Use and Preparation of CD206 Small Molecule Modulators as Therapeutics for CD206-Expressing Cancers

Pancreatic ductal adenocarcinoma (PDA) accounts for more than 90% of pancreatic cancer cases, and it is one of the most aggressive malignancies with a 5-year survival rate of 6%. The high mortality rate caused by PDA is primarily from the lack of early diagnosis – it is often asymptomatic in early stages – and a poor response to conventional chemotherapy and radiotherapy. The major immune cell type present in the PDA microenvironment is a subset of macrophages commonly termed tumor-associated macrophages (TAM). TAMs originate from circulating monocytes upon activation by CCL2, a chemotactic chemokine secreted and then recruited to the tumor microenvironment by cytokines expressed by PDA cells.TAMs consist primarily of polarized M2 macrophages which promote tumor growth by secreting immunosuppressive factors that block effector T-cell activation. TAMs also express scavenger receptors such as CD206 which facilitate tumor angiogenesis and migration. CD206 is a member of the large C-type lectin receptor family which can target and modulate the M2-like macrophages. CD206high expression has been associated with poor clinical outcomes in pancreatic cancer and other solid organ cancers. Current anti-macrophage therapy generally inhibits activation or the recruitment of macrophages (CCL2/CCR2), but lacks specificity towards M2-like macrophages.Researchers at the National Cancer Institute (NCI) have discovered a small molecule that binds to CD206 and induces M2 phagocytosis and cel...
Source: NIH OTT Licensing Opportunities - Category: Research Authors: Source Type: research