New data published supporting monotherapy activity of CCL2 inhibitor NOX-E36 in an additional solid tumor type: liver cancer
Data complements previously published results showing activity of NOX-E36 in pancreatic cancer
Berlin, Germany, February 1, 2019 – NOXXON Pharma N.V. (Euronext Growth Paris: ALNOX), a biotechnology company focused on improving cancer treatments by targeting the tumor microenvironment (TME), announced today the full publication by Bartneck et al. [Cell Mol Gastroenterol Hepatol, 2019; 7:371–390, link] of a series of experiments exploring the potential of CCL2 inhibition in liver cancer with mNOX-E36, a rodent version of NOXXON’s human CCL2 inhibitor NOX- E36. In a mouse model of hepatocellular cancer, researchers found that treatment with mNOX-E36 inhibited the infiltration of tumor-associated macrophages, which resulted in profound changes of the tumor microenvironment, reduced pathogenic vascularization, and reduced liver tumor volume. The article was also highlighted in an accompanying editorial commentary by Avila & Berasain (link).
The preclinical results suggest that blocking the recruitment of macrophages in the liver with an anti- CCL2 molecule such as NOX-E36 is a promising mechanism for the treatment of hepatocellular cancer, which – in addition to previously published data on pancreatic cancer (Lazarus et al., Ann Surg Oncol, 2017; 24 (suppl 1): p. S100) – is the second solid tumor for which monotherapy activity of mNOX-E36 has been demonstrated. The authors conclude that “the clear link between CCR2+ macrophages and pathogenic tumor vascularization supports the exploration of combination therapies (e.g., combining CCR2 or CCL2 inhibition with conventional HCC treatment modalities), and with novel PD1-directed immunotherapies.”