Skeletal muscle exists in a state of continuous synthesis and breakdown of muscle proteins in order to preserve normal metabolic and locomotive functioning. Hormones are well established regulators of this homeostatic process. Chronic systemic inflammation can dysregulate skeletal muscle homeostasis via the disruption of endocrine signalling pathways. This can result in skeletal muscle atrophy, which is strongly implicated in the pathogenesis of type 2 diabetes and sarcopenia. Improving our understanding of the mechanisms underlying this process is therefore important in order to develop novel pharmacological agents capable of preventing skeletal muscle mass loss and disease progression. We have subsequently developed a cell model that simulates this pro-inflammatory state in vitro utilising immortalised human myoblasts (LHCN-M2). We demonstrate that treatment of LHCN-M2 cells with the pro-inflammatory cytokine tumour necrosis factor alpha (TNFα) decreases myoblast proliferation and myotube formation in a dose-dependent manner. The addition of 10 ng/ml, 20 ng/ml and 30 ng/ml TNFα to LHCN-M2 myoblasts for 48 h decreased cell proliferation by 16%, 22% and 31% respectively (r = −0.778, n = 32, P <.001). Similarly, the addition of 2.5 ng/ml, 5 ng/ml and 10 ng/ml TNFα to myoblasts after 7 days of differentiation for 72 h decreased myotube formation by 47%, 59% and 97% respectively (r = −0.911, n = 26, P <.001). We also show that it is possible to pharmacologically modulate the anti-proliferative activity of TNFα, providing a platform for the screening and identification of novel therapeutic avenues to prevent or treat skeletal muscle atrophy.