Dr. Robert Allen, PhD – CSO, Invivyd – Protection From Serious Viral Infectious Diseases
[Music] Welcome to another episode of Progress. potential and possibilities, discussions with fascinating people, designing a better tomorrow for all of us. I’m your host, Ira Panister. Welcome everybody again to another episode of our show. Today bringing another really awesome guest uh involved in science and technology and medicine, creating a better tomorrow for all of us. Uh today, um we have the honor of being joined on the show by Dr. Robert Allen, uh who is the chief scientific officer of Invivid. This is a company that we actually previously profiled about a year ago. They are really interesting biioharmaceutical company devoted to delivering protection uh from serious viral infectious diseases beginning with SARS cove 2 uh by deploying this really interesting and proprietary integrated technology platform to create best-in-class monoconal antibodies. Uh Dr. Allen brings over uh 30 years of experience across the infectious disease space. Most recently as chief scientific officer of smart farm therapeutics. They were a subsidiary of surrento therapeutics and during those initiatives he led various efforts to develop gene encoded monocine antibodies for co 19 that could ultimately be quickly adapted and respond to emerging variants of concern. Uh he also uh concurrently served as senior vice president of antiviral ankalytic imunotherapy development at Sarrento. Uh prior to this time Dr. Allen held multiple scientific uh roles across the pharmaceutical and biotech industry including others at Sarrento as well as at Sega Technologies also at the Oregon translational research and development institute. Uh Dr. Allen holds a PhD in microbiology from Columbia University as well as a master’s uh in applied biology from Georgia Institute of Technology, bachelor’s in biology from roads college. uh and he is ex extensively published in both the worlds of viology completed posttodoc training uh at Washington University in St. Louis and Emory um a lot of really cool topics to get into today a really interesting company uh Dr. Robert Allen, thank you so much for taking time to come on the show today. Thank you, Ira. It’s nice to be here. Nice to have a chance to talk. Absolutely. Absolutely. I I I enjoyed the first discussion I had about Invivid and I’m really looking forward to seeing how everything’s moved forward and and sort of reintroducing the the audience to to a lot of what you’re up to. Um before we go there though, is you know, we typically do I’d like to to hand things over to you to start off uh just to learn a little bit more about you. I I I was reading the you know even prior to your PhD you were uh when when you’re at Georgia Institute of Technology you were initially hanging out at CDC as a research microbiologist your dissertation on on some really interesting transcription factors of of TE-C cell development and then into your your posttock uh with gamma herpes viruses and and beta cell proliferation and the sort of the latent cell uh reservoirs of this virus everything got a really nice intersection of microbiology and immunology. would love to sort of hear the background of it all because it’s it’s fascinating and obviously perfect segue into where we’re going to be going within Vivid. Well, I I think I was lucky enough to be born in a place where nearby once I got to an age where I could put two and two together. Um there was the Centers for Disease Control. So, I was raised in Atlanta and um the CDC was a place where they were welcoming uh young people um in early in their scientific career. I was in my undergrad and I got on with the herpes virus branch under Phil Pellet at the time and they were just doing the the pathogen discovery and characterization for human herpes virus 6 and human herpes virus 7. um at the time you know PCR was a relatively new technology and as you know somebody coming into you know this idea of maybe working in the sciences maybe working in biology it was an incredibly exciting time uh you know for for me and then from there um there were some outbreaks of uh haunt viruses so bona viruses that uh that are synumbre virus was the virus we ended up working on there that moved moved over onto the team in special pathogens and worked on haunt virus outbreaks and then again very very exciting at that time in my career and in my life and then um Ebola virus outbreaks that occurred in the wake of that also um I was lucky enough to join those teams and to learn about how people very intently work on these types of um outbreak scenarios and at that point I ended up going um so at that point it had been mostly characterizing different viruses um and how the basic viology of those viruses, how they replicate, what virally encoded genes were important for replication, um what pathogenesis looked like in different model systems and how that may or may not recapitulate aspects of human disease from those viruses. So that kind of correlative work was all at CDC and then went off to graduate school uh did a did a masters at tech Georgia Tech while I was at CDC in a co-op program and that allowed me to you know again get a little bit more training on the the micro the classic microbiology end of things at tech while I was doing that work um worked on cytogallo virus at CDC as part of that mast’s project and looked at what is still one of the major major contributors to congenital disease um in our population that is cytogallo virus and that still remains in the transplant population and in neonates a considerable concern from a viral disease perspective and I I still reserve a little bit of time in my head for CMV you know to try to think about opportunities to to help out in that direction. There have been some recent small molecule um introductions into the market that have made a big difference in CMV which is nice to see. But um I went to grad school at Colombia uh studied in a microbiology department there at Colombia but then ended up working on T- cell development which was sort of what I was hoping to get into um at the time which was really more this idea of pathogenesis. learning about TE- cell development was a very um was a very formal and thorough introduction into one arm of the immune response. Um but ultimately what I was you know looking to do in the wake of a really interesting uh PhD program there at Columbia was to move into virus pathogenesis which at Wu and Emery I did with a gamma herpes virus that was a virus that could infect and cause disease in mice. We had a we basically had a back system for that so we could do reverse genetics on the virus side of things at the whole genome level. which was really interesting from a molecular biology perspective. And then we had the mouse that um could also be manipulated at that time, right? So we knew that we could make transgenics, we could make knockouts, knockins, and then look to see the conversation between the host and the pathogen, manipulating aspects of that conversation as we went to see what the effect on the overall pathogenesis was as a result of those changes. So again like kind of learning from people who knew very well how to do things and how to get projects moving. Um how to make specific sort of first order levels of understanding at the virus pathogenesis level in the same way that I had started out really just at the viology level trying to make those types of um understandings for myself and maybe even in literature. So and then from from there the idea of interrupting the conversation of pathogenesis um became sort of an interest that I went to a company Sega Technologies and and that’s where I learned about small molecule drug discovery. We had a bunch of biologists that were very interested in biod defense pathogens. So a lot of basic biology needed to happen but then we needed to be able to interrupt those conversations. what I call conversations but are really pathogenesis and in a way that favored the host and was safe for the host and then from there you know kind of I guess you know that kind of that is where um the formal sort of academic education stopped and you know the the industry type of work began. So I can stop there’s no need to go on. Yeah. No, no, it’s it’s it’s a great background story and then it’s important and I’m glad you brought it up that you know at the same time you’re you’re learning all things viology and pathogenesis. Um you’re you’re you’re you’re becoming a hell of a translational drug developer. You’re doing small molecules, antibodies, which obviously we’re getting into. Even the uncle virus stuff which is you know living living products uh that’s a whole other story. Let’s um let’s segue uh a little into again the background issue that um is being focused on currently at Invivid because um I really want to sort of restate this for the audience because you know obviously we’re in this interesting time in 2025 uh in terms of uh all things vaccine hesitancy and people not getting vaccinated. That’s not what we’re talking about today. We’re talking about specific unmet medical needs of imunocmpromised people that just whether it’s a covid vaccine or any other vaccine just cannot mount a proper immune response. And this is everything from uh imunocmpromised people, people undergoing you know cancer therapies for hemalotological malignancies that can’t make a response people on carti therapies that have transplant a big niche that we don’t normally think about as much and I wonder if you could sort of reintroduce us to this area because I think it’s we don’t think much about it but it’s there and it’s big and it’s obviously a major problem that you’re looking to solve with with the products that invivid but reintroduce us to this. Yeah, there’s there’s two major underlying assumptions. One is that the pathogen is dynamic in its genomic identity, right? So, um pathogens they change um aspects of their protein biology in a manner that allows them to continue to um infect and evade the immune system in imuninompetent individuals, right? Um in and then the second major assumption is that not everybody is imuninompetent. that is not everybody has both an has an intact for lack of a better term um cellular and antibbody immune response um to bring to bear on any given pathogen they might encounter right uh so in those individuals that have say a a lesion in their in their antibbody response or in their cellular T- cell response um it’s necessary for them to either avoid getting infected um or to have some sort of augmentation uh of their immune system uh through in this case medical measures. Um we can add antibodies to the system for imuninompetent individuals and provide them the same type of antibbody response in broadstroke to what they would get um if were they to be able to respond to a vaccine immunogen, right? And in that way um we use a monocone antibbody because for manufacturing purposes it’s for us we can generate monocone antibodies considering the fact that the target is dynamic to those aspects of the protein that are less dynamic and therefore remain um in place and provide the susceptibility if you will to the antibbody in those individuals that are provided with the antibbody. Right? So um that’s the way we go about doing things. But for those that are imuno compromised, the reason often times that they’re imuninompromised is due to the fact that they’re suffering from an underlying medical condition. So if they’re in the midst of some sort of encogenic process, right, where they have a primary tumor or they have secondary tumors, um they’re in the under the care of an oncologist and they’re there at the oncologist receiving medications to stem the tide of their cancer progression. Um those medications can lead to an imunompromised state, right? And the reason for that imuninompromised state is ultimately to allow for the cancer to be treated and to favor the host as it relates to the cancer that they’re dealing with. Unfortunately, that also that imuninompromised state also opens them up to susceptibility to pathogens that are in the environment and it actually an increased susceptibility over those that are imuninompetent. And these are functional definitions, but I think you understand what I mean. So the the point here is that we can provide them with protection to specific pathogens in this case COVID right SARS COV2 we can provide them with protection that allows them to basically continue without as much um risk of infection and disease in in the you know after having received this medication so that they’re they can continue uninterrupted in their therapy for cancer in this case right in this example. So the idea of a non-relapsed uh mortality in the context of cancer includes things like infectious disease that infects people that are undergoing you know immune compromising therapies immune suppressive therapies in that in that cancer setting. So Mhm. we can we can basically try to limit those types of non-relapse mortalities in that cancer setting by providing this antibbody for one of the pathogens that they’re very likely to encounter which is SARS COV2. Likewise in the transplant setting where we know that a lot of people are um under an imunosuppressive regimen they are also subject to um respiratory pathogens like SARS COV2 and particularly in cases like lung cancer you don’t want to perturb that lung biology in the you know in the wake of your transplant and also in the leadup to your transplant right you don’t want to interrupt your opportunity for transplant by virtue of having had a you a COVID um sort of episode. So in that setting as well you have imuninompromised people that are imunocmpromised due to the fact that they’re undergoing transplant treatment. Um and we can help with preventing SARS COV2 in that setting with the antibbody with PIMGA. So that’s I think that’s the you know that’s a a good bit of the layout of how it is in the imuninompromised population we can be of assistance. There’s also, you know, and that’s where PIMGA is under authorization right now. Um, there’s a number of, you know, scenarios in life where we find ourselves at risk episodically of infection and I think antibodies can be useful in that setting as well. But that really kind of moves over to the next generation antibbody which is uh VYD 2311. Yeah. Mhm. Mhm. And and and just one other thing before before we go there. Um and you mentioned before about the uh and this goes back to the Invivid sort of you know um platform in terms of antibody discovery and engineering but the the important point there um which we need to state again. um the ability to uh through your technologies and models to to find these areas of the virus that are not under strong immune like the you know the spike protein and all that which is uh you’re looking at other epitopes and and I want you just say a couple words about that again because I want make sure again the audience understands uh what we’re doing here because it’s it’s it’s more you know it’s more than just hey just another antibbody to target this the spike protein here you you have a whole uh system there that’s looking for these on uh these other epitopes that uh are much they’re not under the immune pressure and they’re thus by uh better targets let’s say uh for these antibodies. So there’s I think there’s two important terms here. One is the fact that antibodies that we generate naturally uh to infection or um antibodies that we would engineer in the lab um if they could we could call them antibodies. All antibodies are antibodies and then a subset of those we would call neutralizing antibodies. Right? And a neutralizing antibody means that it binds to the pathogen in such a way that it it shortcircuits or uh prevents infection by the pathogen um and then basically reduces the uh the disease um associated with that pathogen by virtue of its ability to prevent pathogens from infecting cells. Right? it neutralizes infection and those are neutralizing antibodies. Now if you look at a particular target the way that that terminology has been sort of flipped around is that there’s certain ass there’s certain areas of the protein the spike protein that are considered neutralizing epitopes that is if an antibbody bound to that region the neutralizing epitope um then that would be a neutralizing antibbody. So you’re using that sort of functional definition on both sides of the equation there. And what we look for are in spite of the fact that SARS COV2 is rapidly evolving all the time to avoid this the immune response that we generate as a population. Mhm. What are the what are the neutralizing epitopes that are not changing on the target? Right. And how can we characterize those and track those and surveil those to make sure that they are remaining stable and that if we have an antibody that binds to that neutralizing epitope that the binding relationship between our antibbody and that epitope is continual is stable um and is resulting in in neutralization of the virus of the the virus dour right like what part of the variant soup are we dealing with right now? Well, I look at the whole virus, of course, because lots of things can change that could increase the virilance of the virus, but I look very hard at the spike protein um using the team here, the the scientific team here provides tons of data for us to look at um to say is it changing or is it not changing? And we can do that from a um bioinformatic perspective. Like we can model that based on lots of data that we’ve generated empirically that informs our um our model and we can also empirically test that using uh what we call pseudo viruses which are um sort of viruses that carry that same spike protein but are not in they don’t uh infect and replicate the way an authentic virus would. Right? So it allows us to see if can our antibbody stop that pseudovirus from getting into cells in the same way that it would stop an authentic virus from getting into cells. And with that reassurance we can provide you know healthc care providers the information that says that you know the potency of this antibbody is still in very good shape um against the current variant uh variant soup if you will. Yeah. Awesome. Awesome. Okay. So, yeah, let’s let’s go back into the world now of of PEMARP. Um, and again, uh, we talked a little about, you know, last year, uh, and at that point we were in sort of the realm of emergency youth authorization and, uh, amuno bridging studies and all that. Um, clearly have come a long way and there’s a lot going on. Um, and I I don’t want to mix up these terms because I think um, the original characterization was VYD 222 and now there’s VID 2311. Um, take us a little into sort of the little of what happened last year, but then the evolution of the program and then we’ll talk about what h what was just announced actually today in terms of the FDA authorization on the pivotal studies for the the current version. Yeah. So at the time of omocron emergence there was a need to basically um develop an antibbody that could overcome the obstacles that were presented to a previous generation of antibbody at it at invivid. um that was called ADG20 and then ADG20 was engineered um through binding uh screens to omocron emergent viruses to have amino acid changes that basically restored the neutralization potency for VYD 222 that we had become used to with ADG20 prior to the omocrron break. And so that restoration um was very important because it it number one it created an antibbody that was um very relevant at the time but it also demonstrated that we could with very few changes um basically continue to update the activity of this antibbody either in a prospective manner or in a reactive manner should we need to in the future. Right? So the types of changes um that have occurred in the in the virus landscape have basically occurred outside of the epitope for PIMGA and PIMGA’s epitope has remained quiescent and stable since authorization but also since the um omccron emergence right so we’re talking about three years of stability in that in that epitope so it turns out that part of that epitope is critical for interaction with the cognate receptor on the host cell which is ACE2. And I think that you know like that’s a that’s a big part of why this has remained stable is because ACE2 is in sort of a non-changing um force that acts on this particular region of the of the protein our epitope to conserve um the identity of those amino acids as well. And there’s not there’s just not a lot of wiggle room there. There’s some, but there’s not a lot of wiggle room there um that can be taken advantage of by the virus if it’s seeking to um evade the immune system and still maintain fitness as it relates to infection. So, sure, DYD222 or PIMGA was an answer to the challenges presented at the time of the omocrron break. Since the omocron break what we’ve seen is periods of um relatively you know minor changes which we would call evolutionary drift right and we’ve actually seen some periods of u more significant change like number of amino acid changes from one variant to the next um within the RBD or within the spike um and that’s what we call shift right and so at the time of BA.2.86 86 which was um sort of right as we were going from 2023 into 2024 um we saw JN1 come up and that you know that virus bore a number of differences from XBBS that had preceded it right and throughout that time we’ve seen that the epitope has um remained constant in quiescent like I said for for pimgard but what we want to do is we don’t want to lose track of the context that our epitope finds itself in. Like there’s a lot of pressures going on. These are thermodynamic pressures um within the protein. If an antibody changes one of its amino acids, it’s a little bit of that distal effect, right? Um that can you don’t know how to really quantify that. You know that you’re neutralizing still. You know you’re still binding, but the fact is the neighborhood has changed a little bit with respect to the identity of amino acids across that entire protein. And so periodically what we do and we did this for 2311 is we then update the variance that we are going to screen against to a point in time that’s after when the last round of antibbody was generated and that means that varants have changed um amino acid residues have changed outside the epitope and we want to account for that drift or um and in the case of 2311 it was mostly drift we were accounting for But also in cases of shift uh we could do the same thing by updating beyond you know past the point of the shift. So we’ve updated for drift in 2311 as it relates to 222 and by doing so we’ve gained back uh potency by degree over that which we saw from 222. And that’s just reflective of the the minor changes in the structure. Um, and you know, these could be post-transational changes. These could be, you know, just like I said, thermodynamic changes related to amino acid identity, but we’ve gotten back some potency from 2311. And what’s that what that has done is so we could we can see anywhere you know like I think we’ve put out in press releases like on the order of 16 to 17fold increase in activity from 2311 versus 222 head-to-head against you know a given variant JN1 and on that’s been relative that’s been basically consistent. So what that means though is as the potency increases you open up new routes of administration. So whereas it could have required a massive antibbody that that really pointed to IV administration in the past to get the titers necessary to provide protection. With those types of increases in potency, we can now use less material to get the same type of protection. And it now introduces intramuscular as a route of administration which from a patient access perspective is you know is pretty important and um I think that’s one of the drivers is that you know we we think we have a um a very good solution for the populations we were discussing earlier with the imuno compromised and that population also reveals um by degree people who are you at risk of of COVID infection, at heightened risk of COVID infection, either at different points in their lives, um different times in the calendar, even if they’re imunompetent, right? So, how can you provide uh something for them? And so this type of administration has the added benefit of really improving access for other populations beyond the imuninompromised while also very much in including improving access for the imunocmpromised population. So I think that’s you know that’s something that’s really really good to see from our approach. Um we continue to update all the time. We’re always looking for opportunities to update the antibbody and we want to stay ahead of the more substantial time curve which is the time it takes to manufacture this material once you’ve got an antibbody candidate. Right. And so with with 2311, we’re at the ready now with manufactured commercial manufactured material. Um so that the clinical need and the access need can be met with existing manufactured material as opposed to chasing that with a really good antibody but you know less than is needed having been manufactured. So, I think the company is trying to um be reasonable in its pacing and we’ve found an we have an epidote that I think lends itself well to this approach. Yep, absolutely. And and um yeah, clearly um and I obviously some of this is obvious from the your press releases from a few months ago, but um showing you know effects against the the current um variant under monitoring this this XFG variant, which is very important. Um clearly, you know, investors are happy. Uh and then obviously today um the announcement that FDA is is happy with um some of the upcoming clinical programs that you’re designing here. You know, one one’s called Declaration and one’s called Liberty, which is going to be, you know, involved some, you know, head-to-head comparisons with mRNA vaccination and combinations. Um again, take a little time to to walk through both what’s happening with Liberty and Declaration. And then what you were mentioning before I mean I know um Canopy which was the you know the the older studies I know there was some sort of subset analysis back then on on people with you know chronic lympositic leukemia and and other types of malignancies in that population. Is there say you is there like a subset of patients too within um declaration and liberty that that specifically is going to be looked at for for those are sort of what’s the makeup of because I know it’s something like 2,000 patients in declaration 300 in liberty walk us through a little of that what what’s going on here so declaration you know is basically evaluating prevention of symptomatic COVID um at three months right and that’s with either a single dose or monthly doses of the antibbody and each administration is IM it’s compared to a placebo the populations there are going to include imuninompromised individuals okay as well as imunocmpetent individuals who might be at increased risk of COVID um and I think that the whole design of of this trial um the declaration trial is to attend to attend to the FDA’s um I think you know they put a lot of importance on imunocmpromised individuals and protecting them from these pathogens and so the design elements of this trial um are meant to address those concerns on the part of the FDA right and that prioritization on the part of the FDA it’s also meant to open up you know new definitions uh for patient populations that might benefit from this antibbody right and I think those would be imunocmprom compromised individuals along a a spectrum and then also um imuninompetent individuals at increased risk if that can be you know achieved within the enrollment um process itself for for Liberty you know like you’re really looking to see what’s the interaction if any between the antibbody and the vaccine right now you know this is not meant to be a one or the other type of solution for individuals they’re encouraged if they’re indicated to take the vaccine to take the vaccine and then to wait a period of time after vaccination before they are administered the antibbody typically two weeks would be the the guideline there and so I think that what they’re trying to show here is with Liberty a more formal demonstration of what to what degree there’s any interaction between those two as it relates to overall immunity right you one could imagine that for those who are under on B cell deplets, right? Y their T- cell arm is still intact and in the presence of an antibbody, you might be able to um see basically modulations of the T- cell response in the presence of an antibbody that did may or may not exist to the same degree um in the absence of an antibbody response. Right? So even those types of um phenomena, if you will, could be investigated in this context. Got it. Um, all right. There’s there’s one other study that’s happening and and really this is this is extremely interesting because one of the people I I had on the show uh about a year and a half ago was uh Amy Pole from um Poly Bio Research Foundation, you know, working in the long COVID space. I know she’s one of your uh principal investigators for something called the Spear study. And here we’re talking about a long COVID and sort of spear stands for spike protein elimination and recovery. um you know a lot of work has shown that persistent you know spike protein hanging around can lead to all sorts of problems. talk a little bit about what spear is going to be about and again you know what are you learning in terms of um how primitive art ultimately um you know soops up those what do we call reservoirs or whatever uh in comparison I mean I don’t even know what what is being used currently for for long covid and and and this type of stuff but um really interesting and again take us a little into some of the concepts here I think that you know the timing of in the timing of the formation of the spear group and uh the studies that they are carrying out is appropriate here because what we’ve seen from Pimevabart and Pimgarda is a demonstrated in Canopy and also in the field um a demonstrated benefit to patients that are receiving this antibbody when it comes to frequency of infection and severity of infection. Right? So all of that points in a direction that says okay now you have an agent in humans that is showing some uh medical benefit. Let’s see u with that relationship intact whether or not um the syndromatic disease that we called long co right would benefit from an antibbody that we know interacts with the target and can cause benefit or can result in benefit to patients. And so then the question becomes um is is the target in the context of and long co is a syndrome right there’s a number of different I think presentations and and uh symptoms associated with long co but is there a subset of those patients or is there a majority or of those patients that would benefit from a systematic um introduction of antibbody into their system? And if so, would that link to the presence of antigen long term in those individuals? Right? So there’s a number of things that have to be true. You have to have access to the target and we don’t know if there’s, you know, some sort of privileged site that the target is um made its way to, right? This this could be from vaccine or from natural infection. But is spike protein somewhere that is not highly vascularized or is not antibbody accessible and that’s part of the reason that you have long co is that even your natural immune response really can’t get in there and and um clear that you know repository. Is it the case that um the antibbody is present in sufficient amounts can result in a clearance of that of that reservoir and you see an amelioration of the symptoms associated with long co. So I think that you know we have a target we have an antibbody it’s the right time to try these systematic approaches and then the main the main thing is you have to have a clinical team that has got robust reproducible and reliable tractable definitions of what it is that the patient population that they’re going to include looks like. And some of that could include you know biomarkers of disease. It could um include symptom sets. And so all of this is lining up at this point to have a very systematic clinical approach, more systematic than it could have been. I think you know definitely 5 years ago it couldn’t have been this systematic. Um and then you have a very wellestablished um sort of prophylactic effect from the antibbody relative to the target that was present in both the vaccine and in natural infection. So all of this I think that’s kind of why this is happening and how this is happening. There’s a there’s a great deal of demand for rigor in clinical studies and I think we’re at a point where we can to the point of you know uh satisfaction for a number of people um endeavor to do this with our antibbody to see what the effects are. Yeah. Yeah. I mean it’s um again I I I think it’s uh it’s fabulous how this has all evolved since you know we we last talked about it and and clearly seeing you know all these opportunities not just you know beyond prevention but you know going into long co and all the the pathologies that you know lead from that. Um what what else um I mean I know you have you know sort of a little later on in the pipeline you have some stuff going on in influenza. I mean clearly what you’re developing here and again going back to the invivid platform in terms of you know how you predict these varieties and ultimately engineer these antibodies but you can go in all directions here whether it’s you know the stuff you worked on at the we were talking about the beginning from the herpes viruses on to what you were doing at Sega with the the really nasty stuff and sort of biod defense you we’ve had the the Asper folks on a few months ago you know talking about sort of the national stockpile that we we need probably a lot of these types of therapies sort of sit sitting around in case, god forbid, the next thing comes along um that we need to engineer a way out of. But what what else gets you excited as you think about this platform and some of the opportunities? I was, you know, I was just at a respiratory virus meeting um in the last couple weeks and there are a number of respiratory pathogens that I think are relevant um both in the imunompromised population that we’ve been they the adult imunocmpromised population but with with uh nurseab and claimab you know you’ve seen into this RSV uh world in neonates um that’s something that’s very interesting to us we’ve talked about an RSV program and we are very much about the task of um moving that along right now. The other the other unexpected uh pathogen here is measles. And so with measles, what we see is that you know the AR not for for measles is it’s very high even compared to COVID right and so that uh we would not want and I’ve heard this from more than one HCP. The last thing they want is for someone to walk into their oncology waiting room or their transplant biology waiting room and have measles, right? Like that would just be that’s a not that’s a not good scenario. And so keeping the burden of disease low for measles low meaning as low as we’ve become accustomed to and and is a very workable level of of burden in the US, right? like I think the burden is very very low. A lot of the incoming um measles in the US comes from travelers who’ve you know gone outside the US and then come back with a measles infection. They may or may not have been um vaccinated. Their vaccine immunity might have waned. Perhaps they’re imuninompromised. Whatever the case that in that imported measles um presents a real problem. And there are a few populations in the US that have not that are vaccine hesitant almost you know like as a defining quality in time at times um and those populations have fmented measles in the recent past in a way that concerns a lot of people but there’s also been a vaccination rate decrease and so whether we you know without really commenting on that the the state of affairs is fundamentally different than those times when the vaccine rate was higher and the burden of disease was low and potentiated as decreasing. What we have now is a different reality that requires some intervention and right now IVIG is about the only intervention that you have. So I think a monoconal antibbody that was available for those who needed it at the times they needed it would be um we know that it would be very attractive for imuninompromised individuals based on interactions with hcps and these were inbounds from hcp at the time when the measles rates were going up they’re like you know we don’t have anything here besides IVIG and we would love to have a monoconal so we’re we’re working on measles um that’s also going to be lead to other respiratory pathogens I think would fall in line behind that. And then the other thing that you were mentioning before with these sort of syndromatic diseases that could be pathogen associated and therefore could be pathogen encoded protein associated. Um there’s other realms there that we might look at um for those types of diseases. And it’s not really dependent upon anything going on with spear. It’s more the fact that we all live a long time now and we’re all encountering pathogens at different points in our life and there’s a there’s a thread that points from initial acute infection to you know longerterm disease in a number of different pathogen classes that are all worth considering. Um I’ve always been focused you know like a lot of people on therapy but I think prevention is probably the most intelligent way to go about this. That’s why vaccines are very very important and that’s why prep antibodies are very very important. Prevention of disease is prevention of persistent disease as well. Right? And u so I think that’s kind of where we’re you know we’re focused right now in terms of the pathogen world. The list is long and antibodies are are exceedingly safe and rapid um alternative when it comes to providing solutions. So I’m happy about that. I think I can before it’s my time to go then maybe we can get a few of these knocked out. Yeah. Yeah. It’s uh it’s really interesting. Yeah. It was you know you bringing up that whole issue because we we’ve talked also a lot on the show about sort of immunosciness and what happens as we get older and you know the need for hey maybe maybe there we need other approaches to uh you know when we get into our 70s and 80s to how we do these get these more robust responses. But yeah, that’s that’s spot on. So, I’m I’m I’m excited about that angle as well. Uh for you, um Robert, what what what else is on coming up that we should know about? I think I saw that you’re going to be at the uh the World Vaccine Congress next year in Washington. I think that’s coming up in a couple months into 2026. Um anything else, whether it’s on the uh the investor front, the the scientific conference front, and then anything I missed while we have you today that you want to mention, please? Well, I you know, I think that the company is is very interested in providing um access to the populations that that need these types of solutions. And you know, I think that we would our interactions with regulators, we’re kind of a, you know, we’re a company that’s that’s trying very hard to um to meet the medical need in in as you know, a droid a fashion as possible, right? you know, and I think that what we will hope for is that our antibodies can be used in combination with existing therapies um and existing means of prevention um in ways that, you know, we haven’t seen up until this point. And that kind of, you know, I think that kind of pioneering approach is is imshed in the way this this company works and we’re looking for for those types of opportunities. Without going into specifics, I really think that that’s what the company wants to do is to be of utility to the population as it relates to prevention of virus uh respiratory virus disease. I think right now so um yeah, that’s really what we’re most excited about. We’re excited about the fact that we can do this. I think our variant surveillance program is very very good, very very capable at capturing from wastewater or from clinical sequencing the amount of the rate of change that’s occurring and the type of change that’s occurring and staying on top of that, right? And for that reason, you know, like being being involved in the development of preventative uh treatments is extremely exciting because I have a lot of confidence that those things that we develop stand a very good chance of remaining durable in the treatment environment. Right. Absolutely. Absolutely. Yeah. It’s um again it’s it’s it’s an awesome story. I I enjoyed hearing about it last year. I really enjoy hearing uh how you’ve come with the program and then continuing, you know, developing into 2026. The FDA uh very happy with with the design. So, that’s exciting as well. Um but really, you know, great stuff. Um and I look forward to continue to follow it. Um, again for everybody out there that is going to be listening to this episode uh across the uh various podcast networks or who will be watching on the YouTube channel. Again, you’ve been spending time with Dr. Robert Allen, chief scientific officer at Invivid doing really amazing work to develop these best-in-class monoconal antibodies for serious viral infectious diseases. Uh, Robert, I I want to thank you for taking the time out of your schedule to to talk to us, to walk us through how the programs are moving. Thank you for everything you do there in Vivid for Patients, and as we like to say on our show, thanks for helping to create a better tomorrow for everybody out there uh through what you’re doing. Really an awesome story. Yeah, thank you. It was a great conversation. I’m I’m glad to see that you’re doing what you’re doing. It was great having you and really great discussion.
Dr. Robert Allen, PhD is Chief Scientific Officer of Invivyd ( https://www.invivyd.com/ ), a biopharmaceutical company devoted to delivering protection from serious viral infectious diseases, beginning with SARS-CoV-2, by deploying a proprietary integrated technology platform, to create best in class monoclonal antibodies.
Dr. Allen brings over 30 years of experience across the infectious disease space, most recently as the Chief Scientific Officer of SmartPharm Therapeutics, a subsidiary of Sorrento Therapeutics. During that time, he led efforts to develop gene-encoded monoclonal antibodies for COVID-19 that could be quickly adapted to respond to emerging variants of concern. He also served concurrently as Senior Vice President, Antiviral and Oncolytic Immunotherapy Development, at Sorrento Therapeutics.
Prior to his time at SmartPharm Therapeutics, Dr. Allen held multiple senior scientific roles across the pharmaceutical and biotechnology industries including at Sorrento Therapeutics, SIGA Technologies, and the Oregon Translational Research and Development Institute.
Dr. Allen holds a Ph.D. in Microbiology from Columbia University, an M.S. in Applied Biology from Georgia Institute of Technology, and a B.S. in Biology from Rhodes College. He has published extensively in the field of virology and completed his postdoctoral training in virology at Washington University in St. Louis and Emory University.
#RobertAllen #Invivyd #Biopharmaceuticals #InfectiousDiseases #SARSCoV2 #MonoclonalAntibodies #Immunocompromised #RareViralEpitopes #Pemivibart #PreExposureProphylaxis #Covid19 #EmergencyUseAuthorization #EUA #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #ViralPodcast #STEM #Innovation #Technology #Science #Research