Navidea Biopharmaceuticals, Inc. (AMEX:NAVB) Q3 2022 Earnings Call Transcript

Michael Rosol: Sure. So one of the interesting things of our constructs is what we’re doing is we’re attaching these known therapeutics like paclitaxel, doxorubicin and now bisphosphonate, which in general are known drugs, although importantly, we’ve created a novel bisphosphonate. So that’s also very exciting. But those drugs have known mechanisms of action. When they are attached to our molecule our Manocept platform and delivered through the CD206 pathway. They actually have different mechanisms of action than the free drugs themselves. And what they’re doing is they are actually changing the phenotype of the macrophage rather than doing what they do as pure cancer drugs for example, the paclitaxel and doxorubicin, they’re not achieving their effect in that same way where they go in and stop cell division or call it death.

They’re actually going into the macrophage and changing the phenotype. In this case more, or in these cases more towards the pro-inflammatory type, which rallies and stimulates the body’s immune response in our animal models against the tumors. And this is very exciting. So we had a number of questions related to that, that mechanism of action and that led to a lot of excitement. And then the results themselves, and I’ll post the poster onto our website in the coming days we’re posting the American College of Rheumatology posters on the website later today or tomorrow as well. You can look at the poster. But in our data, what we’ve done is not only are we driving the phenotype more towards the pro-inflammatory state, but we’re also having other effects, like we’re reducing the SIRPalpha signal, which relates to the macrophage €“ I’m sorry, the tumor cell don’t eat me signal.

So what we’re doing is we’re SIRPalpha, which would then work in a roundabout way to €“ get over the hurdle that the tumor cells present, where they stop the macrophages from eating them, basically keeping things simple. So we have a kind of €“ we have a surprising and really cool, unexpected additional mechanism of action that’s really on the cutting edge immunotherapy’s and cancer. So not only do we, can we drive the phenotype a certain way in so doing, we’re actually stimulating the phenotype in a way that is the €“ at the leading edge of what’s going on in the immunooncology space. So we had a large number of people who were very excited by that. And the encouraging thing for this small company from Columbus, Ohio or Dublin, Ohio specifically is worth the forefront €“ out data alright.

They’re the forefront of this kind of medicine. So our need is to get the accelerant as I said earlier, to drive these things more rapidly into the clinic. But the technology is there, the science is there, and we’re doing all we can to advance it, uh, as rapidly as possible, but it’s really very exciting.

Mike Rigali: So would that forefront, would that kind of like we be driving the CD163 as an example?