Sona Nanotech Inc (CSE:SONA, OTCQB:SNANF) chief medical officer Dr Carman Giacomantonio talked with Proactive about the company’s latest findings related to its targeted hyperthermia therapy (THT), which he described as showing “very enabling immunogenic” effects in recent experiments.
The THT platform works by delivering controlled heat to the core of a tumour, triggering a natural cell death response and activating the body's immune system.
Giacomantonio explained that this process exposes tumour proteins to immune cells, increasing the chance that they will be recognised and attacked.
He noted that “all cancer cells have this kind of evolutionary quality” of resisting cell death, but THT stresses the cells enough to induce it.
Looking ahead, he said the company plans to expand testing to demonstrate systemic immune responses, with the goal of treating metastatic cancers by targeting a single tumour site.
Proactive: Hello. You're watching Proactive. Joining me is Sona Nanotech Chief Medical Officer, Dr Carman Giacomantonio. Carman, very good to speak with you. You're up with an update on your targeted hyperthermia therapy or THT. And it looks pretty encouraging.
Dr Carman Giacomantonio: Yeah. We're very excited about this latest round of experiments. So THT, or targeted hyperthermia, as you know, is really what we're doing — we're driving heat, very controlled heat, kind of fever temperature in 42 to 48 degrees into the core of a tumor. And in doing so, we're stressing the tumor cancer cells specifically to enter into a death cycle.
It's a natural evolutionary phenomenon that we've taken advantage of through this kind of very precise technology. And in doing so, when it triggers that targeted cell death, the natural innate immune response to the heat is to generate a clearing phenomenon where immune cells come in, dissolve or eat up the cancer cells, and then in the process, introduce anything that's abnormal about those cells to the immune system. That's where the core of the immunity lies.
So is it really targeting, I suppose, immunotherapy-resistant cancer cells or tumors?
You know, so it's not resistant — that's again the beauty of it. It's in fact targeting any cancer cell. All cancer cells have this kind of evolutionary quality, if you will. Cancer cells naturally don't die. That's the biggest mistake in a cancer cell — it doesn't have the programmed cell death trigger anymore.
But they are fragile. And stress, particularly heat stress, activates a protein-driven process called heat shock protein. Those heat shock proteins trigger a lot of pathways, and one of them is cell death. So it doesn't matter whether the cancer is immune-sensitive. This could be even an immune-sensitive cancer — this would trigger that cell death.
A cancer that's sensitive to immunotherapy is sensitive because the protein that makes up the cancer is recognized by the host's immune system. A cancer that isn't immune-sensitive just hasn't been seen in that way. The abnormal protein that's associated with the development of a cancer is no longer or it has not been recognized. And so what this does is present innumerable proteins to the immune system, and the odds are that one of those proteins will be interesting enough to the immune system to pursue.
So Carman, this builds on preliminary results that you released back in December. That was in a colorectal study. Does this give you increased confidence in the THT?
Oh, absolutely. What we did was we repeated the experiments. We added in extra numbers — reproducibility is a big part of science. In repeating the experiments and increasing the numbers and seeing the exact same response in the data, one would see that if we treated the tumors with a control, which is nothing — just saline — or if we treated the tumors with a standard checkpoint inhibitor, so a standard immune therapy that essentially turns off the controls and the checks and balances so the immune system is enabled to pursue whatever it can see… in either of those cases, the tumor just grew without any inhibition.
And then when we treated the tumors with the targeted hyperthermia and then exposed them to the same immune modulating agent — the checkpoint inhibitor called a PD1 (programmed death receptor 1) inhibitor — it led to absolute complete control, prevention of tumor growth. And in fact, it completely flattened a number of the tumors. So it was very enabling immunogenic.
Carman, what are the next steps then?
So the next steps are — we're continuing to do this. We're expanding it into the model. What we're intending to show is that the immunity we've generated in this model will prevent new tumors from growing. And when generated in a single tumor, it will treat any other tumors that are growing. So we're treating metastatic — this is essentially a metastatic model — but we're treating multiple tumors now by just activating immunity in a single tumor.
So this is what people talk about — abscopal effects — an effect beyond the targeted tumor. The hypothesis we're working on is that if we were to treat a single tumor in a patient, we can generate a generalized systemic response by activating immunity in that single tumor.
Quotes have been lightly edited for clarity and style