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In the initial screening, we used inflammatory cytokine\u2010induced atrophy of C2C12 myotubes as a phenotypic screening platform to assess the protective effects of TCMs. The selected TCMs were then evaluated for their abilities to protect\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                      <\/jats:styled-content>\n                      from age\u2010related reduction of mobility and contractility, followed by the C\u201026 colon adenocarcinoma mouse model of cachexia to confirm the anti\u2010muscle atrophy effects (body\/skeletal muscle weights, fibre size distribution, grip strengths, and serum IL\u20106). Transcriptome analysis, quantitative real\u2010time polymerase chain reaction, and immunoblotting were performed to gain understanding of the potential mechanism(s) by which effective TCM protected against C26 tumour\u2010induced muscle atrophy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Of 29 widely used TCMs,\n                      <jats:italic>Dioscorea radix<\/jats:italic>\n                      (DR) and Mu Dan Pi (MDP) showed a complete protection (all\n                      <jats:italic>P<\/jats:italic>\n                      values, 0.0002) vis\u2010\u00e0\u2010vis C26 conditioned medium control in the myotube atrophy platform. MDP exhibited a unique ability to ameliorate age\u2010associated decreases in worm mobility, accompanied by improved total body contractions, relative to control (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001 and &lt;0.01, respectively), which, however, was not noted with DR. This differential\n                      <jats:italic>in vivo<\/jats:italic>\n                      protective effect between MDP and DR was also confirmed in the C\u201026 mouse model. MDP at 1000\u00a0mg\/kg (MDP\u2010H) was effective in protecting body weight loss (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.05) in C\u201026 tumour\u2010bearing mice without changing food or water intake, accompanied by the restoration of the fibre size distribution of hindleg skeletal muscles (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.0001) and the forelimb grip strength (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0&lt;\u00a00.05). MDP\u2010treated C\u201026\u2010tumour\u2010bearing mice were alert, showed normal posture and better body conditions, and exhibited lower serum IL\u20106 levels (\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a00.06) relative to vehicle control. This decreased serum IL\u20106 was associated with the\n                      <jats:italic>in vitro<\/jats:italic>\n                      suppressive effect of MDP (25 and 50\u00a0\u03bcg\/mL) on IL\u20106 secretion into culture medium by C26 cells. RNA\u2010seq analysis, followed by quantitative real\u2010time polymerase chain reaction and\/or immunoblotting, shows that MDP's anti\u2010cachectic effect was attributable to its ability to reverse the C\u201026 tumour\u2010induced re\u2010programming of muscle homoeostasis\u2010associated gene expression, including that of two cachexia drivers (MuRF1 and Atrogin\u20101), in skeletal muscles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>All these findings suggest the translational potential of MDP to foster new strategies for the prevention and\/or treatment of cachexia. The protective effect of MDP on other types of muscle atrophy such as sarcopenia might warrant investigations.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcsm.13028","type":"journal-article","created":{"date-parts":[[2022,6,19]],"date-time":"2022-06-19T22:35:33Z","timestamp":1655678133000},"page":"2073-2087","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Development of a traditional Chinese medicine\u2010based agent for the treatment of cancer cachexia"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5920-0064","authenticated-orcid":false,"given":"Kun\u2010Chang","family":"Wu","sequence":"first","affiliation":[{"name":"School of Pharmacy, College of Pharmacy China Medical University  Taichung Taiwan"},{"name":"Research Center for Healthy Aging China Medical University  Taichung 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