BPC 157 (acetate)
(Synonyms: GEPPPGKPADDAGLV, Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val) 目录号 : GC46946
A pentadecapeptide with diverse biological activities
Cas No.:1628202-19-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Body protection compound 157 (BPC 157) is a pentadecapeptide fragment of BPC that has been found in gastric juice and has diverse biological activities.1 It increases cell migration of, and F-actin formation in, primary rat tendon fibroblasts when used at a concentration of 2 µg/ml.2 BPC 157 (0.01 and 10 µg/kg, i.p.) reduces paw swelling, bone erosion, and inflamed joint mononuclear cell infiltration in a rat model of rheumatoid arthritis induced by complete Freund's adjuvant (CFA).3 It decreases the lesion size of gastric ulcers induced by indomethacin , aspirin , or diclofenac in rats at the same doses. BCP 157 (0.01 and 10 µg/kg, i.p.) decreases the duration of catalepsy and reduces tremor severity in a mouse model of Parkinson's disease induced by MPTP.4
1.Sikiric, P., Seiwerth, S., Rucman, R., et al.Brain-gut axis and pentadecapeptide BPC 157: Theoretical and practical implicationsCurr. Neuropharmacol.14(8)857-865(2016) 2.Chang, C.-H., Tsai, W.-C., Lin, M.-S., et al.The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migrationJ. Appl. Physiol.110(3)774-780(2011) 3.Sikiric, P., Seiwerth, S., Grabarevic, Z., et al.Pentadecapeptide BPC 157 positively affects both non-steroidal anti-inflammatory agent-induced gastrointestinal lesions and adjuvant arthritis in ratsJ. Physiol. (Paris)91(3-5)113-122(1997) 4.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-tetrahydropyridineJ. Physiol. (Paris)93(6)505-512(1999)
| Cas No. | 1628202-19-6 | SDF | |
| 别名 | GEPPPGKPADDAGLV, Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val | ||
| Canonical SMILES | C[C@@H](C(N[C@@H](CC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](C)C(NCC(N[C@@H](CC(C)C)C(N[C@H](C(O)=O)C(C)C)=O)=O)=O)=O)=O)=O)NC([C@@H]1CCCN1C([C@@H](NC(CNC([C@H]2N(C([C@@H]3CCCN3C([C@@H]4CCCN4C([C@@H](NC(CN)=O)CCC(O)=O)=O)=O)=O)CCC2)=O)=O)CCCCN)=O)=O.CC(O)=OC[C@@H](C(N[C@@H](CC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](C)C(NCC(N[C@@H](CC(C)C)C(N[C@H](C(O)=O)C(C)C)=O)=O)=O)=O)=O)=O)NC([C@@H]1CCCN1C([C@@H](NC(CNC([C@H]2N(C([C@@H]3CCCN3C([C@@H]4CCCN4C([C@@H](NC(CN)=O)CCC(O)=O)=O)=O)=O)CCC2)=O)=O)CCCCN)=O)=O.CC(O)=O | ||
| 分子式 | C62H98N16O22.XC2H4O2 | 分子量 | 1419.5 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.7045 mL | 3.5224 mL | 7.0447 mL |
| 5 mM | 0.1409 mL | 0.7045 mL | 1.4089 mL |
| 10 mM | 0.0704 mL | 0.3522 mL | 0.7045 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats
World J Gastroenterol 2004 Apr 1;10(7):1032-6.PMID:15052688DOI:10.3748/wjg.v10.i7.1032.
Aim: To investigate the protective effects of gastric pentadecapeptide BPC 157 on acute and chronic gastric ulcers in rats and to compare the results in therapy of human gastric ulcers by different administration methods. Methods: Gastric pentadecapeptide BPC 157 was administered (initial single or continuous administration) into rats either intragastrically or intramuscularly before (induced acute gastric ulcer) or after (induced chronic gastric ulcer) the applications of inducing agents, and each animal was sacrificed to observe the protective effects of BPC 157 on gastric ulcers. Results: Both intramuscular (im) and intragastric (ig) administration of BPC 157 could apparently reduce the ulcer area and accelerate the healing of induced ulcer in different models and the effect of im administered BPC 157 was better than that of ig. The rats treated with higher dosages (400 ng/kg, 800 ng/kg) of BPC 157 (im and ig) showed significantly less lesion (P<0.01 vs excipient or saline control), the inhibition ratio of ulcer formation varied between 45.7% and 65.6%, from all measurements except 400 ng/kg BPC 157 in pylorus ligation induced model (P<0.05), in which the inhibition rate was 54.2%. When im administered (800 ng/kg BPC 157) in three models, the inhibition ratio of ulcer formation was 65.5%, 65.6% and 59.9%, respectively, which was better than that of famotidine (its inhibition rate was 60.8%, 57.2% and 34.3%, respectively). Continuous application of BPC 157 (in chronic acetate induced gastric ulcer) could accelerate rebuilding of glandular epithelium and formation of granulation tissue (P<0.05 at 200 ng/kg and P<0.01 at 400 ng/kg and 800 ng/kg vs excipient or saline control). Conclusion: Both im and ig administered gastric pentadecapeptide BPC 157 can apparently ameliorate acute gastric ulcer in rats and antagonize the protracted effect of acetate challenge on chronic ulcer. The effect of im administration of BPC 157 is better than that of ig, and the effective dosage of the former is lower than that of the latter.
Clopidogrel-Induced Gastric Injury in Rats is Attenuated by Stable Gastric Pentadecapeptide BPC 157
Drug Des Devel Ther 2020 Dec 21;14:5599-5610.PMID:33376304DOI:10.2147/DDDT.S284163.
Aim: Although Clopidogrel is safe in healthy volunteers, it can induce recurrence of gastric ulcers in high-risk patients. Here, we investigated the protective effect of the natural product, stable gastric pentadecapeptide 157 (BPC 157) on Clopidogrel-induced gastric injury. Methods: We used acetic acid to induce gastric ulcer in Sprague Dawley rats. Clopidogrel alone or in combination with BPC 157 or L-NAME (nitric oxide system blockade) were administered after healing of acetic acid-induced ulcer. One percent methylcellulose solution was used as control. Ulcer recurrence rate and the ulcer index were compared between these groups. Gastric mucosal apoptosis rate, microscopic inflammation activity and angiogenesis markers vascular endothelial growth factor A (VEGF-A) and CD34 were examined by TUNEL, histological evaluations (HE) and immunohistochemistry (IHC). Pathways involved, expressions of endoplasmic reticulum (ER) stress apoptosis marker CHOP, angiogenic markers VEGF-A and its receptor VEGFR1, and endothelial NO synthase (eNOS) were all analyzed by Western blot. Results: This study indicated that Clopidogrel significantly induced the gastric ulcers recurrence, severe inflammation and ER stress related apoptosis of the gastric mucosa, suppressed the synthesis of angiogenic markers and eNOS. Furthermore, Clopidrogel intervention resulted in the activation of protein kinase B (AKT) and p38 mitogen-activated protein kinase (p38/MAPK). BPC 157 attenuated the gastric mucosal damage caused by Clopidogrel and reversed these molecular effects. However, NO blockade L-NAME weakened the protective effect and thus the molecular effects of BPC 157 on gastric mucosa. Conclusion: In conclusion, these results suggest that BPC 157 inhibited Clopidogrel-induced gastric mucosa injury partially by inhibition of gastric mucosa cell ER stress-mediated apoptosis and inflammation, and promoting gastric mucosa angiogenesis via VEGF-A/VEGFR1 mediated-AKT/p38/MAPK signaling pathways.
BPC157 as Potential Agent Rescuing from Cancer Cachexia
Curr Pharm Des 2018;24(18):1947-1956.PMID:29898649DOI:10.2174/1381612824666180614082950.
Cancer cachexia, one of the metabolic syndromes caused by cancer, is a devastating and miserable condition encountered in more than 50% of terminal cancer patients presenting with significant weight loss associated with skeletal muscle atrophy and fat loss. Though cachexia may account for up to 20% of cancer deaths, no significant treatment is still lacking and is of urgent unmet medical need in cancer treatment. Therefore, understanding the underlying molecular mechanisms is essential for anticipating therapeutic approaches. Since the primary events driving cachexia are mediated via either the central nervous system relatedor inflammation related-anorexia, hypoanabolism, and hypercatabolism, therapy usually targets nutritional support to compensate reduced food intake along with some anti-inflammatory agents to cover specific inflammation-related metabolic derangement, and encourages exercise to supplement reduced physical activity, but all proven to be not so effective so far. Therefore, combination therapies such as a standard multi-modal package including an anorexic agent, megestrol acetate, and anti-inflammatory agent coupled with the development of potential novel therapeutics promise a new era in rescuing patients from cancer cachexia. In this review, we propose the potential application of BPC157, one of the active cytoprotective agents isolated from gastric juices for cancer cachexia. Before clinical trial, we introduced the evidence showing BPC157 rescued from cancer cachexia supported with explored mode of actions.