Cachexia is a multifactorial syndrome characterized by progressive loss of skeletal muscle and adipose tissue. Cachexia is observed in the later stages in most types of cancer with a high prevalence in pancreatic cancer. Approximately, 50-80% of cancer patients suffer from cachexia regardless of the type of cancer and around 20% of cancer deaths are due to cachexia. It is attributed to increased catabolism and decreased anabolism of the skeletal muscle and increased lipolysis in adipose tissue. This leads to impaired functional activity and quality of life. Pro-inflammatory and pro-cachectic factors produced by tumor cells are thought to mediate weight loss. In addition, it has been recently proposed that tumor-derived exosomes also play an important role in cancer-associated cachexia. Exosomes are nanovesicles ranging from 30-150 nm in diameter secreted from multiple cells and contain various biomolecules reflecting their cellular origin. In this study, the role of exosome in cross-talk between tissues was studied. Cachexia causing cancer cell (C26)-derived exosomes were isolated by differential centrifugation coupled with ultracentrifugation. The isolated exosomes were characterized by Western blotting and electron microscopy. To understand the protein cargo that regulates cancer cachexia, quantitative proteomics analysis was performed on the isolated exosomes. The analysis highlighted the presence of many exosomal markers as well as cachexia inducing factors.