Kok Yung Lee

1 Introduction Complement therapeutics has evolved from limited applications in a few ultra-rare conditions to the application of complement inhibition to more common diseases [1]. C5 emerged early as a favoured therapeutic target; indeed, the first human C5-blocking monoclonal antibody (mAb) was reported in 1991 [2, 3]. Progress toward the clinic was spearheaded by the C5 blocking mAb eculizumab, FDA approved for paroxysmal nocturnal haemoglobinuria (PNH) in 2007.

Abstract The TNF-related apoptosis-inducing ligand (TRAIL) has potential as a therapeutic agent as it has previously been shown to induce apoptosis in triple-negative breast cancer. Recombinant human TRAIL has shown promise in pre-clinical studies of breast cancer. TRAIL exhibits specificity for triple-negative and treatment-resistant disease subsets. However, several studies have demonstrated that patient tumours exhibit resistance to TRAIL and TRAIL-receptor agonists.