• M402 modulated tumor-stroma interactions involved in metastatic and desmoplastic pathways in two pancreatic cancer models. • In the genetically engineered mouse model: • M402 in combination with gemcitabine prolonged survival, decreased metastases and local invasion, and inhibited epithelial-tomesenchymal transition. • In the orthotopic Capan-2 pancreatic cancer model: • M402 monotherapy showed a dose-dependent reduction in primary tumor weight, while M402 in combination with gemcitabine almost completely inhibited primary and metastatic tumor growth, which may be related to M402’s effect on SHH signaling. • These results provide a rationale for investigating the clinical use of M402.
A first-in-human study has been initiated that will evaluate the safety,pharmacokinetics, efficacy, and biomarker profiles of escalating M402 doses in combination with gemcitabine in patients with metastatic pancreatic cancer.
• M402 can inhibit angiogenesis, tumor progression and metastasis in animal models by modulating a variety of polysaccharide-based binding proteins, which may support the clinical investigation of M402 in a range of cancers.
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