Home Questions What is the recommended dosage for TB-500 and BPC 157 in humans?
Answer from top 10 papers
The recommended dosage for TB-500 (Thymosin Beta-4) is not explicitly provided in the context of the papers. (Esposito et al., 2012) discusses the detection of a fragment of TB-500 for doping control but does not mention a therapeutic dosage. As for BPC 157, the papers indicate that it has been used in various experimental models at different dosages. For instance, (Suran et al., 2014) and (Drmic et al., 2015) mention a dosage of 10 μg/kg in rat models, while (Park et al., 2021) references doses of 10, 20, and 40 μg/kg for antinociceptive effects. However, these dosages are specific to the animal models used in the research and may not directly translate to human use. It is important to note that while BPC 157 has been studied in various contexts, such as neurotoxicity, NSAID-induced damage, and endothelial impairment ((Suran et al., 2014; Sikiric et al., 2012) and (Strbe et al., 2021)), the exact dosage for humans has not been established and would likely vary depending on the specific condition being treated and the individual's characteristics. Furthermore, the use of these peptides in humans outside of clinical trials is not well-regulated or standardized, and their safety profile has yet to be fully established. In summary, while experimental studies suggest certain dosages of BPC 157 in animal models, there is no established recommended dosage for TB-500 or BPC 157 for human use. Any potential therapeutic use of these peptides in humans should be under the guidance of a medical professional and within the context of clinical trials or approved therapeutic protocols ((Suran et al., 2014; Sikiric et al., 2012; Strbe et al., 2021; Drmic et al., 2015) and (Park et al., 2021)).
Source Papers
10.1096/fasebj.28.1_supplement.1143.11
The effect of pentadecapeptide BPC 157 in metamphetamine‐induced dopaminergic neurotoxicity (1143.11)
Apr 1, 2014 The FASEB Journal
We investigated the effect of stabile gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, M.W. 1419), an original antiulcer peptide studied in inflammatory bowel disease and now multiple sclerosis clinical trials (LD‐1 not achieved, no side effects reported), in methamphetamine (METH)‐induced neurotoxicity, representing an animal model of monoamine disruption.METH dose of 40 mg/kg b.w. (s.c.) was administered to Wistar rats 24 h prior to random assignment to control (saline, 1 ml/200 g b.w., i.p.) or BPC 157 (10 μg/kg, i.p.) group. Rats were monitored (phenotype, locomotor activity) for 7 days and histopathological analysis of striata was performed.All animals had neurodegenerative phenotype, but these traits became more pronounced in controls compared to BPC 157 rats. Gradual decline in locomotor activity in BPC 157 rats was similar to behavior of healthy rats, while there was a marked hyperactivity in controls 7 days after METH administration. A higher number of red neurons counted in control rat striata and significantly higher number of normal‐appearing neurons in BPC 157 rats imply its beneficial effect on striatum. Therefore, we propose BPC 157as a potential therapeutic agent in monoamine disorders.Grant Funding Source: Supported by Grant 108‐ 1083570‐3635, Croatia
35 10.2174/1381612811306010076
Toxicity by NSAIDs. Counteraction by Stable Gastric Pentadecapeptide BPC 157
Nov 1, 2012 Current Pharmaceutical Design Predrag Sikiric + 18 more
Stable gastric pentadecapeptide BPC 157 is an anti-ulcer peptidergic agent, proven in clinical trials to be both safe in inflammatory bowel disease (PL-10, PLD-116, PL 14736) and wound healing, stable in human gastric juice, with no toxicity being reported. Recently, we claim that BPC 157 may be used as an antidote against NSAIDs. We focused on BPC 157 beneficial effects on stomach, duodenum, intestine, liver and brain injuries, adjuvant arthritis, pain, hyper/hypothermia, obstructive thrombus formation and thrombolysis, blood vessel function, counteraction of prolonged bleeding and thrombocytopenia after application of various anticoagulants and antiplatelet agents and wound healing improvement. The arguments for BPC 157 antidote activity (i.e., the role of BPC 157 in cytoprotection, being a novel mediator of Robert’s cytoprotection and BPC 157 beneficial effects on NSAIDs mediated lesions in the gastrointestinal tract, liver and brain and finally, counteraction of aspirin-induced prolonged bleeding and thrombocytopenia) obviously have a counteracting effect on several established side-effects of NSAIDs use. The mentioned 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. Unlike NSAIDs, a very high safety (no reported toxicity (LD1 could be not achieved)) profile is reported for BPC 157. Also, unlike the different dosage levels of aspirin, as a NSAIDs prototype, which differ by a factor of about ten, all these beneficial and counteracting effects of BPC 157 were obtained using the equipotent dosage (μg, ng/kg) in parenteral or peroral regimens. Keywords: NSAIDs-gastrointestinal tract lesions, NSAIDs-liver lesions, NSAIDs-brain lesions, aspirin-prolonged bleeding/ thrombocytopenia, stable gastric pentadecapeptide BPC 157, counteraction, antidote against NSAIDs, clinical trials, inflammatory bowel disease, anticoagulants
Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157
Oct 20, 2021 Biomedicines Sanja Strbe + 19 more
Due to endothelial impairment, high-dose lithium may produce an occlusive-like syndrome, comparable to permanent occlusion of major vessel-induced syndromes in rats; intracranial, portal, and caval hypertension, and aortal hypotension; multi-organ dysfunction syndrome; brain, heart, lung, liver, kidney, and gastrointestinal lesions; arterial and venous thrombosis; and tissue oxidative stress. Stable gastric pentadecapeptide BPC 157 may be a means of therapy via activating loops (bypassing vessel occlusion) and counteracting major occlusion syndromes. Recently, BPC 157 counteracted the lithium sulfate regimen in rats (500 mg/kg/day, ip, for 3 days, with assessment at 210 min after each administration of lithium) and its severe syndrome (muscular weakness and prostration, reduced muscle fibers, myocardial infarction, and edema of various brain areas). Subsequently, BPC 157 also counteracted the lithium-induced occlusive-like syndrome; rapidly counteracted brain swelling and intracranial (superior sagittal sinus) hypertension, portal hypertension, and aortal hypotension, which otherwise would persist; counteracted vessel failure; abrogated congestion of the inferior caval and superior mesenteric veins; reversed azygos vein failure; and mitigated thrombosis (superior mesenteric vein and artery), congestion of the stomach, and major hemorrhagic lesions. Both regimens of BPC 157 administration also counteracted the previously described muscular weakness and prostration (as shown in microscopic and ECG recordings), myocardial congestion and infarction, in addition to edema and lesions in various brain areas; marked dilatation and central venous congestion in the liver; large areas of congestion and hemorrhage in the lung; and degeneration of proximal and distal tubules with cytoplasmic vacuolization in the kidney, attenuating oxidative stress. Thus, BPC 157 therapy overwhelmed high-dose lithium intoxication in rats.
Optimization of the Rifampin Dosage to Improve the Therapeutic Efficacy in Tuberculosis Treatment Using a Murine Model
May 15, 2013 American Journal of Respiratory and Critical Care Medicine Jurriaan E M De Steenwinkel + 8 more
The dosage of 10 mg/kg/d rifampin, as currently used in the treatment of tuberculosis (TB), is not an optimal dose. Shortening of treatment duration might be achievable using an increased rifampin dose. Determination of optimal rifampin dosage in mice, resulting in maximum therapeutic effect and without adverse effects. Assessment of associated pharmacokinetic parameters and pharmacokinetic/pharmacodynamic indices. A murine TB infection using a Beijing genotype Mycobacterium tuberculosis strain was established by intratracheal bacterial instillation followed by proper inhalation, while keeping mice in a vertical position. We assessed dose-dependent activity of rifampin in single-drug treatment during 3 weeks. The maximum tolerated dosage, pharmacokinetic parameters, and pharmacokinetic/pharmacodynamic index were determined. Therapeutic efficacy of a range of rifampin (R) dosages added to a regimen of isoniazid (H) and pyrazinamide (Z) was assessed. Maximum tolerated dosage of rifampin in the murine TB was 160 mg/kg/d. Pharmacokinetic measurement in HR(10)Z and HR(160)Z therapy regimens showed for rifampin a C(max) of 16.2 and 157.3 mg/L, an AUC(0-24h) of 132 and 1,782 h·mg/L, and AUC(0-24h)/minimum inhibitory concentration ratios of 528 and 7129, respectively. A clear dose-effect correlation was observed for rifampin after 3-week single-drug treatment. Administration of HR(80)Z allowed 9-week treatment duration to be effective without relapse of infection. Our findings indicate that the currently used rifampin dosage in the therapy of TB is too low. In our murine TB model a rifampin dosage of 80 mg/kg/d enabled a significant reduction in therapy duration without adverse effects.
The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration
Oct 28, 2010 Journal of Applied Physiology Chung-Hsun Chang + 4 more
Pentadecapeptide BPC 157, composed of 15 amino acids, is a partial sequence of body protection compound (BPC) that is discovered in and isolated from human gastric juice. Experimentally it has been demonstrated to accelerate the healing of many different wounds, including transected rat Achilles tendon. This study was designed to investigate the potential mechanism of BPC 157 to enhance healing of injured tendon. The outgrowth of tendon fibroblasts from tendon explants cultured with or without BPC 157 was examined. Results showed that BPC 157 significantly accelerated the outgrowth of tendon explants. Cell proliferation of cultured tendon fibroblasts derived from rat Achilles tendon was not directly affected by BPC 157 as evaluated by MTT assay. However, the survival of BPC 157-treated cells was significantly increased under the H(2)O(2) stress. BPC 157 markedly increased the in vitro migration of tendon fibroblasts in a dose-dependent manner as revealed by transwell filter migration assay. BPC 157 also dose dependently accelerated the spreading of tendon fibroblasts on culture dishes. The F-actin formation as detected by FITC-phalloidin staining was induced in BPC 157-treated fibroblasts. The protein expression and activation of FAK and paxillin were determined by Western blot analysis, and the phosphorylation levels of both FAK and paxillin were dose dependently increased by BPC 157 while the total amounts of protein was unaltered. In conclusion, BPC 157 promotes the ex vivo outgrowth of tendon fibroblasts from tendon explants, cell survival under stress, and the in vitro migration of tendon fibroblasts, which is likely mediated by the activation of the FAK-paxillin pathway.
51 10.2174/1381612826666200523180301
BPC 157 Rescued NSAID-cytotoxicity Via Stabilizing Intestinal Permeability and Enhancing Cytoprotection
May 23, 2020 Current Pharmaceutical Design Jong M Park + 3 more
The stable gastric pentadecapeptide BPC 157 protects stomach cells, maintains gastric integrity against various noxious agents such as alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), and exerts cytoprotection/ adaptive cytoprotection/organoprotection in other epithelia, that is, skin, liver, pancreas, heart, and brain. Especially BPC 157 counteracts gastric endothelial injury that precedes and induces damage to the gastric epithelium and generalizes "gastric endothelial protection" to protection of the endothelium of other vessels including thrombosis, prolonged bleeding, and thrombocytopenia. In this background, we put the importance of BPC 157 as a possible way of securing GI safety against NSAIDs-induced gastroenteropathy since still unmet medical needs to mitigate NSAIDs-induced cytotoxicity are urgent. Furthermore, gastrointestinal irritants such as physical or mental stress, NSAIDs administration, surfactants destroyer such as bile acids, alcohol can lead to leaky gut syndrome through increasing epithelial permeability. In this review article, we described the potential rescuing actions of BPC 157 against leaky gut syndrome after NSAIDs administration for the first time.
10.1096/fasebj.29.1_supplement.771.13
BPC 157 Counteracts Convulsions after Continuous Haloperidol Overdose Administration in Rats
Apr 1, 2015 The FASEB Journal Domagoj Drmic + 5 more
Aim. We focused on haloperidol induced convulsions in rats and stable gastric pentadecapeptide BPC 157. BPC 157 is an antiulcer peptide tested in clinical trials, for inflammatory bowel disease and multiple sclerosis, showing particular central effects, affecting brain 5-HT release, particularly in substantia nigra, counteracting amphetamine-acute and chronic disturbances as well as gastric lesions and catalepsy induced by various neuroleptics, particularly haloperidol. However, BPC 157 was not tested against continuous application of haloperidol throughout 14 days, in a haloperidol over-dose of the 25 mg/kg/day ip that might induce progressive convulsions. Materials and methods. Rats were daily monitored and filmed 10 minutes before and throughout next 2h after haloperidol administration (25 mg/kg ip) for convulsions presentation (sec), BPC 157 was given (10μg/kg, 10ng/kg i.p.) immediately after haloperidol as described (Jelovac et al., Eur J Pharmacol. 1999;379(1):19-31; Sikiric et al. Curr Pharm Des. 2014;20(7):1126-35.). Results. Convulsions were consistently attenuated since day 1 (means±SD, i.e., for first 30 min 70±10 sec μg vs. 150±10 sec control *P<0.05, at least); day 4, (i.e., for first 30 min 350±30 sec μg vs. 750±40 sec control *P<0.05, at least), day 7, (i.e., for first 30 min 500±30 sec μg vs. 850±40 sec control *P<0.05, at least), day 14, (i.e., for first 30 min 300±30 sec μg vs. 950±40 sec control *P<0.05, at least). Conclusions. Applied after haloperidol, the deleterious course was attenuated after BPC 157 administration, and particularly, severe haloperidol convulsions markedly attenuated. Supported by Grant 108-1083570-3635, Croatia.
Antinociceptive Effect of BPC-157 in the Formalin-induced Pain Model
Jun 30, 2021 Kosin Medical Journal Sang Yoong Park + 6 more
Objectives Body protective compound-157 (BPC-157) is a stable gastric pentadecapeptide that has been effective in trials aiming to increase wound healing capabilities and decrease inflammatory cell influx, including studies on the healing of muscles and tendons. There are no studies about the effect of BPC-157 on pain transmission via nociception. This study examined the antinociceptive effects of BPC-157 using formalin tests and immunohistochemistry. Methods Rats were randomly divided into the control, morphine and BPC-157 groups. Pain behavior was quantified periodically at 5- and 35- min intervals (representative values of phases 1 and 2) by counting the number of flinches exhibited by the injected paw after injection. The dorsal root ganglia (DRG) and spinal cords (SC) were collected, and then, the number of cytokine-positive cells was determined via immunostaining. Results BPC-157 dose-dependently decreased the number of flinches during phase 1 but did not decrease the number of flinches during phase 2. During phase 1, interleukin-1β (IL-1β) in the DRG tissue was significantly different in the morphine, 10 μg/kg BPC-157, and 20 μg/kg BPC-157 groups. During phase 2, statistical significance was achieved in the DRG tissue in the morphine, 20 μg/kg BPC-157, and 40 μg/kg BPC-157 groups. During phase 1, interleukin-6 was significantly different in the DRG tissue in the morphine group and the SC tissue in the 10 μg/kg BPC-157 group. During phase 2, statistical significance was achieved in the morphine group and the BPC-157 20 μg/kg group in both the DRG and SC tissues. There were no significant differences in tumor necrosis factor-α between the DRG and SC tissues. Conclusions BPC-157 was effective during phase 1 but not during phase 2, as determined by the formalin test. BPC-157 decreased the expression of IL-1β in the DRG tissue in phases 1 and 2.