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Current Pharmaceutical Design


ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Review Article

BPC157 as Potential Agent Rescuing from Cancer Cachexia

Author(s): Eun A. Kang, Young-Min Han, Jeong Min An, Yong Jin Park, Predrag Sikiric, Deok Hwan Kim, Kwang An Kwon, Yoon Jae Kim, Donghwa Yang, Hann Tchah and Ki Baik Hahm*

Volume 24 , Issue 18 , 2018

Page: [1947 - 1956] Pages: 10

DOI: 10.2174/1381612824666180614082950

Price: $65


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.

Keywords: Cancer cachexia, BPC157, muscle atrophy, cytoprotection, hypercatabolism, hypoanabolism.

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