Jul 2, 2026 · 23 min · 8 segments
We love to hear from our listeners. Send us a message. Episode 132 of Cell & Gene: The Podcast features Host, Erin Harris' conversation with…
Jay HartenbachGuestErin HarrisHostSo we know it's a patient-derived double-loaded dendritic cell immunotherapy, and it combines a patient's own dendritic cells with mRNA and proteins for-- from freshly obtained tumor specimens.
So, okay, how-- from your perspective, how does this double-loaded design address key limitations that have really historically restrained dendritic cell therapies in our space?
Y-yeah, I think, you know, to start, the, the first differentiator is that we believe, and, and what we are seeing clinically, is that we're actually generating a significant immune response.
Uh, dendritic cells have somewhat the reputation that they are really safe, but they are not effective, and Diakonos is hoping to change that narrative with DOC-1021 and this double-loaded approach.
Uh, that's unique to us, and we believe is really the secret sauce as to why dendritic cells have not worked in the past and why we're actually able to generate a very powerful immune response, uh, in general.
And so when we look at prior dendritic cell therapies, you really could put them into two different groups.
There's a couple that, that tried some, uh, you know, really, uh, off the charts approaches, but most approaches were either taking the patient's tumor-derived lysate or mRNA and loading that into the dendritic cell.
And when we think about dendritic cells, they're the master regulator of adaptive immunity.
And so the thought behind dendritic cells was, if we can get dendritic cells to recognize the cancer as a threat, then we'll get the benefits of a complete top-down immune response.
You know, if you talk to most immunologists, and you ask them, "If you could get dendritic cells to work, would that be an ideal immunotherapy modality?" And, and the large consensus, if not all, would say yes, but it's that if.
And so these single-loaded approaches that were either using the tumor-derived lysate or mRNA were not, uh, stimulating or activating the, the dendritic cell in a way that ultimately initiated an immune response.
And so this double-loaded approach really came about somewhat serendipitously by our chief science officer.
He was building dendritic cell vaccines, uh, for patients in a-- or, or for preclinical samples and was just trying different approaches, you know, loading via lysate and loading via mRNA.
And he thought one day, "What happens if you do both at the same time? What if ha- what happens if you load the mRNA and the lysate simultaneously? Do you get this one plus one equals two effect or, or maybe even a little bit better?" And what his initial experiment showed was that one plus one equals 11, right? The double-loaded dendritic cells were demonstrating an 11 times greater, uh, cytotoxic immune response that had been activated by those dendritic cells.
And what he ultimately discovered was by doing the double loading, we were effectively mimicking a viral infection in dendritic cells.
And so we take a step back, and we think about how a virus infects a dendritic cell or how the body even detects a viral infection, which is through dendritic cells.
You'd have the virus directly infecting the dendritic cell, where the mRNA would ultimately get passed and transcribed by the nucleus.
So we know it's a patient-derived double-loaded dendritic cell immunotherapy, and it combines a patient's own dendritic cells with mRNA and proteins for-- from freshly obtained tumor specimens.
So, okay, how-- from your perspective, how does this double-loaded design address key limitations that have really historically restrained dendritic cell therapies in our space?
Y-yeah, I think, you know, to start, the, the first differentiator is that we believe, and, and what we are seeing clinically, is that we're actually generating a significant immune response.
Uh, dendritic cells have somewhat the reputation that they are really safe, but they are not effective, and Diakonos is hoping to change that narrative with DOC-1021 and this double-loaded approach.
Uh, that's unique to us, and we believe is really the secret sauce as to why dendritic cells have not worked in the past and why we're actually able to generate a very powerful immune response, uh, in general.
And so when we look at prior dendritic cell therapies, you really could put them into two different groups.
There's a couple that, that tried some, uh, you know, really, uh, off the charts approaches, but most approaches were either taking the patient's tumor-derived lysate or mRNA and loading that into the dendritic cell.
And when we think about dendritic cells, they're the master regulator of adaptive immunity.
And so the thought behind dendritic cells was, if we can get dendritic cells to recognize the cancer as a threat, then we'll get the benefits of a complete top-down immune response.
You know, if you talk to most immunologists, and you ask them, "If you could get dendritic cells to work, would that be an ideal immunotherapy modality?" And, and the large consensus, if not all, would say yes, but it's that if.
And so these single-loaded approaches that were either using the tumor-derived lysate or mRNA were not, uh, stimulating or activating the, the dendritic cell in a way that ultimately initiated an immune response.
And so this double-loaded approach really came about somewhat serendipitously by our chief science officer.
He was building dendritic cell vaccines, uh, for patients in a-- or, or for preclinical samples and was just trying different approaches, you know, loading via lysate and loading via mRNA.
And he thought one day, "What happens if you do both at the same time? What if ha- what happens if you load the mRNA and the lysate simultaneously? Do you get this one plus one equals two effect or, or maybe even a little bit better?" And what his initial experiment showed was that one plus one equals 11, right? The double-loaded dendritic cells were demonstrating an 11 times greater, uh, cytotoxic immune response that had been activated by those dendritic cells.
And what he ultimately discovered was by doing the double loading, we were effectively mimicking a viral infection in dendritic cells.
And so we take a step back, and we think about how a virus infects a dendritic cell or how the body even detects a viral infection, which is through dendritic cells.
You'd have the virus directly infecting the dendritic cell, where the mRNA would ultimately get passed and transcribed by the nucleus.
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