DUBLIN, Ohio–(BUSINESS WIRE)–Navidea Biopharmaceuticals, Inc. (NYSE American: NAVB) (“Navidea” or the “Company”), a company focused on the development of precision immunodiagnostic and immunotherapeutic agents, today announced the publication of a manuscript entitled “Increased Macrophage Specific Arterial Inflammation has a unique relationship with non-calcified plaque and specific immune activation pathways in people with HIV: a targeted molecular imaging approach,” based on work conducted at Massachusetts General Hospital (“MGH”) and Harvard Medical School, Boston MA, and sponsored by the company. The research, which appears in The Journal of Infectious Diseases (PMID: 35856671), was led by lead investigator Steven Grinspoon, MD, chief of the Metabolism Unit at Mass General Hospital and professor of medicine at Harvard Medical School.
Sustained immune activation and downstream macrophage-specific arterial infiltration are believed to contribute to an increased risk of atherosclerotic (plaque) cardiovascular disease in people with HIV receiving antiretroviral therapy (“ART”). In this study, Tc99m tilmanocept imaging was applied to investigate macrophage-specific arterial inflammation in participants with versus matched participants without HIV. It was hypothesized that people with HIV would exhibit higher levels of aortic arterial inflammation in relation to atherosclerotic plaque and immune activation.
The results showed that patients with HIV who received antiretroviral therapy (N=20) had significantly higher macrophage-specific arterial inflammation demonstrated by Tc99m tilmanocept than matched people without HIV (N=10). Total, non-calcified and calcified aortic plaque volume calculated from CT scans did not differ significantly between the groups. Macrophage-specific arterial inflammation related to non-calcified plaque in HIV patients (and not in participants without HIV) and furthermore related to levels of specific inflammatory markers. The uptake of Tc99m tilmanocept into the aorta was significantly higher at different uptake thresholds in participants with HIV (p=0.03) and showed a stronger association between arterial inflammation and non-calcified plaque volume (p=0.0001 for HIV interaction status and plaque volume) but not calcified plaque volume (P=0.83 for interaction). In people with HIV (and not in participants without HIV), the volume of non-calcified aortic plaque was directly related to aortic Tc99m tilmanocept uptake at different uptake thresholds.
Macrophage-specific arterial inflammation, quantified using a novel molecular imaging approach, was higher in patients with HIV on ART compared to matched participants with similar atherosclerotic cardiovascular risk without HIV. Arterial inflammation related to non-calcified plaque volume only in patients with HIV. Cellular biomarkers of inflammation are also associated with macrophage-specific arterial inflammation. These important immune pathways may contribute to an increased risk of cardiovascular disease in people with HIV and are thus relevant for identifying new therapies.
These data suggest that increased macrophage-specific arterial inflammation of uncalcified plaque may be a mechanism of increased cardiovascular risk in people with HIV. Using Tc99m tilmanocept imaging may help identify future targets for new immunomodulatory therapies to reduce the risk of atherosclerotic cardiovascular disease in people with HIV on ART.
dr. Michael Rosol, Chief Medical Officer of Navidea, said: “We are delighted to have completed this important work with Dr. Grinspoon at MGH. This is another one of the research collaborations we’ve had with top-level researchers at leading institutions.” dr. Rosol continued: “Today’s announcement is an example of the broad reach of our tilmanocept platform. The development of applications of Tc99m tilmanocept as a biomarker in people with HIV could have far-reaching implications for patient management and therapeutic benefit decision making.”
dr. Grinspoon said: “This study provides another important evidence of increased arterial inflammation in relation to monocytes and activation and important innate immune activation pathways in people living with HIV. Tilmanocept may be useful to assess new immunomodulatory strategies to reduce inflammation and reduce the risk of cardiovascular disease in PWH.”
Navidea Biopharmaceuticals, Inc. (NYSE American: NAVB) is a biopharmaceutical company focused on the development of accurate immunodiagnostic and immunotherapeutic agents. Navidea is developing multiple precision-focused products based on its Manocept platform to improve patient care by identifying the sites and pathways of disease and enabling better diagnostic accuracy, clinical decision-making and targeted treatment. Navidea’s Manocept platform is based on the ability to specifically target the CD206 mannose receptor expressed on activated macrophages. The Manocept platform serves as the molecular backbone of Tc99m tilmanocept, the first product developed and marketed by Navidea based on the platform. Navidea’s strategy is to deliver superior growth and shareholder returns by bringing new products to market and advancing the company’s pipeline through global collaboration and commercialization. For more information, visit www.navidea.com.
This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. We have based these forward-looking statements largely on our current expectations and projections about future events and financial trends affecting the financial condition of our company. Forward-looking statements include our expectations with respect to pending lawsuits and other matters. These forward-looking statements are subject to a number of risks, uncertainties and assumptions, including, but not limited to: our history of operating losses and uncertainty about future profitability; the final outcome of any pending lawsuits; our ability to successfully complete research and further development of our drug candidates; the timing, cost and uncertainty of obtaining regulatory approvals for our drug candidates; our ability to successfully commercialize our drug candidates; reliance on royalties and grant income; our ability to implement our growth strategy; expected trends in our business; our limited product line and distribution channels; advances in technologies and development of new competitive products; our ability to comply with NYSE American rolling listing standards; our ability to maintain effective internal control over financial reporting; the impact of the current coronavirus pandemic; and other risk factors described in our most recent Annual Report on Form 10-K and other SEC filings. You are urged to read the disclosures in our SEC filings, which are available at: http://www.sec.gov or at http://ir.navidea.com.
Investors are urged to consider statements containing the words “will”, “may”, “should”, “should”, “plan”, “continue”, “intended”, “target”, “forecast”, “future”. ” contain. “believe”, “intend”, “expect”, “anticipate”, “estimate”, “project” and similar expressions, as well as the negatives of those words or other similar words, as uncertain forward-looking statements.
You are cautioned not to place undue reliance on forward-looking statements, all of which could prove to be incorrect. We undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events or otherwise after the date of this report. In light of these risks and uncertainties, the forward-looking events and conditions discussed in this report may not materialize and actual results could differ materially from those expected or implied in the forward-looking statements.