Recently, we had the opportunity to interview Rick Kiessig, the co-founder of Kimer Med, a company developing a broad-spectrum antiviral that has the potential to destroy a wide range of viruses.
Its drug, known as VTose, is a variant of an older antiviral drug known as DRACO, which unfortunately failed to gain sufficient funding a few years ago and became a victim of the valley of death, like so many other promising drugs and therapies do.
Kimer Med are building upon the work that went into DRACO and developing its own variant with the aim of creating an antiviral that can knock out multiple viruses. Needless to say, if such a drug could be successfully developed, it would have implications for a myriad of infectious and age-related diseases.
Can you explain in plain language how VTose works?
VTose is a protein with three functional pieces.
On their own, proteins don’t normally pass through cell walls and into cells. So, the first piece is a short “tag,” which solves that problem, allowing the protein to enter the cell.
The other two pieces are parts of proteins that already exist in every cell in the body. One of them binds to long segments of double-stranded RNA (dsRNA), which are only produced by viruses, not healthy cells.
The binding process then activates the final piece, which causes the cell to commit suicide. This process, called apoptosis, is normal and natural in the body and happens to billions of cells every day. We’re actually helping cellular machinery and the immune system do what viruses are preventing them from doing.
After apoptosis, scavenger cells clean up what’s left of the cell. Viral proteins and the virus itself are destroyed.
Why did the name change to VTose?
As defined by Rider, “DRACO” is actually his name for a family of compounds, not just one. DRACO is ultimately Rider’s thing, done a certain way. We will certainly end up doing some or perhaps many things differently, and don’t want to claim to be something we’re not.
We also want our own trade name for a compound that will reflect our changes, investigations, effort, and innovations.
What kinds of viruses could VTose potentially address?
Rider found DRACO was effective against every virus he tested against: 15 different ones, including a number of different types.
One of the early viruses that we want to look at is SARS-CoV-2, of course. Influenza, HIV, Hepatitis B, Herpes, CMV, HPV and EBV are also of interest, as are viruses in pets and livestock, such as FIP in cats.
We know all viruses create dsRNA, so it’s possible that VTose could end up being effective against all of them. However, we also know that viruses have quite a wide range of defenses, including doing things like interfering with the cell’s normal ability to bind with dsRNA and to self-destruct. It’s possible that those same defenses will prevent VTose from working in certain viruses. We won’t know for sure until we test.
Fortunately, we have different formulations we can try for VTose to work around viral defenses, should we eventually run into any that prevent it from working.
Making the project a success is going to take lots of work and specialist knowledge. Can you tell us a little bit about yourself, your co-founder, and your team and why you think you can succeed where Rider failed?
My co-founder Phil and I both have an entrepreneurial background. I ran my own business in Silicon Valley for about 20 years. I’ve also worked with or for about a dozen start-ups, so I’m very familiar with what it takes to start and run a company. By trade, I’m a software architect. In addition, I studied biochemistry in school, and it’s been an ongoing interest of mine in the 40+ years since then. Phil’s degree was in Biomedical Engineering, and he also has a software background.
We strongly believe in the vision and promise of broad-spectrum antiviral technology and that this work is important.
We have the scientific background needed to understand Rider’s work in depth and to work with experts to specify and manage in vitro and in vivo testing. In areas where we have knowledge gaps, or as the company grows, fortunately, expert skills can also be hired. We are already getting advice from specialists at places like Callaghan Innovation, University of Otago, and Massey University.
I admire Dr. Rider and his work greatly. One area where I think we differ is my focus is less on research and more on bringing a product to market.
We’re fortunate these days that much of the work involved with bringing a new drug to market can be contracted out, and we have the project management experience needed to make that happen.
With something as promising as DRACO, you would have thought it would have had no problem finding funding, given its broad antiviral potential. Why did DRACO fail to gain traction in your opinion, when the attempt was made to fundraise for it a few years ago?
Dr. Todd Rider, the inventor of DRACO, said he found that government grant and NIH-type funding related to pharmaceuticals is largely limited to two broad areas: either basic research or the final step of bringing a new drug to market. However, they apparently don’t like to fund the middle part (where we are now), which involves clinical trials.
He also felt that investment from pharma companies would require showing effectiveness against commercially interesting viruses, such as herpes, which is why that was one of the goals of his 2015/2016 crowdfunding campaigns.
My view is a bit more cynical. Pharma companies have a number of drugs to treat viral illness (antivirals and others). Many of those drugs require regular use for a long period of time, because they don’t make the virus go away, they just temporarily keep the symptoms at bay as long as you continue to take them.
Those drugs represent significant revenue streams. Introducing what could be a cure therefore might not be seen in a positive light. To compound the problem, pharma companies also have a significant influence on government funding.
It’s been almost a decade now since the Riders PLoS ONE paper about DRACO, why hasn’t anyone done anything with it before now?
One reason nothing was done before now with DRACO is that it was patented by Rider and MIT Lincoln Labs, where he worked at the time. However, it turns out that MIT/LL recently abandoned those patents. Patents normally last 20 years, but you have to pay maintenance fees to keep them active. If you don’t pay the fees, the patents expire; that’s what happened here.
It’s worth noting that the rest of the world hasn’t completely ignored Rider’s work: two labs have replicated the basics. One in China in 2015, and another in Iran just this year.
Patents certainly aren’t the only reason nothing much has been done with DRACO since 2011, though. The objections that come up when discussing the subject are actually a very interesting reflection of human nature. Quite a few people simply don’t believe the previous results. They think if it was real, surely someone would have already stepped in and done something, or they think the work wasn’t published in a “serious enough” journal and is therefore questionable. Others have fundamental misunderstandings about the underlying biochemistry.
The idea that it wasn’t published in a high enough impact journal (and Plos is hardly a minor player) says everything about how broken the journal system is and how it is holding back scientific progress. We supported the 2018 Jason Schmitt film Paywall: The Business of Scholarship, by getting an interview with the owner of Sci-Hub, the site that provides free access to scientific papers. What is your view on how journals lock scientific knowledge behind extortionate fees and what needs to change to make sharing scientific knowledge work better?
I run into paywalls myself all the time, and they drive me crazy. I completely support the idea of open access to scientific papers.
My view is that journals currently have a successful yet problematic business model and that the current reward system for academics reinforces the problems with journals.
However, scientific research is stifled not just due to the lack of open access to published papers, but also by the way journals select articles to publish and the way peer review is done. I believe lots of very good work is being lost due to these controls.
My suggestion for a place to start with change would be that the terms of all government-sponsored research should include a requirement that the results are published open access. That would also cause academic institutions to re-evaluate their reward systems, since so much of their work is government sponsored.
It is hard to believe people think the science that Rider did was not of high enough quality; I understand that he actually went above and beyond with his experiments. You obviously must think so, or you would not have decided to take this project on. What convinced you in particular that the scientific merit was there despite its vocal critics?
First, I actually read Rider’s paper. Many of Rider’s critics clearly didn’t even get that far. In fact, I’ve read it now at least five times, and each time through, I pick up some new and fascinating insights.
I consider the paper to be a tour de force. He did much more work than he had to in order to get published. My guess is that he may have suspected that he wouldn’t be believed, so instead of reporting results on one virus, he tested 15. Not just one virus family, but seven. Not just one genome type, but 4. Not just one tissue type, but 11. Not just in vitro, but also in vivo in mice. He even verified mechanisms of action and ruled out effects by secondary compounds.
I also read Rider’s patent; all 250 pages’ worth. Mixed in with the horribly repetitive legal and technical language, there were a number of additional valuable insights.
Considered as a whole, I found the weight of the technical evidence and the proposed mechanisms of action to be very convincing. In addition to that, it also helps that the basics of his work have now been reproduced in two other labs.
Obviously, our focus is on aging and age-related diseases here at Lifespan.io. With that in mind, in what ways do you think VTose might potentially influence aging?
One area where a broad-spectrum antiviral could help improve longevity is by reducing or eliminating the inflammation caused by chronic viral infections of all kinds. Excessive inflammation is a known contributor to aging.
There is also evidence that viruses are associated with a surprisingly wide range of diseases, including multiple sclerosis (HHV6A) in addition to chronic conditions, such as ME/CFS.
What about the persistent virus cytomegalovirus (CMV), which is thought to contribute to the age-related decline of the immune system?
There is evidence that CMV infections are associated with an age-related decline in the function of the immune system (immunosenescence).
Finding a way to cure CMV may therefore help reverse this age-related decline. That makes CMV an important target for longevity research. It’s a priority for us, too, for the same reason.
In addition, CMV may also be involved in several other widespread health problems, including ME/CFS.
Ditto on HSV-1 & HSV-2?
These are also important early targets for testing, both due to the obvious reason that they are common viral infections and also due to recent evidence showing a connection between HSV-1 and Alzheimer’s.
Given that viruses frequently infect large populations of cells, is there a danger that VTose could end up killing a large number of cells at once and, with that, pose a significant risk to health?
Although possible in theory, massive cell death was never seen by Rider during his testing in mice.
There are several factors at play here; some work in our favor, and some don’t. It’s not just the number of cells that are infected. It’s also their location, the tissue type(s) involved, the density of infection, the current status of the viral replication cycle, and so on.
Ultimately, we won’t know for sure until we test; it’s certainly something that we will be watching for.
If it does end up being an issue, we have a number of work-arounds in mind. As an example, one obvious approach would be to use micro-dosing so that only a small number of cells at a time have a concentration of the drug high enough to trigger apoptosis.
What would be your timeline to Phase 1 clinical trials?
There are a lot of moving parts that feed into an answer to that question: everything from which viruses we end up testing against to which tests we run, which labs we use, what our results look like, and so on. In addition to funding, of course!
If we end up with enough funding, our preference would be to focus on clinical trials first and foremost.
With less-than-optimal funding, we are planning to work with veterinary specialists in New Zealand, and other vets internationally, to treat one or more viral diseases in pets and/or livestock. This will allow us to bring a product to market sooner than would otherwise be possible but might also slightly delay a product for humans.
With enough funding, a relatively narrow focus, and no significant distractions, we believe it’s possible to complete pre-clinical trial testing and analysis and an Investigational New Drug (IND) application and be ready for Phase 1 clinical trials in 18 to 24 months.
However, we don’t know what we don’t know. As with any drug development program, surprises are always possible.
A successfully working broad antiviral has significant implications for aging, especially in the context of the decline of the immune system, where persistent viruses put additional strain on dwindling cellular resources, and in reducing the level of chronic inflammation known to impair tissue regeneration and other critical cellular communication. We would like to thank Rick for taking the time to speak with us about this fascinating drug and would like to wish the Kimer Med team the very best of fortune in its journey to bring VTose to market.