This video features a discussion with Adam Rogers, M.D., CEO of NervGen, and Rich Macary, a board advisor for the company. They discuss NervGen's lead candidate, NVG-291, a peptide therapy aimed at neuroregeneration, particularly for spinal cord injuries. The conversation covers Adam Rogers' strategic shift for the company, including moving to NASDAQ for increased visibility, early results from clinical trials, the broader therapeutic potential of NVG-291 in neurotrauma, and future development plans. Rich Macary also shares his background in RNA therapeutics and neurology, and how he connected with Adam Rogers and NervGen.
Here are the questions and answers, presented as closely as possible to the speakers' original words from the transcript:
Q1: How did you meet? Uh what were the circumstances uh that that led you uh Adam and Rich to Nerve Gen? A1: (Rich) "Yeah. Well, that's a that could be a long story, but the the short version of it is I was already an adviser to the company. uh I got involved really because I saw a ton of parallels between work that I had done in RNA therapeutics with Avi Bioarma which became Serepta. I saw a lot of parallels and got involved as an adviser to the company. But uh in 2022 uh I actually had David Rogers, Adam's son, intern with me and uh I had him focus on the company that I was putting a lot of attention into which was NerveGen. uh he shared that research with Adam uh and uh the rest is history. We ended up connecting actually through his son in that internship." A1: (Adam) "Exactly. And it was really I think you know if we have to put a date on this it was probably January, February, March of 2022. And so my son was a senior in college. He was getting ready to work for Rich. I think Rich told him to go do some work on this company. He read the papers of Jerry Silver. He's like, he writes me up. He goes, he he he emails me. He goes, 'You got to take a look at some of these papers. There's some really really interesting stuff.'"
Q2: Adam, you mentioned you're an opthalmologist by training and a professor, but you previously founded Himero Biosciences, uh, a gene therapy company that was targeting, uh, age-related macular degeneration. You sold that company, uh, you were CEO, I guess, for for from 2017 to 2020, sold it to J&J in 2020, uh, in a deal, I think, worth over $400 million. Um what what made you want to become a biotech CEO uh initially Adam and you know what was that experience like? A2: (Adam) "Well you know if you um the company was really started from scratch. It was um we started this in the lab at TUS. It was ideas that a few of my partners in the retina department um had of how do we treat individuals with dry age related macular degeneration... And so I just sort of naturally grew into the role of running the company. It wasn't like I want to become a CEO. It was almost I had to become the CEO and run this company because we, you know, we were raising money. we were manufacturing the drug. There were four of us in the in the company and I was the only one that was really wanted to put forth the time and and keep it going. And so I wouldn't say I wanted to be it. I would say I just sort of evolved into becoming the CEO of of Hamira. So, everyone in the lab's kind of looking around at each other. Uh, you know, who who's going to take this forward? Who's going to actually be the CEO? And you, uh, you rose rose to the top there in Exactly. It's it's really how it how it came about."
Q3: Rich, I wanted to ask you about you know you you were at the the precursor to Serpa did early work in RNA therapeutic development and you've advised uh company executives and investors at a number of different organizations. is your chairman and co-founder and president of Synaptica Therapeutics, a neurology company that's developing a unique approach to the treatment of of Alzheimer's. What how did your uh interest in uh in neurology originate, Rich? And maybe tell me a little bit about Synaptica therapeutics. A3: (Rich) "Sure. Sure. Yeah. I mean, my whole uh evolution really started by jumping into biotech through RNA therapeutics almost 20 years ago. that led me uh you know the idea of programmable drugs uh was exciting... Around the time I was leaving my mom developed Alzheimer's and so my direction into neuroscience and neurology was driven by that situation. I first took a personal interest trying to find something to help her and then that became a professional interest when I started to realize everybody was focused just on amaloid and tao and I was looking at all these other things in my research like neuroinflammation uh like microgle dysfunction and then I started to look at synaptic dysfunction and plasticity mechanisms mechanisms... I saw their research. I happened to be there when they turned over the cards on their first phase 2 and the data was amazing. Still the best data I've seen in slowing the progression of Alzheimer's. I saw the ability to file IP, get breakthrough designation from the FDA. I helped create the company around them."
Q4: I have to ask Adam, is there anything that you have learned from Paul? Uh any advice uh that he's given you that that you might share? A4: (Adam) "Absolutely. Listen, I mean, when you when you get to work with someone like Paul who's had so much has basically expansive business experience, you can't help but learn from him. And you know, I learned a few things from Paul and he sat on he was one of our investors at Himera and he sat on our board at Himeira and the one thing I learned from Paul is he listens and he listens very intently and he listens far more than he ever speaks. And so he he he he literally embibes everything that's going on and really just kind of digests it and then synthesizes it. He really has fourdimensional views of of the world and has phenomenal business sense and making decisions. And you know I just when I'm with him I just sit I listen to him I watch how I watch how he operates and those are really the main takeaways that I've I've received from him. He's also a very decisive person and knows where where he wants to go."
Q5: Um sticking with you for a minute, Adam. You joined NerveGen. Uh it's a clinical stage company last summer I believe. Um what what did you do first? Uh did you and Rich work together on a strategy for the first few months? I mean, what's your approach to kind of coming into a company like NerveGen? What, you know, what was your game plan? A5: (Adam) "Well, Ben, I I had been on the board of NerGen since July of 2022. So, I had some pretty decent insight of the company. I was the acting president actually when I started with the company back in 2022 for about six months while we had an interim CEO who was one of the founders. Um, and you know, getting back to my days at Hamira where you, you know, you said, 'Look, you must have learned a lot of things at Hamra, I did.' And one of the things I learned is you've got to, you know, when you're a small company, you've got to be nimble and you have to make decisions and you have to know where you want to go. And so, obviously, when Rich and myself, um, and others sat down at the company, when I sat down with the board, I knew exactly where we needed to go. you know, we needed we needed to really digest all of the clinical data that that we had just finished in our 1B2A connect SCI study. We needed to take that out there. We needed to be aggressive. um we made moves to um leave the Toronto Stock Exchange and get on to NASDAQ where where you know we when you're up in Canada and and this is not a bad thing, but not a lot of companies or investors know who you are up when you're up on the Toronto Stock Exchange. And so we we needed to gain visibility. um and so that's so we really made we're going to we're going to get this into a phase three. We're going to get on to the major uh stock exchanges in the US for for visibility and for and you know um everything else that comes with that funds that can only invest in US companies. And so we just made a lot of changes. I wanted the company to become very efficient and very nimble and make decisions and be very decisive."
Q6: So moving over to the NASDAQ, gaining visibility, did that also improve uh the the fundraising situation? I mean, was there an immediate impact uh after that after that transition? A6: (Adam) "Well, what it what it does what that does is it gets you onto the um it gets you into the world of the analysts and the analysts then interact with you. You speak with them. You tell them what's going on and then you know obviously when when they take up coverage of your company they have readers and they have people that follow investors that follow them and then obviously you you become more of a known commodity. We didn't have that up up on the Toronto Stock Exchange and so we we were sort of toiling away in anonymity up there and so we really needed to improve our visibility and so yes that that that when people know about you then then you're on the radar. We needed to be on the radar."
Q7: Um, Adam, are there are there specific things that you look for in a candidate aside from kind of like technical knowledge and skills? I mean, are there cultural aspects that you look for uh, in in terms of growing out, you know, the team and personnel? A7: (Adam) "Well, I'll take for example you first of all the the easy answer is yes and then I'm going to walk you through like one of the key hires I made this year which was Shim Ruff and she is head of our regulatory affairs and Shamim was at Serepta and she was also at Stoke Therapeutics. NDG291 while while spinal cord injury in and of itself is too large of a group of individuals to be considered a rare disease or an orphan stage disease, the FDA looks at this as as such an unmet need that it's almost rare. So, I I needed to find individuals that have experience in moving um drugs through the regulatory uh process um like Shamine and she's done that at many different companies and so I need to bring in people with that type of experience. OB obviously you're always looking for people that fit in as well and and you know look you need that but I I'm looking you know we're a small company. I'm making very very strategic hires for people that will dramatically help the company and keep moving this NVG291 into not only just the clinic but into the hands of individuals that desperately need this drug as as rapidly as possible."
Q8: Um is it similar to peptide therapies like like GLPS? A8: (Adam) "It it's very similar. It's a 35 amino acid peptide. Uh we manufacture here in the United States. Um it's very very similar."
Q9: Is there any capacity issues given the you know the absolute explosion of of interest and of uh of development of various GLP one therapies u primarily for diabetes and obesity. Um, but I I'm curious about the the capacity uh with, you know, with partners with CDMOs. Has that been an issue at all finding uh partners that that can manufacture particularly now that you're, you know, gearing up for a phase three trial? A9: (Adam) "No, it's it's not been an issue for us. We we've actually um invested heavily in the manufacturing side of things. That's the one thing that I also learned from from my days in Hamira is, you know, you've got to have a strong source of drug and a really, you know, strong partnership with uh with the manufacturers and and we've done that. And I've uh Charles Olsen, Chuck Olsen works for us out in California. He's he heads up our CMC. He's phenomenal, highly experienced um and he runs everything. So, we are we have a very scalable model. um that is able to supply drug. And so we've had no issues with that given our really our our large investment in that area."
Q10: And you guys are planning to initiate the phase three uh in the second half of this year. Is that is that correct? A10: (Adam) "We we you we're calling it mid 2026."
Q11: You had a um an end of phase 2 meeting with the FDA. Uh this is the um I guess technically the tetra plegia. Tell me how to tetroplegia indicate this spinal A11: (Adam) "it's tetroplegia which is what we used to call quadriplegia but now now it's termed tetroplegia. And so we we've had two meetings with the FDA. won a type C meeting which was on on Zoom, not an in-person meeting. Back in the fall of 25, the end of Q1 um 26, we had a type-c inperson, what you would call an end of phase 2 meeting with FDA. I would call this a very very collaborative meeting with the FDA. Um we um have really from a collaborative st collaborative standpoint have an understanding of both our primary and secondary endpoints and are moving rapidly into starting a single uh registrational study this summer in individuals that you would call chronic tetraplegia or you may call motor incomplete cervical spinal cord injury."
Q12: you guys are both excited about the potential of this development candidate. I wonder um if you could tell me a little bit about uh why maybe some of the early results that that you've seen in patients receiving this therapy uh you know what what makes you so bullish about this this development candidate. A12: (Adam) "So let let me group our results in really like two buckets. The first one we did electrical testing in these individuals because what this drug does, the drug is a 35 amino acid peptide. It's injected into the abdomen. So it's a very easily administered drug... A daily administration of the drug. Correct. We give it for up to 12 weeks at this point in time. And so in the individuals in the study, they they received it just that way daily uh for 12 weeks. Um, it can be self- administered at home as well. So, it's not like you've got to be in you've got to be in the hospital to have it administered. It's no different like you we you brought up GLP1s. It's very much the same. So, our our what we looked at was, you know, well, let me get into how this drug works. There are inhibitory uh molecules called CSPGs or chondroitin sulfate proteoglycans that really in in an injury state get upregulated... So your body and you know your body will say look the neurons that are damaged are like I'm you know will try to regenerate but these CSPGs which inhibit neur inhibit the neurons they block these these small neurons that are sprouting after the injury from reconnecting. So the first thing that we wanted to see was okay how does this drug which interferes with the CSPG cascade do we improve uh neuronal conductivity? Are we able to measure the electrical impulse from around the area of the injury out to the out to an extremity and we showed we we had a positive result there. And then we looked at functional outcomes. And so the the first and main functional outcome that we looked at was hand function. And we measure it through something called grasp, which is an acronym grssp. It's called grasp quantitative apprehension. And it's four small tests that a person does and they're and they're graded on time and and um how correct they do it... So, so we had an 825% improvement from day zero to week 12 in individuals with hand function. And and that exceeded a point which physicians or key key people in the field would say beyond that point an individual can hold a fork and feed themselves, comb their hair, brush their teeth, button, you know, button their shirt or their sweater, uh zipper up their pants, do certain functions that on a day-to-day basis improves their ability to live an independent life. And that's what we found with the hand function. and hand function in in individuals with spinal cord injury especially cervical spinal cord injury is probably the most important function that they can gain back because if you think about it Ben everything that we do in the world is either v looking at it vision or hand function just picking up your phone and texting people or you know how do you eat and make a meal it's those are vital vital uh aspects um and then we we did blinded eggs interviews so actually before that we discontinued the drug at week 12 and then we measured the hand function again at week 16. And what we saw was that there was even continued improvement in the hand function test after they had been off the drug for 4 weeks, which which demonstrates to us that the new neuronal connections that are being made are permanent and we're seeing this permanence in the functional outcome that they're having. We also did blinded exit interviews with these individuals and they did not know whether they received the drug and those were on average up to 250 to 260 days after they left the clinical trial and we had about a twothirds improvement in bladder function and a 56 to 60% improvement in um reduction in spasticity. So muscles are are a big problem as well. And so we saw really dramatic whole body improvements in these individuals. Two individuals that were received the drug could not complete a 10-meter walk test at the beginning of the trial and they were able to do so um at the end. So, we really are seeing some wholebody global um therapeutic impact of the drug based on their functional um improvements that we're seeing."
Q13: The the grasp outcome or or the the kind of uh hand related outcome, is that uh is that what you talked about with FDA? Is that what did the you know the kind of primary endpoint in phase three? A13: (Adam) "Yes, we to we talked with them about that back in September and then we spoke with them about that um in the first quarter this year and so we we had to become aligned. they had to understand the grasp study um you know and and understand you know it's just an understanding of that it's a validated study um and how how important it is for an individual to regain hand function for someone that has spinal cord injury and I may have overlooked this to you the individuals that we enrolled in this clinical trial were one to 10 years out from their injury and so so these are individuals that by all means you know, there's no standard of care for anyone for for these for these for people that have suffered a spinal cord injury. So, for all intents and purposes, this is the, you know, the only therapeutic option that they have that's in testing right now to uh to improve their functional outcome."
Q14: And this mechanism that you just described, Adam, uh that uh comes from from Jerry Silver, Rich, is that, you know, is that also, you know, what excited you about the company and and brought you, you know, to to NerveGen initially? A14: (Rich) "Completely. I mean, when I first started getting involved in RNA therapeutics, uh, and I saw the original, uh, MDX rodent models for Duchane musculardrophe that showed proof of concept. Again, that's a genetic model. I got excited. This is, as Adam said, a physical mechanical model. You're not emulating the disease. You're literally... Exactly. And so, you know, even when that was graduated to uh canines and DMD and we saw that improvement, you're hoping it was going to translate in seeing this model. I I made the bet early on and that's why I got excited that this was going to translate into humans. And that's exactly I've never seen anything translate like this. If you look at the rodents, even the videos of it and then ultimately see we did capture videos uh in this trial, it is it is unbelievable."
Q15: So, so CSPGs are an inhibitory uh molecule in the extracellular matrix. And so they really prevent neurons from going into aaron areas. And like I said earlier in in neurot trauma um especially in the area around trauma, these CSPGs are upregulated. And then what they do is sprouting neurons will just interact with the CSPG and they'll think they're they're perfectly happy and they're doing something but they're just interacting with the CSPG. We don't get rid of the CSPG. What we do is we the inhibitory um signals that that are being sent out by the CSPG, we downregulate those. So we're not we're not ridding the body of the CSPG. we're diminishing the the inhibitory effect that the CSPG has on a neuron from respouting and reconnecting to its normal location. A15: (Adam) "So, so CSPGs are an inhibitory uh molecule in the extracellular matrix. And so they really prevent neurons from going into aaron areas. And like I said earlier in in neurot trauma um especially in the area around trauma, these CSPGs are upregulated. And then what they do is sprouting neurons will just interact with the CSPG and they'll think they're they're perfectly happy and they're doing something but they're just interacting with the CSPG. We don't get rid of the CSPG. What we do is we the inhibitory um signals that that are being sent out by the CSPG, we downregulate those. So we're not we're not ridding the body of the CSPG. we're diminishing the the inhibitory effect that the CSPG has on a neuron from respouting and reconnecting to its normal location."
Q16: So in a healthy body uh you would want I guess you know that the CSPG I guess what what what are what kind of role are they performing A16: (Adam) "in a healthy in a healthy body they form CSPGs form what's called a peruronal net. Think of it almost like um around a wire. How there's like um there's some insulation around a wire. They're almost like an insulation around the wire. They form this perinuronal net and they keep the neurons going in a in a in a certain location. Um this drug has no effect on individuals that have a normal amount of CSPGs unless there is an aarent upregulation of the CSPGs. Will will this drug have an effect on someone? So in in healthy individuals, we we don't see any there there's no benefit whatsoever that we that we identify."
Q17: I saw in your pipeline slide you've received some funding uh from the Department of Defense. uh I think a couple of different groups within the Department of Defense and I I'm assuming that that's due to the the injury aspect and that you know that this could perhaps be used uh in the military but I I I'm making assumptions here. Can you tell me maybe about how, you know, and I think it was before your time, Adam, you know, when this when this funding came in, maybe Rich, you could speak to it, but um what I I guess how did that funding come in the door and and what um what does that collaboration if if there is one look like? A17: (Rich) "Yeah, sure. Again, even going back to when I was at SERP that people forget that in the early days, we had a lot of funding that came from uh the DoD. It came from work that we were doing with us and Ebola Marberg that was an infectious disease here given that this mechanism in spinal cord injury is of interest to the department of defense but beyond that the field of neurot trauma I believe they've spent billions in research in this area this is one of the things that they're trying to improve on for the war fighter and for veterans and so um we actually predating me uh we uh had uh the uh departing head of the uh US combat casualty the care research center at the DoD, now the DO. Um, he ended up becoming a consultant to the company. His name is Dr. Mike Davis. Um, he really was excited, believed in the science the way all of us do, uh, as somebody who looked at all of these things on behalf of the DoD for many years. And he got involved in helping us navigate where to go and telling the DoD, 'This is something different and unique than you've seen before. We're not trying to just go after inflammation. Uh this is a completely new mechanism and so helped us get money. Some of it's congressionally directed funding. Uh some of it's coming from directly from agencies of the government within the military. There so many different funding pockets, but that allowed us to do the blast induced hearing loss study with the Air Force. It allowed us to do a peripheral nerve injury study that's involving uh the the DoD, but also uh that came with through Washington University and ongoing. We don't have the results yet, but uh we're doing a study in traumatic brain injury with Walter Reed. All that non-diluted funding coming from various sources. So the the partnership and involvement of the DoD I think is really really important."
Q18: Um uh I would be uh remiss if I didn't mention the the other candidate that NerveGen has. It's in pre-clinical stages, NVG300. Uh is there anything that at this stage that you can tell me about that candidate? Is it also a peptide? A18: (Adam) "Yeah, Ben, it is also a peptide and would be administered very similar to NVG291. Obviously look I mean part part of what we want to do is ease of administration but that that is still in you know from from our standpoint we are internally still uh discussing and deciding how to uh deploy it and and which indications we'll be using it for. So as we you know we will come out publicly with that in the future on NVG300."
Q19: Got it. Got it. All right. Well uh we are getting to the end of our time here. um maybe we could just end with your top priorities for the company for the rest of the year and and also you know what you see as the biggest challenges that that NerveGen faces uh for the rest of let's call it a year for the next year. A19: (Adam) "So listen, in the immediate future and and I and I would group this into the challenges too is our look, I'm a very focused person as far as getting, you know, I know where we need to go and and I have a group around me that helps helps this company move forward to get there. And so our goal, we are uh steaming ahead with getting our phase three study up this summer on MDG291 for individuals with chronic uh cervical SCI. Um we are you know that's our main number one focus uh right now and then obviously over the summer we will also uh discuss publicly what our next indications will be. But our our number one goal get the study up and running get it get enrollment going as as efficiently and quickly as possible and enroll those individuals within a 9 to 12 month period. That that's our that's our probably one through 10 most important list of things to do this year."
Q20: Um uh do you guys plan, I mean, do you have a strategy to potentially, uh, if if it sails through phase three, uh, you file, you get approval, are you prepared to commercialize this drug as NerveGen yourself or or is it more of a kind of must partner or or must sell type of strategy that that you're working on? How do you think about that aspect? A20: (Adam) "The way I look at it and I have this exact same uh same same approach of homera. Our goal is to take this drug all the way and commercialize it. And I don't think you can think any other way. I I I did not join this company and we're not building this company to be sold. We're building it to get a drug to market and to improve the lives of individuals with spinal cord injury. And that's that's just my focus and the way I I I view the world. You know, it it I I can't tell you what's going to happen down the road. I don't know. I don't have a crystal ball. But all I know is we're going to start a phase three study. We're going to take our results to the FDA and we intend to take that drug to market and to improve the lives of all those individuals that that you know have this enormous unmet need of spinal cord injury. And then right after that, what we want to do is we want to expand it to everyone with the spinal cord injury. You know, we're we're not including individuals with lumbar or thoracic injury. And there's no reason that just because they've got a, you know, this works in cervical spinal cord injury that it's not going to work in thoracic or lumbar injuries at all. So my goal is to get everyone with a spinal cord injury um give them get them access to this drug as as efficiently as possible. And Ben, if I could add to that, you know, the experience that I had at Serpa, you know, when we started talking about DMD outside of like the Jerry Lewis teleathon, a lot of investors didn't know about this area, but more so there wasn't a built therapeutic model to go out there and bring that forward. So, you know, Serea created that model and that's exactly the opportunity we have here. We have no therapeutic for SEI. So, not only do we expect to be the first ones to go over the line and get a approved drug, but to build that call point and that infrastructure to deliver this to these patients is an opportunity. Uh, and and you know, we we think that that is very very doable for a company like this. There isn't a bigger company that already has a footprint to do this. So, we'll build it and that will probably make us more valuable as a company and do a service to the community by putting together really that delivery infrastructure."
