Navidea Biopharmaceuticals Announces Acceptance of Abstract for Presentation at the Tumor Myeloid-Directed Therapies Summit Annual Meeting
Navidea Biopharmaceuticals (AMEX: NAVB) announced the acceptance of its abstract for a poster presentation at the Tumor Myeloid-Directed Therapies Summit scheduled for June 14-16, 2022, in Boston, MA. The poster will highlight new bisphosphonate drug constructs developed using Navidea’s CD206-targeted drug delivery platform, Manocept. These constructs successfully shifted human macrophage phenotypes towards a proinflammatory state and significantly reduced SIRPα expression, which may enhance cancer immunotherapy applications. Chief Medical Officer Dr. Michael Rosol emphasized the potential of these constructs in treating severe illnesses.
- Acceptance of an abstract for a poster presentation at a significant summit.
- Development of novel bisphosphonate drug constructs shows promising results in changing macrophage behavior.
- Potential implications for enhanced cancer immunotherapy through targeted drug delivery.
- None.
The 2nd annual Tumor Myeloid-Directed Therapies Summit meeting will be held
The poster will present information related to the synthesis of two novel bisphosphonate drugs that have been attached to Navidea’s CD206-targeted drug delivery platform molecule, Manocept. These constructs use a novel degradable linker to release the therapy only once they have been internalized into a CD206-expressing cell, such as a tumor associated macrophage. The new therapeutic constructs were evaluated in human macrophage cell culture assays to compare the ability of the new constructs with unbound free therapy to shift the phenotype of macrophages toward a proinflammatory gene expression pattern. The new drug delivery constructs successfully shifted the phenotypes of human macrophages towards a proinflammatory state and compared favorably to the unbound free therapy. The new drug constructs also induced a highly significant reduction in macrophage expression of signal regulatory protein alpha (“SIRPα”), the receptor for the “don’t eat me” signal that, when activated, suppresses the ability of macrophages to attack and phagocytize disease associated cells such as cancer cells. The ability to induce this type of phenotypic change in macrophages could have far-reaching applications in cancer immunotherapy.
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