Gut Inflammation (60 Capsules) (Stable BPC-157, KPV, PEA, Tributyrin)
$325.00
Synergy for Gut Inflammation and Gut Repair: BPC 157, KPV, PEA, and Tributyrin
BPC 157, KPV, PEA, and tributyrin are all compounds with important functions in the gastrointestinal tract. Their properties overlap, but are different enough that researching them together may provide synergistic benefits in the setting of intestinal inflammation. The next step into research of these peptides would be to determine if their combined properties might offer substantial benefit in the setting of inflammatory bowel disease and other intestinal inflammation.
To understand how these peptides work together in the gut, it is important to first understand their individual properties. Those looking to develop experimental protocols for combinations of these peptides would do well to start with the lengthy research supporting each. Overarching these include control of systemic inflammatory responses, improvement of intestinal barrier function, reduction of inflammation in adipose tissue, control of inflammatory cytokine signaling (especially TNF-alpha), and reduction in immune responses to intestinal inflammatory signals.
Each of these products is naturally occurring, making them of even great interest to inflammation researchers because they are easier to isolate and produce, offer a reduced risk/side effect profile, and can be used to explore natural inflammatory pathways and the interactions that occur between them.
What Is BPC 157 and Stable BPC157 Arginate?
BPC 157 is a synthetic derivative of the naturally occurring protein known as body protection compound (BPC). BPC was first isolated form the human gastrointestinal tract where it is known to have anti-inflammatory and healing properties. It has been investigated in phase I clinical trials for the treatment of gastrointestinal ulcers as well as tendon and muscle injuries. BPC 157 is one of the rare anti-inflammatories to also possess angiogenic properties as well.
Sequence: Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val
Molecular Formula: C62H98N15O22
Molecular Weight: 1419.556 g/mol
PubChem CID: 108101
Source: PubChem
It is important to note that not all forms of a peptide are equivalent. In the case of BPC 157, there are two forms of the peptide: an Arginate salt and an Acetate salt. Research with oral administration of standard BPC 157 (acetate salt) has shown that it tends to break down in gastric acid more than the ariginate salt form. The body’s response to this is to simply produce a lot of BPC 157 and only in the areas where it is needed. Of course, this solution is not tenable when delivering the peptide orally and so scientists set out to produce a more stable form of BPC 157 by adding additional chemical structures to the peptide that resist gastric acid but do not alter overall function. The more orally bioavailable “stable” form of BPC 157 is the arginate salt. Studies show that just 5% of BPC 157 arginate is degraded after 5 hours in gastric acid as compared to 98% of the acetate salt. By reducing the degradation of BPC 157, the arginate salt makes the peptide more effective as an orally administered compound. The enhanced oral bioavailability of the arginate salt makes it the preferred choice in BPC 157 oral research[1].
What Is KPV?
KPV is a synthetic analogue of alpha-melanocyte stimulating hormone. Made up of three amino acids, KPV is known to retain the properties of the much larger alpha-MSH protein including anti-ischemic and anti-inflammatory properties. It is under active investigation as a potential treatment for inflammatory bowel disease[2].
KPV is a potent general anti-inflammatory, but its true benefit is in its ability to reduce intestinal inflammation in mouse models of inflammatory bowel disease. Research shows that the peptide can reduce inflammatory infiltrates, MPO activity, and histological evidence of inflammation. Research in mice shows that KPV can accelerate clinical recovery and improve weight gain in the setting of IBD[3].
Research shows that KPV is a potent suppressor of TNF-alpha and that its effects can be targeted to the intestine with the proper delivery mechanism[4]. This is important because TNF-alpha is a driver of inflammation in IBD and a target of current therapeutics like infliximab (Remicade/Inflectra) and adalimumab (Humira). These medications are effective early in their use, but lose efficacy due to the formation of systemic antibodies against them over time. They also carry with them a host of substantial, if rare, side effects. The ability to target anti-TNF-alpha activity to the intestine could help to thwart these drawbacks and would also allow for higher dosing and thus better disease control.
Amino Acid Sequence: Lys-Pro-Val
Molecular Formula: C16H30N4O4
Molecular Weight: 342.43 g/mol
PubChem CID: 125672
CAS Number: 67727-97-3
Synonyms: MSH (11-13), ACTH(11-13), alpha-MSH(11-13)
Source: PubChem
What Is PEA?
Palmitoylethanolamide (PEA) is a naturally occurring fatty acid amide produced from a combination of palmitic acid and ethanolamine. It binds to the peroxisome proliferator-activated receptor alpha (PPAR-a) as well as to cannabinoid-like G-coupled receptors GPR55 and GPR119 to influence pain and chronic inflammation. It also inhibits cyclooxygenase-2 signaling.
Research shows that PEA influences pain perception in at least two different ways. The first, and perhaps most important way in which PEA alters pain is via its anti-inflammatory actions. These actions are mediated through the PPAR-a receptor and through effects on NF-kappaB signaling[5].
Research in mouse models shows that PEA attenuates inflammation by activating PPAR-alpha. PPAR-alpha is a nuclear receptor protein that acts as a transcription factor[6]. While originally of interest for its ability to regulate lipid metabolism in the liver, PPAR-alpha has since been found to have anti-inflammatory properties. PPAR alpha is found in liver, kidney, heart, muscle, and adipose tissue in high quantities and in many other tissues in somewhat lower quantities. A number of prescription anti-diabetic and metabolic syndrome drugs target PPAR-alpha.
The ability of PEA to alleviate pain via an alternative to PPAR-alpha stimulation has been demonstrated in mouse models. In these studies, PEA was found to bind to the cannabinoid CB2 receptor in a manner similar to the endogenous cannabinoid (endocannabinoid) anandamide. This allows PEA to alleviate the perception of pain (nociception), but this effect is limited to pain controlled by the CB2 receptor, which has no impact on thermal pain or capsaicin-induced pain[7]. Because PEA is a naturally occurring molecule, it is likely that the cannabinoid CB2 receptor is its native target along with PPAR-alpha.
PPAR-alpha and endocannabinoid action are not the only mechanisms by which PEA seems to operate though. Research in mice indicates that PEA inhibits NF-kappaB nuclear signaling in the dorsal rout ganglia of spinal nerves[8]. This results in significant reductions in cyclooxygenase-2 (COX-2) expression in the central nervous system and subsequent reductions in nerve pain and pain signaling in general. COX-2 is the target of anti-inflammatories like ibuprofen, Celebrex, and Aleve.
Molecular Formula: C18H37NO2
Molecular Weight: 299.5 g/mol
PubChem CID: 4671
CAS No: 544-31-0
Alternative Names: PEA, N-PEA, Palmidrol, Impulsin, Loramine P256, Hexadecanamide
Source: PubChem
The properties of PEA extend beyond pain relief and reduction in inflammation. Research in mice shows that PEA has anticonvulsant activities. The effective dose is similar to that of prescription anticonvulsants, but PEA does not appear to cause neurological impairment[9]. The anti-convulsant effect of PEA is likely mediated through its actions on the CB2 receptor of the endocannabinoid system[10]. This is the same receptor that mediates PEA’s anti-nociceptive activity. Action at this receptor has been shown to attenuate neurological damage and reduce infarct size following simulated stroke in the laboratory. It is thought that CB2 activation may help to reduce inflammation in the central nervous system and that this may lead to improvements in seizure thresholds and offer neurons protection against inflammatory processes[11].
What Is Tributyrin?
Tributyrin is a triglyceride (fat) found naturally in butter. Research shows that, within the body, tributyrin is converted to butyric acid. Butyric acid has been found to have anti-proliferative effects, slowing the growth of certain cells like colon cancer cells. Research shows that this anti-proliferative effect is the result of overexpression, induced by tributyrin, of the vitamin D3 receptor[12].
Molecular Formula: C15H26O6
Molecular Weight: 302.36 g/mol
PubChem CID: 6050
CAS No: 560-01-5
Alternative Names: tributin, butyrin, tributyroin, NSC 661583
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