer agent with a cyto/organoprotective activity, such as the novel stomach pentadecapeptide bpc 157, was investigated in two rat depression assays. First, a forced swimming test (a porsolt’s procedure) was used. As a more severe procedure, chronic unpredictable stress (after 5 d of unpredictable stress protocol, once daily drug application during stress procedure, open field-immobility test assessment at fourth or sixth day of medication) was used. In a forced swimming test, a reduction of the immobility time in bpc 157 (10 microg, 10 ng x kg(-1) i.p.) treated rats corresponds to the activity of the 15 mg or 40 mg (i.p.) of conventional antidepressants, imipramine or nialamide, respectively, given according to the original porsolt’s protocol. In chronic unpredictable stress procedure, particular aggravation of experimental conditions markedly affected the conventional antidepressant activity, whereas bpc 157 effectiveness was continuously present. The effect of daily imipramine (30 mg) medication could be seen only after a more prolonged period, but not after a shorter period (i.e., 4-d protocol). In these conditions, no delay in the effectiveness was noted in bpc 157 medication and a reduction of the immobility of chronically stressed rats was noted after both 4 and 6 d of bpc 157 (10 microg, 10 ng) medication.”
Last, but not least, BPC-157 has a strong effect on addiction-related neurotransmission. It enhances GABA transmission and reduces benzodiazepine tolerance.
“A novel gastric pentadecapeptide bpc 157 with different beneficial activities and anticonvulsant effect interacting with gabaergic system could improve diazepam efficacy coadministered (10 microg/kg, 10 ng/kg i.p.) with diazepam (5.0 mg/kg i.p.) twice daily for 10 days, since diazepam chronic medication would otherwise predispose for diazepam- tolerance/withdrawal development (shorter latency to convulsion after convulsant). In diazepam chronically treated mice, it attenuated diazepam tolerance (provoked by later acute administration of diazepam together with convulsant) and postponed physical dependence/withdrawal effects (provoked by later administration of isoniazid). In tolerance assay, at 42 h after the end of conditioning regimen, shorter preconvulsive latencies than in healthy (non-diazepam conditioned) mice following isoniazid (800 mg/kg i.p.) (as hallmark of tolerance) were observed if diazepam (5.0 mg/kg i.p.) was again given acutely to mice previously conditioned with diazepam alone (use of picrotoxin 3.0 mg/kg i.p., as convulsant, with acute application of diazepam in previously diazepam conditioned mice did not lead to tolerance hallmark). This was completely avoided in diazepam+bpc 157 10 microg or diazepam+bpc 157 10 ng chronically treated animals. In physical dependence assay (isoniazid challenge assessed at 6, 14, 42 and 72 h after conditioning medication), when compared to diazepam non-conditioned healthy mice, in diazepam conditioned mice residual anticonvulsive activity was not present already at the earliest post-conditioning interval (i.e., not different latency to isoniazid-convulsions), whereas shorter preconvulsive latencies (as physical dependence/withdrawal hallmark) were noted in diazepam conditioned mice following isoniazid challenge at 42 h and at 72 h after end of conditioning treatment. In diazepam+bpc 157 10 microg- conditioned mice, a residual anticonvulsive activity (i.e., longer latency to isoniazid convulsion) was noted at 6 h post-conditioning, whereas shorter preconvulsive latencies appeared only at 72 h-post-conditioning period. In conclusion, taken together these data (lack of tolerance development (tolerance studies), prolonged residual anticonvulsive activity, and postponed physical dependence/withdrawal hallmark in diazepam+bpc 157 chronically treated mice) with common benzodiazepines tolerance/withdrawal knowledge, it could be speculated that bpc 157 acts favoring the natural homeostasis of the gaba receptor complex as well as enhancing the gabaergic transmission, and having a mechanism at least partly different from those involved in diazepam tolerance/withdrawal, it may be likely used in further therapy of diazepam tolerance and withdrawal.”
And also reduces the hyperactivity that occurs when methamphetamine was administered to rats.
“Stabile gastric pentadecapeptide bpc 157, gly–glu–pro–pro–pro–gly–lys–pro–ala–asp–asp–ala–gly–leu–val, mw 1419, has a variety of protective effects in different organs, as well as nervous system. It antagonizes haloperidol-induced behavioural supersensitivity to amphetamine which, results in dopaminergic neurotoxicity and nigrostriatum damage due to increased lipid peroxidation. Currently, bpc 157 neuroprotective effects are evaluted in a model of haloperidol- and methamphetamine-induced neurotoxicity. These models result in impaired motoric function and increased lipid peroxidation in different brain regions. The purpose of this research was to asses bpc 157 protective effects on nigrostriatum in rat model of haloperidol and methamphetamine induced neurotoxicity using fine motoric in rats as indicator of nigrostriatum function and malondialdehyde (mda) levels as lipid peroxidation marker.”
THE GOODS OFFERED BY THE SELLER IS INTENDED FOR SCIENTIFIC AND DEVELOPMENT PURPOSES ONLY. The goods offered by the Seller include chemical substances that shall not be used as a drug, medicine, active substance, medical aid, cosmetic product, a substance for production of a cosmetic product neither for human consumption that is any food or food supplement or otherwise similarly used on humans or animals.