Senolytx Therapeutics and How they Are Tackling Senescent Cells: Simple BioTech Podcast #1

James:

Today, I have the honor of talking with Tim Cash. Tim Cash is the Chief Science Officer of Senolytx. Senolytx is one of the six daughter companies of David Sinclair’s Life Biosciences. Senolytx is a company working on one of the biggest hallmarks of aging, senescent cells. In this episode, we go over what senescent cells are, why we have them, and why we need to get them under control. Hi, Tim. Thank you so much for joining me today.

Tim:

Hi, James. Pleasure to speak with you.

James:

So let’s just jump right into things. First off, who are you, what are you working on and tell me a little bit about the company, Senolytx?

Tim:

Sure, James. So my name is Tim Cash. I’m the Chief Scientific Officer of Senolytic Therapeutics. Senolytic Therapeutics was founded in Barcelona in February of 2017, by our academic founder Manuel Serrano, who was a key opinion leader in the field of senescence, as well as Mark Ramez, our CEO. We later set up a mirror company in the U.S. in June of the same year. And the reason for that is that our seed investor was a company called Life Biosciences, based in Boston, who has a major goal of curing aging. We started R&D operations in September of the same year, when I joined the team and moved to Barcelona. So as you may know, there are many strategies to tackling this problem of curing aging. Ours happens to be targeting a phenomenon known as senescent cells, developing small molecules and antibody-based therapies to attack these cells, which we believe, and that there’s a lot of evidence now to support, are a cause of aging. And we can go into more detail about exactly what that means in the interview.

James:

As a casual observer, someone who’s just on the sidelines, paying a good amount of attention to the companies that are springing up. It seems like fixing this senescent cell problem is on the radar for a lot of companies. It seems like it’s a really big deal. In terms of figuring out aging, it seems like it may be one of the biggest deals.

Tim:

So as you know, there are many theories of aging. There’s about eight major theories of aging at this point in time, and we like to think that senescent cells are one of the most important contributors to the phenomenon of aging. And now there’s a lot of good data out there to support that fact. The senescent cells were actually described in the 1960s, by two guys named Hayflick and Moore as a phenomenon of cells and culture to stop dividing and to just kind of sit there, not die, but just kind of sit there and hang out. And it was later appreciated many, many years later, mainly by the laboratory of our academic founder, Manuel Serrano, that senescence is indeed an in vivo phenomenon that it’s not just an in vitro cell culture artifact, but it can happen in vivo.

Tim:

And this really led people to start thinking, “Well, this could be a cause of aging.” Because it was later appreciated that not only are the cells just sitting there arrested as damaged cells, not undergoing apoptosis or undergoing cell death, but they’re also secreting a myriad of inflammatory cytokines that can drive pro aging processes such as fibrosis. And so it was speculated that these senescent cells could really drive many aging processes. And it was just maybe about five or six years ago that really one of the landmark pieces of work came out from the Mayo Clinic from a couple of groups there that when you genetically delete senescent cells in the mouse at least, shockingly and very significantly, you can prolong healthspan by multiple parameters in these mice and you can also prolong their lifespan. So this was really a proof of concept that senescent cells cause the aging process.

James:

Awesome. And so my understanding of sentence cells, basically they’re not dead cells, they’re just cells that have kind of stopped replicating and now they are excreting some sort of toxins that are pro inflammatory. These are things that are starting the aging process. Basically, these are cells that we do not want.

Tim:

That’s right James. I think that’s a pretty good nutshell explanation of what a senescent cell is. So we like to think of three major important characteristics of a senescent cell. First and foremost, they’re a damaged cell. They are a cell that has stopped dividing and has not undergone apoptosis. Normally when you have a damaged cell, the body likes to get rid of it. So it’s not hanging out there, so it undergoes apoptosis. But a senescent cell does not do this for multiple reasons.

James:

So I just wanted to pause really quickly because you mentioned apoptosis, but I think a lot of the listeners may not know exactly what that is. Apoptosis is basically the programmed death of a cell. It’s what your cells are supposed to do. A healthy cell will experience apoptosis. Essentially, this is just when a cell dies and gets wrapped up in this nice little present for the immune system to come along and clear it out. Anyways, go ahead, apoptosis.

Tim:

Apoptosis. So senescent cells have this characteristic of being resistant to apoptosis, or cell death. And actually, I should point out that the first generation of senolytic drugs actually target factors that get at this achilles heel of senescent cells. They’re kind of poised to undergo cell death, but they don’t quite get there. So the first generation of senolytic drugs, which include a drug called Navitoclax get at that vulnerability of senescent cells and drive them into apoptosis. And then as you pointed out, an important characteristic of senescent cells that really drives the pathology behind their existence is this feature of the SASP, or Senescence-Associated Secretory Phenotype, which encompasses the secretion of inflammatory cytokines, as well as factors that drive fibrosis, such as TGF Beta.

James:

Yeah. When I was reading about S-A-S-P, Senescence-Associated Secretary Phenotype, it really seems like the boogeyman of the cellular world, and I’m going to read here from Wikipedia, or just give a quick summary of it, but basically S-A-S-P, SASP. It causes chronic inflammation, induction of fibrosis, and the inhibition of stem cells. Not to mention it reduces NAD levels in non-senescent cells, which has a whole list of problems that can cause, but DNA repair being one of them, and DNA repair being a huge factor when it comes to aging. It seems that getting SASP under control would be incredibly beneficial for the longevity industry and life extension as a whole.

Tim:

Yeah, that’s right. So that goes to the evolution of the way we have been thinking about attacking senescent cells. So I alluded to the fact that there has been a first-generation cadre of senolytic drugs. And when I say senolytic, these are drugs that go to the heart of the senescent cell and kill the senescent cell, in a siliconomas manner. So directly eliminating it. But the more we’ve thought about senescent cells and strategies to get them under control, we realized that maybe we don’t need to completely kill the senescent cell. Maybe we can just suppress this SASP that we’ve referred to, which is the most pathologic feature of the cell. So this has led to a change in thinking, or an alternate way of thinking, that perhaps we can just suppress the SASP. And so this has led to the discovery of a cadre of what we call senomorphic drugs. Senomorphic being drugs that don’t kill the cell, they’re not senolytic, but they simply inhibit this pathologic, biologic feature of the senescent cell, namely the SASP.

James:

So my question is, why would you think that senomorphics would be more beneficial than Senolytx? If Senolytx is just completely removing the cell, the senolytic cell, and senomorphics is more modulating the toxins, for lack of a better word, that it’s excreting. Curious why senomorphics is the better option in your opinion.

Tim:

Yeah, so I think the jury is still out as to whether senomorphics are superior to Senolytx. So on the one hand Senolytx can be said to be superior, because they’re kind of a permanent solution to the problem at hand. We just get in there and get rid of the senescent cells permanently, or periodically as they arise. One problem that we can foresee there is that if you have a diseased organ, such as a fibrotic lung, or a fibrotic kidney and there’s a heavy senescent cell burden, you may have a combination of senescent cells that are contributing to the pathology, but you may also have some senescent cells that are still retaining their function, are important for the continued healthy function of the organ. So you may not want to get rid of all of the senescent cells in that tissue per se.

Tim:

I don’t think that there’s firm evidence out there to say that this is the case, yes or no, we’re working on that. But that’s one concern I can say that’s in the field currently about Senolytx. So one advantage of the senomorphics would be that you could avoid that kind of eradication. Potentially it’s still functioning senescent cells in the organ. But one downside of the senomorphic would be that you would need to continually administer it to the patient because you’re not permanently eradicating those senescent cells. So it would require more chronic treatments. That being said, the senomorphic would still… So I didn’t get into the phenomenon of senostatic.

Tim:

So senescent cells also have this interesting property in that they can spread in an organ. So you may start with a few senescent cells in an organ and then after some time you’ll notice that the senescence has spread, a phenomenon called paracrine senescence or some people call it bystander senescence. Some people call it secondary senescence. But it can actually spread like a cancer. And that’s thought to be mediated by the SASP itself. So primary senescent cells can secrete these toxins, as you referred to, or SASP factors, which can induce senescence in neighboring cells and can lead to an accumulation of senescent cells through time in a particular tissue.

James:

And so this is why senescent cells are so often referred to as zombie cells, because of the fact that they can actually turn other cells around them into senescent cells.

Tim:

So senomorphics would get that under control without killing potentially functional senescent cells that may be important for the function of the organ.

James:

That makes complete sense. So basically Senolytx is dropping a nuclear bomb into the system and you may take out some friendly senescent cells that are doing good work. And senomorphics come in and basically, I guess, manage the damage the senescent cells are doing. Would that be an accurate representation?

Tim:

I think that’s a pretty good summary. I might hesitate to say, nuclear bomb. That’s when I refer to Senolytx. As I said, the jury is still out there about how harmful senolytic therapy may be and I think this is going to be different in different diseases, and maybe different between different individuals. And it may require that we develop a diagnostic to assess the initial senescent cell burden of an individual before we apply senolytic therapy to determine whether it’s going to be an atomic bomb or an actual treatment. But I think your summary is pretty accurate, what you’ve just stated there.

James:

Cool and Senolytx, the company Senolytx, what are you guys working on? You’re working on Senolytx as well, or senomorphics, and I think you mentioned something about training the immune system, something potentially totally different.

Tim:

We’re actually, since the jury is still out about what’s actually better, Senolytx versus senomorphics versus a third strategy, which you just alluded to, which is training the immune system to eradicate the senescent cells. We are taking a broad approach and we’re actually developing all three strategies. So we have a first program where we are developing a senomorphic strategy for the treatment of kidney fibrosis with a focus on a condition called chronic allograft nephropathy, a feature of which is kidney fibrosis through time after kidney transplant.

Tim:

So we’re developing senomorphic therapy to treat that particular disease as a first-in-human trial with the idea of extending that to other kidney fibrotic conditions. The reason for that is that we have very good proof of concept data in animal models to suggest that our senomorphic drug can treat kidney fibrosis very well. We have a second program, which is actually focused on a senolytic. It’s a little bit counterintuitive, the order that I’m describing this since, as I previously said, Senolytx came first and then the concept of senomorphics. But we also have a senolytic approach, which is going after a novel target in the setting of lung fibrotic conditions and we are focusing on the disorder called idiopathic pulmonary fibrosis, as well as a secondary interest in COPD, Chronic Obstructive Pulmonary Disorder.

Tim:

And then we have a third program, which in my opinion is the most exciting and innovative because it’s well developed by ourselves, but not by the field in general, which is this idea that as we get older we accumulate senescent cells. And that’s consistent with the idea that senescent cells can cause aging. But when we’re younger, we get senescent cells when we have injuries. So for example, if you have a wound on your skin, you will develop senescent cells there.

Tim:

And the senescent cells actually serve a function. They serve a biological function that has been evolutionarily developed to protect us from injury. So the senescent cells in that context of wound healing, their purpose is to manage the repair process. So through this SASP, or the secretion of these inflammatory cytokines, they recruit the immune system to come in and clear any bad stuff there. And they also stimulate the repair process by stimulating the beneficial fibrotic program that lays down the extracellular matrix, repair the wound. But at the end of that process, those senescent cells have to go away and the immune system has evolved to clear the senescent cells up in that process. If they hang around, we have a problem. That’s when we have pathologic scarring and fibrosis, but the young body can manage that. But as I was saying before, as we get older, for some reason, for reasons we don’t completely understand, as we get older, the immune system becomes less efficient at clearing senescent cells and they accumulate. There could be two reasons for that in our opinion.

Tim:

Some people speculate that it’s just as we get older, our immune system doesn’t function as well, so it can’t clear up these senescent cells as well, so they accumulate. But another interesting possibility is that the senescent cells evolve mechanisms through time to evade the immune system. That’s actually our favorite hypothesis, and our academic founder Manuel Serrano has carried out a [inaudible 00:16:33] approach in his lab to identify cell surface proteins and targets that contribute to this process of invasion of the immune system by senescent cells. And we have focused on one lead target there and are developing therapies against that target of course, both monoclonal antibodies and small molecules as a potential way to get the immune system to come in and clear those senescent cells.

James:

That’s quite a bit there, but doing my best to follow along. I’m going to try and repeat that back to you in my understanding of it. Essentially, as we grow older, the senescent cells learn to hide themselves in a way. Would that be accurate?

Tim:

That’s a pretty good description.

James:

So using some sort of protein or molecules of some sort, they’re able to hide themselves and you guys think that you found, you figured out which protein, which molecule it is that helps hide them. And you want to basically, what do you want to do with that information?

Tim:

We are developing monoclonal antibodies and small molecules that inhibit the inhibition of this molecule and allow the immune system to come in and clear the senescent cells. So basically this protein that we have identified is a break on the senescent cell that blocks the immune system from clearing it. So when we block that break, we allow the immune system to come in and clear those senescent cells.

James:

That’s perfect. So basically, you clear out this protein that’s keeping things hidden, and once that’s cleared out, the immune system comes in and does what it’s supposed to do.

Tim:

That’s right. And the protein is actually expressed on the senescent cell itself. So upon blocking that protein, the immune system can immediately come in and clear those senescent cells.

James:

That’s super interesting. And you think that this is a more effective way of clearing senescent cells than Senolytx and senomorphics potentially?

Tim:

My personal opinion is yes, it’s a very natural way to clear the senescent cells, because you’re allowing the body to do its job naturally.

James:

It seems like you guys are basically just setting up the immune system to do what it does best and to have the highest chances of success of finding and removing the senescent cells. It does seem a lot more natural than say Senolytx, which would just be killing off the cells and senomorphics, which as you mentioned, would likely be a treatment that you would have to continuously do. So I want to talk about the delivery system that you guys are going to be using to inject this. I guess you would be injecting this?

Tim:

Yeah, so I think you’re referring to the nanoparticle technology?

James:

Yes. The nanotechnology that you guys are working on. When I was reading about this and when I watched your video that I probably had to watch this part about five to 10 times, it almost seems like science fiction.

Tim:

So this was the initial technology that we focused on and we continue to explore its applications on the side. It’s not related to any of the therapies I have just described. It’s an entity of its own, but the idea behind the nanoparticle technology is again, getting at vulnerabilities of senescent cells. So senescent cells are known to highly express a particular enzyme called beta galactosidase. Now this enzyme is expressed in all cells, but at low levels, and for reasons we don’t quite understand it’s expressed very highly in senescent cells. It’s related to the increased lysosomal mass that senescent cells have, an interesting unique feature of senescent cells that’s still being explored.

Tim:

But by virtue of this high level expression of beta galactosidase we have designed a mesoporous silica nanoparticle that can be loaded with a cytotoxic, our prototype for that is a drug called doxorubicin, which is a very well known chemotherapeutic in the field of oncology.

Tim:

This nanoparticle can be loaded with cytotoxics such as doxorubicin and then coated with a natural substrate for beta galactosidase, in this case it’s a polymer, the galactose itself. And so, the strategy there is to treat cells in culture or animals in vivo with these nanoparticles. And by virtue of that special polygalactose coats only the senescent cells can uncoat the cytotoxic that’s inside and allow for its release and allow for killing of senescent cells.

Tim:

Now these particles are taken up by non-senescent cells, but because the particles are coated in this substrate that’s very specific to an enzyme common to senescent cells they aren’t uncoated and they’re just cycled back out of the non-senescent cell. So this vehicle targets senescent cells by virtue of this coat, and by virtue of the fact that senescent cells highly express this enzyme called beta galactosidase.

James:

Beta galactosidase, that’s quite a mouthful.

Tim:

Beta gal.

James:

Beta gal. Yeah, that’s much easier. So my understanding is basically you’ve got these incredibly small nano size balls that you guys fill up with your drug doxorubicin, which is a chemotherapy drug.

Tim:

That’s right. That’s right. But in theory, these nanoparticles can be filled with any drug of choice.

James:

Any drug of choice. So once this is injected into, it’s injected, I assume, correct?

Tim:

Our current route of administration is injection. Yes, that’s correct.

James:

So once this is injected, it goes into your bloodstream. It can find these senescent cells because senescent cells give off this red flag, the beta gal, correct?

Tim:

Well, it’s a little bit different from that. The nanoparticles actually enter also, it’s not until it gets inside the cell that the specificity comes into play because the nanoparticle’s encoded inside of the cell, inside the lysosome where this enzyme, beta gal lives. It’s only in the senescent cell where the nanoparticle becomes uncapped. In non-senescent cells it will go into the cell, but it will come back out uncapped.

James:

So essentially once these nanotechnology balls get inside of the cell, if the cell is highly expressing beta galactosidase; beta gal, then it would be a senescent cell. And because it’s expressing that beta galactosidase the balls would be uncapped and the doxorubicin, or whatever drug has been inserted into the balls, will be released and effectively terminate the senescent cell. However, these little tiny nanotechnology balls will be going into all of the cells. If a cell is not highly expressing the beta galactosidase, then these nanotechnology balls, let’s just call them nanoparticles, will cycle out of the cell and it will not be uncapped, leaving the non-senescent cell completely unharmed. That is a pretty neat little system. So, that brings me to my next question. What happens to these nanoparticles? Do they just stay in your body forever or do they get cycled out, excreted somehow? Is there any evidence that there’s levels of toxicity?

Tim:

So we have preliminary animal data that they are excluded by the normal routes of excretion.

James:

Well that’s great to hear because in my research, when I’ve been looking into other companies, I have seen that a lot of companies that are developing nanoparticle technology are actually having issues with toxicity and especially toxicity in the liver. But again, this is, it’s not one of Senolytx’s, Senolytx the company, it’s not one of your company’s main focuses.

Tim:

So as I said, the nanoparticles are not a component of our more mature programs at this point in time, but we continue to develop the material.

James:

I’m obviously not an expert on the industry, but the concept of being able to deploy any number of drugs directly into a cell, especially as new drugs, new molecules continue to be developed that would benefit greatly from this type of deployment, the use cases for this type of technology are only going to continue to grow as time goes on. So now I just want to talk about what type of results you guys are seeing with these Senolytx. You mentioned you guys have done animal trials.

Tim:

That’s right. That’s right. So since we’re on the topic of nanoparticles, I can start with that, since that was our first senolytic prototype that was developed in the lab of Manuel Serrano, that we carried over into the company. And that work is actually now published. And so with that, that’s actually a senolytic, that qualifies as senolytic since it kills the senescent cells.

Tim:

What they saw is that, and again this is published work, that the nanoparticle-based therapy can have efficacy in an animal model of idiopathic pulmonary fibrosis. So they took a mouse model of lung fibrosis and administered the nanoparticles after the fibrosis developed and almost miraculously saw that the lung function of the animals with lung fibrosis was restored after two weeks’ treatment. And in that work they also saw that the nanoparticles can synergize with standard chemotherapeutics in a model of melanoma xenograft in animal models to completely eradicate tumor growth.

Tim:

And so the topic of Senolytx in the field of oncology is beyond the realm of what we study within Senolytx. We have seen some interesting signals with some of our assets inside Senolytx in the field of oncology. And actually we are currently out-licensing the concept behind the immunotherapy we’re developing to a company that’s interested in developing therapies related to cancer and senescence-induced therapy in cancer. So with our senomorphics so far we’ve seen, in the first program, we’ve seen efficacy in animal models of kidney fibrosis. With our senolytic therapy we’ve seen efficacy in animal models of lung fibrosis. And with a third molecule, the immuno molecule, we’ve seen strong signals in animal models of cancer.

James:

The world of oncology has gotten pretty exciting over the past few years with tons of strides being made in the methods of how we are treating cancer. And especially as we learn more about the role of the immune system in cancer treatment. So I want to talk a little bit about regulatory hurdles. I know when it comes to getting these things through the trials, you have your phase one trials, your clinical trials, you kind of have to choose a target. And so for Senolytx, your guys’s target is fibrosis, correct?

Tim:

That’s correct. So kidney fibrosis and lung fibrosis are key indications in Senolytx.

James:

So even though on paper you guys are kind of forced to choose a target to get through all of the regulatory hurdles, ideally your guys’s technology will be used in a much broader sense, in a much broader anti-aging life extension sort of use case.

Tim:

That’s right, and that’s our ultimate hope. The ultimate goal at the end of the day is to find molecules that don’t just cure one age-related disease, but to find molecules that can actually treat aging itself. As you may know right now it’s a bit contentious about whether or not aging is a disease. A lot of effort is being put into getting aging on the books as a disease to be treated in general, but to start in trials, and so the idea here is to treat age-related diseases one at a time in clinical trials because that’s all we can do right now, but with the hope that we can broadly apply these treatments, not just to one age-related disorder, but the broad spectrum.

James:

I think we’ll get there sooner rather than later. I’m hearing more and more people on Facebook, on Instagram, just in general talking about longevity, talking about the fact that yeah, maybe aging is a disease as a whole that we should be working on fixing instead of putting band-aids on all of the other little problems. Really exciting. Really interesting stuff. Thank you so much for taking the time to explain all this to me, Tim. I really appreciate it. To finish things off, I just want to ask you some fun questions about the longevity and biotech industry. If you’ve still got a little extra time?

Tim:

Sure. Sure. Shoot.

James:

Well, first of all, there’s ton of companies working on senescence at the moment. Why do you think Senolytx will be the company to figure it out?

Tim:

Well, I think one of our advantages, and one of the things that puts us ahead of everybody else is the fact that we have Manuel Serrano on our team who is a key opinion leader in the field of senescence. He’s made many of the fundamental discoveries that have driven the field forward, including the discovery of the important cell cycle arrest factor B16, as well as the concept of oncogene-induced senescence, as well as the first observation that senescence can occur in vivo. So having that expertise on our side definitely puts us ahead of the rest.

Tim:

In addition, one of our advantages is that we are really looking for new targets and strategies beyond those that have been tried before. And so I alluded to the fact that there are a first generation of targets and senolytic drugs out there, namely going after the target BCL-2 and BCL-XL, MDM2 and the drug dasatinib. And so we think that there’s future generations of targets and drugs beyond that and we are taking approaches to screen those targets both internally, but also via collaboration with Manuel Serrano’s lab. And doing strategies beyond just simple standard drug screenings. We have novel screening approaches that we think will lead us to novel targets that will yield better efficacy when targeted.

James:

Not to mention you guys are a daughter company of Life Biosciences, which is, if people don’t know, that’s David Sinclair’s company. I imagine that has a lot of benefits.

Tim:

That’s right. So Life was our seed investor and got us off the ground very successfully. We’ve had a very good relationship with Life Biosciences thus far, and David certainly is a key opinion leader in the field of aging and developing therapeutics to treat this thing that we call aging. And so that definitely, that relationship has definitely given us a fantastic jumpstart to move forward.

James:

Yeah, absolutely. David Sinclair is actually the guy that got me into it about two years ago when he was on Joe Rogan, so he’s definitely been a positive member of the community for getting the word out. I mean before, two years ago, I never thought that it was even possible to extend your lifespan beyond 80 to 90 years old. He’s definitely a benefit to have on your team.

Tim:

Yeah. David is a key driver in this field of aging and moving just the thought forward in the field that we can actually have a cure for aging.

James:

So a couple more questions. What are you most excited about in the biotech industry right now?

Tim:

Oh, there are so many things to choose from, but if I had to think about this off the top of my head in relation to what we’re working on, I think the field of immuno-oncology is really the most exciting thing out there right now. This field of anti-PD1-based therapies has really revolutionized the way that we see cancer therapy. Revolutionized the way we do trials now. I think almost every trial includes a co-treatment with an anti-PD1 therapy. It goes at this idea that how important the immune system is in treating cancer, which links to the idea of how we can also train the immune system to eradicate senescent cells, much like tumor cells, from the body to treat age-related disorders. So this whole revolution in the field of immuno-oncology is a paradigm for how we can think about aging and age-related, this sort of therapies.

James:

It seems more and more that there’s a ton of similarities between the oncology cancer research and senescent cell research.

Tim:

That’s right. That’s right. As I suggested earlier, senescent cells are a lot like cancer cells. The only difference is cancer cells divide like crazy, senescent cells don’t divide at all. But senescent cells, like cancer cells can spread within organs and wreck havoc on organs. The ultimate goal is to eliminate them, just like we want to eliminate tumor cells.

James:

What an exciting time to be alive, hey? To potentially see a cure for cancer and the drastic increase in human lifespan. You can’t help but feel a little bit lucky. A little bit like we’re very lucky to be born at this time. Ideally, we don’t just miss the boat. One last question. Where do you think the longevity industry will be in five, 10, 15 years? I want to try and get excited about this. What do you think we’re going to be looking at in that time period?

Tim:

That’s a very interesting question, James. So I think in the next five years we can look forward to the completion of some early phase clinical trials focused on specific age-related disorders. And so we should have a collection of different molecules and different age-related diseases to kind of assess and see where there’s commonalities and see where things work and don’t work. And that should allow us to maybe move to doing trials specifically on aging on multiple age-related disorders within 10 years.

Tim:

Once we have the information from individual diseases and individual molecules within the first five years, we can expand that to look at more than one disease at a time in clinical trials within the next 10 years. And then maybe within 15 years we can start to focus on molecules that can be given to the general population, molecules that have been proven to be safe. And I’m just talking about starting to think about doing this, which maybe 10 years ago people thought this would be possible. So just the fact that we can start to think about this in 15 years, about specific molecules that can be applied as a general anti-aging strategy I think will be revolutionary. That’s where I see the field moving over that timeframe.

James:

Yeah, it’s going to be a different world in 15, 20 years. I keep telling people this.

Tim:

It seemed like science fiction 10 years ago. Now it still seems a little bit like science fiction, but more of a reality than it was before.

James:

For sure. Well thank you so much for joining me, Tim, and if anybody wanted to reach out to you in terms of doing what they can to help out Senolytx, if you guys are money at any point, how can they be a part of this?

Tim:

So we are going to be in fundraising mode to support R&D-enabling studies, and first-to-human trials for the mature programs I previously mentioned starting in quarter two, quarter three of this year. We have a website that’s Senolytx.com, you can easily reach out to us there, as well as myself personally, or our CEO. And we are also open to partnerships to develop our own internal mature clinical assets as well as external assets that may have been developed for other purposes but may have an application in the field of aging, as well as any clinical partnerships that could facilitate the development of our kidney fibrosis and lung fibrosis programs.

James:

Awesome. I’m so excited to follow along with Senolytx and see what you guys come out with. Once again, thank you so much Tim. This was a great conversation and I learned a ton.

Tim:

Thanks James, it was a real pleasure to talk to you.

James:

If you got this far, I just want to say thank you so much for listening. If this was at all interesting to you, I’d love to connect on Instagram and hear you feedback. I’ll also be posting clips from the latest episodes, as well as anything else I find interesting about the biotech industry. You can find me on Instagram at Simple Biotech, and if you’re interested in the companies that I’m looking at and the companies that I’m excited about, connect with me on Angel List at angel.co/jamesruhle. That’s James R-U-H-L-E. Thank you so much, and be safe out there.