Treating Previously Undruggable Diseases: Dr. Ian Taylor at Arvinas
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Most likely everyone reading this has been affected by cancer or knows someone who has had cancer. Using natural cell degradation, today's guest and the team at Arvinas are treating previously undruggable diseases like cancer and Parkinson's. Their goal is to cure cancer or at a minimum, reduce it to a disease where you take your medication and continue living a full life without the terrible side effects of today's treatments.
Dr. Ian Taylor, Chief Science Officer at Arvinas, explains how his team is accomplishing this with PROTAC. Arvinas is a clinical-stage biopharmaceutical company focused on developing new therapeutics for cancers and other difficult-to-treat diseases.
If you are hoping for another treatment for cancer besides historical approaches (like chemotherapy), you need to listen to what Dr. Taylor has to say. It's innovating and extremely exciting.
More about Dr. Ian Taylor:
Dr. Taylor came to the company after nearly 10 years at Pfizer Oncology, most recently as an Early Development Team Leader. In this role, Dr. Taylor was responsible for leading a cross-functional drug development team that conducted Phase 1 and Phase 2 clinical trials for multiple assets in several cancer indications. His initial role at Pfizer Oncology was as Senior Director of Translational Oncology. In this role, he was responsible for directing translational science activities, which included designing and executing translational research plans and leading companion diagnostic partnerships for programs in both preclinical and clinical (Phase 1 -3) stages. Prior to Pfizer, Dr. Taylor worked at Bayer Healthcare, Pharmaceuticals, holding positions of increasing responsibility, including Vice President of Cancer Biology. In this position, he led the department responsible for all biology aspects of small molecule drug discovery of cancer therapeutics in the mechanistic areas of signal transduction, cell cycle regulation, angiogenesis and apoptosis. During his tenure, the Cancer Biology group delivered numerous molecules to the Development organization. He also started and led the Biomarker group, which contributed to the development of sorafenib. Dr. Taylor earned his B.A. from Bowdoin College and his Ph.D. in Molecular Biology and Genetics from Harvard University. He also completed his postdoctoral training in the laboratory of Dr. Harold Varmus at the University of California, San Francisco and the National Institutes of Health (NIH).Enjoy!
- Arvinas treatment pipeline: https://www.arvinas.com/pipeline-programs/pipeline
- Be a guest on the show: https://docs.google.com/forms/d/e/1FAIpQLSeEU7Owi8VDv30hzmWbj4JsXPKyfsWvKXHMeghEAyirAbR18A/viewform
Hi, everyone. Thanks so much for tuning in. If this is your first time being here - welcome! We share inspiring stories of people on the front lines of life sciences, bringing life saving products to market. And if that sounds like you, or you want to share your story, we'd love to hear from you. There's a form in the show notes here to apply, to be on the show. if you have an idea or know somebody, please submit their name. We'd love to get in touch.
Today's guest is Dr. Ian Taylor, the chief scientific officer at our Venus. He came to our Venice after nearly 10 years at Pfizer oncology. most recently as an early development team leader, his role there at Pfizer was cross functional in drug development treatment and conducted phase one and phase two clinical trials for multiple assets and several cancer indications.
And he's had a whole career in oncology as well with Bayer healthcare pharmaceuticals, and it got us. BA from Bowdoin college and his PhD in molecular biology and genetics from Harvard university. And Ian today talks about the mission of our Venus and pioneering science to develop new transformative treatments for patients with limited treatment options or for whom existing treatments have not been very effective.
He and his team work in targeted protein degradation. And Ian goes more into this, but basically tagging cells in a unique way to naturally degrade. He also goes into the advantages of this type of treatment, as well as the future of being able to treat what is now 80% of untreatable diseases. And the possibilities of making treatments or reality for those who suffer from them.
let's bring him in…
[00:01:49] Grant: Ian, thank you so much for joining the podcast today.
We're excited to have you on the show.
[00:01:53] Dr. Ian Taylor: Oh, it's my pleasure. Thanks for having me. I'm really
[00:01:54] Grant: excited too.
Yeah. We are excited to talk to you about what you're doing at Arvinas and the field, a really interesting field and the technology that you're working on over there to treat previously undruggable diseases.
But maybe before we get into that, just for those who may not know about Arvinas, tell us about what you folks are up to there and your company.
[00:02:12] Dr. Ian Taylor: Yeah. So at Arvinas, we're looking into new Haven, Connecticut, and our mission is to serve unmet medical needs, particularly the fields of oncology or cancer and neurodegeneration.
And we're expanding it to other areas as well. And we do that by what we is known in the field as targeted proteins. For us specifically, we use a technology called Protacs or proteolysis targeting cameras. These are small molecules that are designed, excuse me, to eliminate disease, causing proteins from cells.
A lot of drug therapies that people may be aware of are largely inhibitors. They inhibit the catalytic function of a particular disease causing target like an enzyme, which is fine, but there's a lot of limitations. It's hard to fully inhibit a protein. If it's really overexpressed in a cell saying like in a cancer cell, whereas our technology uses the natural way that cells degrade proteins or turn over proteins because cells are constantly doing that.
They're making new proteins, they're getting rid of old proteins. If they're misfolded or they're mutated, or they've just outlived their natural life. So we're hijacking, we're tapping into that system with a small molecule and degrading the protein, just completely eliminating it from the cell. And we think that has a lot of advantages.
Longer-term benefits of keeping that cell from being expressed lower doses of the therapy different functions that proteins might have other than their Intermatic function that leads into the undruggable space. And w and applying that to oncology cancer and neurodegeneration such as diseases like Alzheimer's or Parkinson's.
[00:03:46] Grant: Yeah. And one thing I think is really interesting about you're doing there is you're. I think you used the term hijacking you're using the body's normal function. Eliminating these abnormal proteins. And I think that is something that will capture people's attention because it's something that's natural to the body.
So how are you, like, how did you get into that type of technology and how are you advancing that? Yes. So
[00:04:08] Dr. Ian Taylor: this is a technology that was spun out of Yale university. So our scientific founder, Dr. Craig Cruz was the inventor of Protacs 20 years ago. Now, when we first published a paper on Protacs, so he had the idea of.
If you could somehow bring the way cells normally degrade proteins and make it attack a certain specific protein that you want it to degrade. Then right now in this cell, that could be really powerful. So the way it works as a small molecule, Binds to what we call a hetero bifunctional molecule actually has multiple functions and that's why we call it Kymera.
It's basically three structural features in one small molecule. So one end of the molecule binds to the target that you want to degrade. So the disease doesn't protein, the other end of the molecule binds to an enzyme in the what's called the ubiquitin proteasome system. That's the natural system that the cell uses to degrade, or at least one of the natural systems.
There's actually. And so what you're doing is you're bringing this workhorse enzyme and ubiquitin proteasome system called ubiquitin ligase. You're bringing it right to the target that you want to degrade. And the ether ubiquitin ligase is job is to. Add a ubiquitin chain of molecules. This is a tag that the cell recognizes, oh, once the protein has this ubiquitin tag, it's the cell says, oh, this protein is now ready to go off and be degraded.
So once that, once the ProTech actually brings together the disease causing protein in this ether, ubiquitin, ligase, the rest of the process is exactly how the cell would normally do it. But you realize this, you pick what needs the protein. That tag of ubiquitins the cell recognizes and off it goes to what's called the proteasome, which is this collection of enzymes that chops up the protein into its component peptides and ultimately into amino acids and completely eliminates it from the cell.
So it's really, it's very intuitive. It's really cool. Actually the way it works and it actually does work. We can completely eliminate proteins from cells by treating with the small.
[00:06:01] Grant: Wow. I think I saw on your website which is fantastic, where there's a lot of great videos that kind of show exactly what you're talking about here in a a very visual way for our us visual learners.
But you said that I think 80% of the proteins. Today is currently undruggable. And your technology is going to be able to address a lot of that, with being able to target specific cells to then tag them this way. So just curious how with this huge potential with neurodegenerative diseases, cancer, like you mentioned, how is your team focusing on where to advance and continue to research this technology?
And what eventually gets into.
[00:06:36] Dr. Ian Taylor: Yeah, that's a great question. So yeah, the undruggable space, so you're right. 80% of the proteome, which is the collection of proteins in a cell are considered undruggable. And for those of us who are working in drug discovery for a long time, and for me, it's been a long time.
There's always been this great collection of proteins that are clearly linked to disease, but just have been intractable to traditional small molecules. And we've had to move away from those over the course of time. And there's just a one list. Some of them are called these holy grail targets that boy, if we're going to.
We would probably be able to treat disease. And this has been something that I focused on for a long time. It's really what attracted me to come to our business was the ability to go after these undruggable. And the reason protests can do it is because really all you need to do is with the protect is bind to the target protein and then bring that to it.
And it only has to bind. It only has to bind transiently just long enough to form that tremor complex of the protect, the target and E three ligase, get that protein ubiquitinated and then go off. It goes to degradation. You don't have to have any other function than binding finding a transient body, but traditionally with traditional small molecules, you would have to attack.
What's known as an active site, right? An enzymatic site, the way that protein is working, but some proteins don't have active. Sometimes. And sometimes those proteins active sites are really hard to get a small molecule in. There are things like transcription factors to just bind to DNA, but drive transcription in particular, in oncology, that's a big problem.
Inappropriate gene expression leads to to inappropriate tumor cell growth, which leads to tumors. There's a whole group of transcription factors that just, and they're like bowling balls almost right there. You can picture it as a book. They're very smooth. There's not that many nooks and crannies.
Where can you bind a small molecule to inhibit the dysfunction? It's largely impossible with a ProTech I have to do is bind a little bit in one of those nooks and crannies, get that there you pick and can degrade. And so that's, those are the kinds of targets that we are looking. And also we're really attracting the struggles, but also where does degradation have an advantage over traditional small molecule inhibition or even inhibition by antibody?
So other therapeutic modalities, certainly there are a lot of successful drugs that are working. We want to make sure that we're attacking phase where degradation actually has an advantage. So it's not just a meeting. But the by Dick by actually removing, approaching from the cell, it has an advantage over other, any other modality.
And that's how we, that's how we select our targets. That's how we prioritize our targets. That's what we prosecute our targets with that fundamental aspects. What we call like the the tenants of protests. We have a collection of where does the degradation have an advantage over other modalities?
[00:09:15] Grant: a lot of sense. Okay. Yeah. I appreciate you explaining that. What are some of like you said, With some treatments, you can have unintentional growth. What are potentially some of the risks involved with this type of technology, like perhaps binding to the wrong type of protein or something like that?
What are some of the risks involved?
[00:09:33] Dr. Ian Taylor: Sure. That's what people always focus on. Several risks, we get a non-selective degradation, right? We'll be degrading other proteins that you want a degree. And that's something we obviously tracked during the course of our lead optimization program.
When we're developing the drug, we can we can track that using what's known as proteomics. You look at as, thousands of proteins in the cell and make sure you're only degrading. The one that you're going after. We've actually shown that for our weed programs that are in the clinic, , it's going after the androgen receptor for prostate cancer, every 4 71, that's going up to the estrogen receptor for breast cancer.
We've actually looked and say, okay, are we degrading anything other than the estrogen receptor rest of your center? Cancer is no, at least for the large part of the proteome that we can look at it. So we optimize for that. As we go, the other thing that people say is. You're hijacking ubiquitin proteasome system.
So are you affecting its ability to degrade other proteins that would normally degrade and then they'll build up and cause a problem? The answer to that is no, as far as we, as far as we can see, it was looked at many times and that's because our molecules are really potent. So we're only using a small fraction of the ether, ubiquitin ligase, for example, we're only using a small fraction of the total capacity of the proteasome.
And so we've not seen a buildup of other proteins because we're hijack. Because the molecules are potent and we're just using a fraction of it. So those are the main issues that they're concerned about. Of course, it's your, when you're doing drug discovery, drug development, you're always looking for toxicity.
So we certainly track that in the clinic, in our patients. And we try to minimize those. And the other thing with pro-tax is we can use lower dose. Because of the way the ProTech works. You don't have to overwhelm the target with a lot of compounds because it's an event driven pharmacology, the event being the Pequot nation.
It's not an occupancy driven pharmacology, like traditional small molecule inhibitors. They'd have to occupy that active site and you need an excess of small molecule to make sure you're constantly occupying the site. So that allows for lower doses would also help with the safety profile.
[00:11:30] Grant: That is fascinating.
And I can't think of. It might be so bold as to say that everybody listened to the podcast. And certainly no one in my circle has been unaffected by somebody with cancer or neurodegenerative diseases. And so the idea of having something that is safer and allows the person to recover faster than a lot of these overwhelming treatments available today.
That sounds really exciting. This is really innovative, the cusp of this field moving forward into the future. So this is just an exciting, and one quick, one quick side note that you mentioned a couple of the treatments in your pipeline right now. We'll link to this in the show notes, but there are, I love how your website lists a lot of.
The program's going on and their current phase, if it's research or and where they're listed here. So I think in some of the partners that you're involved with, I just love the transparency on your website. We'll link to that in the show notes. So people can see actual more information about some of the treatments that you just.
[00:12:25] Dr. Ian Taylor: we actually have, we have three compounds in the clinic. Now we have another androgen receptor called IRB 7, 6, 6, which you'll see on the website. We actually have over 20 programs that we're working on at various stages, both in oncology, immuno-oncology immunology we're getting into and also neural degeneration, as you mentioned.
So that, and that just speaks to the power and breadth of Protacs. We view it as what we call therapeutic area. Can really be applied almost anywhere. We actually have a joint venture. You'll see on our website with bear farms who called it a bear health care, which is called the earth by which is bringing Protacs into the agricultural space.
Interesting. So beyond human disease. And to be honest, one of the surprises that I've had over the course of my career or Venezuela, when I started a little over five years ago, we were essentially the only company to. Protests and targeted protein degradation protects is applied to targeted protein degradation.
Now there are so many companies doing large. Biotechs like us academics. I honestly can't think of a field that's exploded as much within five years, at least in the drug discovery space as targeted protein degradation and protects as because everyone recognizes what you've already said, the potential power of it, the advantages in terms of adverse events or toxicity.
Now it's easier to name companies that aren't doing. Protests are targeted protein degradation than are cause it's, they're just, everyone is doing it. Literally everyone is doing, and that's been great for us as a, as pioneers in the space. All those people buying it, but it's really been eye-opening it's wow.
And people were bringing in until the therapy, other companies were bringing it to other therapeutic areas. Again, just speaking to the breadth and the power, potential power of the technology.
[00:14:07] Grant: Yeah. So Ian, I guess I'm curious, let's take a second to see a look in the rear view mirror a little bit.
And how did you get here, in your career. So we'll link, we went over your bio a little bit. We'll link to it in the show notes as well. But you were at Pfizer oncology for a number of years. You worked with Dr. Harold Varmus, the Nobel prize winner. And so just, from some of the experiences within your career how has your experiences led to how you where you got to today, first of all, and then just some of the ways that you approach your work today from experiences early on in your career, for those who are just starting out in.
[00:14:35] Dr. Ian Taylor: Yeah, it actually touched on I'll come back to it. You touched on it earlier in one of your comments. Yes. I got my PhD at Harvard and then I grew up outside of Boston, so it was a nice area for me to stay local. I went to college in Maine, then I was lucky enough to get a post.
With Harold Varmus, who was at university of California, San Francisco at the time he basically just won the Nobel prize sharing it with Mike Bishop for discovering oncagenes. So cancer causing genes and spent three years there. And then he became the director of NIH national Institute of.
And so he moved there and I was lucky enough to move with him and finish up my post-doc a year at NIH was really very interesting. NIH is huge, down to Bethesda, Maryland. And at the time I was I was finishing up my post-doc and I start to apply for academic jobs. It'd be, become a professor, but I actually had a couple of offers, but right around that same time, and I was deciding I got a call from a down.
For a job at bear pharmaceuticals up in west Haven, Connecticut. And I said, oh, that's interesting. I didn't really know much about the pharma industry, but I went on the interview and went on a second interview and decided to take the job. Cause a lot of what I was doing, health lab looking for new genes, applied to what they were looking for.
Harold. I was going to take this job at Baron. Yeah, I thought you were taking this academic job. And I said to him, Harold, I'm not going to win the Nobel prize. I'm just not like you. But I think the next coolest thing would be to be involved in a project where you brought a drug to help patients.
And he looked at me said, yeah, I can see that again. Plus I didn't really want to write grants. And that, that just, wasn't my thing. I wanted to do applied research. That philosophy of wanting to develop drugs and help patients has carried me through my entire career. And I've been lucky enough to be involved with over my course of career at bear and at Pfizer where I went after bear shut down in Connecticut.
And I was in oncology drug development. So at bear, I was in research and then at Pfizer, I was in drug development. So clinical trials. And I've been lucky enough to be involved in six programs that have made it to the market. That's really fortunate. A lot of people work their whole career and they're not involved in one that gets to the market.
And I've always been drawn to oncology now, our vascular and neuro science as well, because of exactly what you said, you, you tell people you're working in cancer. Immediately can resonate with that, right? Because everyone knows cousin, a grandmother, a nephew, any, neighbor who's been touched by cancer and then same with neurodegeneration, Alzheimer's becoming more prevalent.
And so it's been gratifying to be able to connect with people with the research that you do and trying to. Yeah, maybe not their spouse or their family member. But the next generation, and really, we're trying to cure cancer. We're trying to cure these neurodegenerative diseases.
That's really hard to do, but we're really trying to extend people's lives. Make these diseases more. But improve their quality of life. Not just their length of life kind can turn it into like diabetes or something where you can take a pill and control that disease for a really long time. And that, that would be a success, right?
For people to make that next graduation or the wedding or whatever that next family milestone. That's constantly what I strive for. When I think about, now that we're a public company, there's a lot of focus on investments and that stock price or whatever. I always say. So to the folks here, focus on the patients, the rest will take care of itself.
And that's been a thread throughout my whole career.
[00:17:54] Grant: Yeah. That's very sound advice in the corporate world. We hear, when you focus on your customers, you can't really miss. Yeah, you can't really go too far if you're very customer obsessed as a phrase, I hear a lot in the technology space.
So with that as a background, thank you for going through that career history though. That's really fascinating to hear how people get to where they are. What are some of the guiding principles that maybe govern your day to day as the chief scientific officer?
[00:18:16] Dr. Ian Taylor: It's high quality science is the first thing, right?
Making sure that everyone's doing experiments the way they need to be done so that we can really interpret our data, develop the best compounds we possibly can. So it's all about designing the right experiments to answer the next critical question. And of course, to do that, you need to hire great people surround yourself with great people.
I think that's common to almost any organization. That's really great is oftentimes the people that surround the leaders, whether it be a CEO or CSO are actually smarter than you are Eh, but just need, but need leadership and to really Excel. And so my, I always say that my job is to make the people that are in the research group, their job easier, remove barriers, allow them to be creative, innovative, do the best possible work that they can do because they're actually doing the work. I don't do any real. No I've reviewed data. I I give suggestions, but I'm not in the lab anymore, which I think everyone is thankful for doing the experiments.
You gotta, you got to enable the people who are actually doing the work to do the best that they possibly can. So remove barriers, give them advice, give them leadership, give priorities, make decisions. That's what I've learned throughout my career. A lot of times people just want somebody to make a decision and have it be clear.
Understandable. And they're like, okay, they may not agree with that, but at least they know, okay, this is what the priority is. This is a decision and this is the direction we're going. And so that's how I approach it. Hire great people, point them in the right direction, remove the barriers and then get out of the.
[00:19:48] Grant: Yeah that's very sound leadership advice. And with with hiring great people and where Arvinas is today and my mind's still blown at the potential of all the technology that you're working on over there. So much has happened over the last decade with technology advancing and just the tools to be able to research, do high quality research.
Like you're saying. Where do you see if we look towards the future? Where do you see the next five to 10 years going in the spaceman? Not, maybe not just for Arvinas, itself, but also just in the field overall. Where do you see things evolving?
[00:20:17] Dr. Ian Taylor: Yeah, targeted protein degradation.
I feel like in general, we've just scratched the surface. I mentioned Craig Cruz, the Yale university professor who started the company published the first ProTech I sent to him probably a year or so ago. I said, Craig with protests, you've not just opened up a new therapeutic modality new approach to treating these diseases.
We've opened up a whole new area of science, right? Understanding system, how to hijack. Effectively, and it's really spawned this whole other area of what's called induced proximity. So what, with the ProTech, we're reducing the proximity of our target protein and the east green lights to degradation, but you can Excel in PE and now companies are expanding that beyond protein degradation to other enzymatic functions, like plus four relation or dephosphorylation acetylation.
People have now taken what we've done with targeted protein degradation and bringing it into other areas. And it's just expanding like exponentially, this whole idea of hijacking normal systems that the cell uses to basically modulate disease causing proteins and therefore be able to treat diseases.
So that's where I see it going where we are in the next five to 10 years is moving beyond degradation. Where I, as I said, companies are flooded. So now going through these other processes that you can hijack and different ways of them treating diseases and ultimately combining those approaches, right?
Certainly in oncology, the way cancers are treated now it's rarely by just a single drug. It's usually it's multiple drugs. You only have to do your clinical trials and that kind of thing. But ultimately it gets combinations because I always say cancer cells are smart. They figure out what they're trying to stay alive.
And it's accelerated. There they have new mutations, new ways of bypassing the pathway to stay alive. And they're trying to stay one step ahead. It's the same as if you're trying to stay alive, you're going to do everything you can to stay alive or cancer cells doing everything I can to stay alive, trying to kill it.
So that's why you need to take multiple avenues. One avenue could be targeted protein degradation another could be dephosphorylation by induced proximity. So that's where I see it going. Just taking many, many different approaches to to ultimately make cancer either again, it's hard to cure cancer, that's our goal, but to make it more of a chronic disease. And have people live 10, 20, 30 years with a cancer and just take their medication and live their life as fully as they possibly can. And not have the terrible side effects. With well, with chemo and debilitating and not wanting to get, that's what, high quality of life.
Extended like that's, that would be that's that's the, to go, that's
[00:22:51] Grant: a glorious vision for the future is to have that as a possibility. And it seems within our lifetimes that with how things are going for the first time, it feels like human ambition and technology are starting to intersect, and we could see it. Yeah.
[00:23:06] Dr. Ian Taylor: Listen, Artificial intelligence has a hot topic right now. I We use it at Arvinas, but the power of what you're seeing with artificial intelligence technology, where you're going beyond, you're now seeing things that a human couldn't see using computer networks to to analyze data, to see trends that we wouldn't be able to pick up on our own.
That's obviously being applied all over the place, including in our work. So that kind of speaks to what you're saying. That's really going to, I think, push the evolution of technology even quicker to bring therapies to market even quicker, help patients again, coming back to that, helping patients even more.
[00:23:45] Grant: Yeah. You mentioned artificial intelligence really quickly. Just a quick side question here. I'm curious, we, at the quality we provide a quality management system to help people meet certain federal regulations and qualities of standard. What at Arvinas, what does your technology stack look like?
You mentioned artificial intelligence, what are some tools or other things that you're using? You don't have to go into any, I guess to specific if there's any competitors listening to the show, but like w if what's your normal tech stack, what is it that you're using?
You mentioned AI, or there was other machine learning things you have that are helping you advance, not just the core technology that you have there, but supporting technologies. Yeah.
[00:24:22] Dr. Ian Taylor: So we have a lot of technologies. I mentioned proteomics before, right? So this is where you take cells and grind them up and run them through mass spectrometers and see all the different proteins that are there.
And hopefully only degrading the one that you're going after. We use a lot of bioinformatics, a lot of computing power, so bioinformatics data analysis computational chemistry. So we have. We were in the cloud, we have chemists to basically do virtual screening. So you'll take us a structure of a protein.
You'll know what the structure of protein is and try to dock molecules in there that are warheads for ultimate protests. So we do virtual screening. So you don't have to actually do real screen. You can do virtual screen with a whole library of compounds. It just a way to go really much, much, much faster.
Now it's always supplement. What I'll call it traditional biology, traditional medicinal chemistry. In the end, you have to test these compounds in cells. You have to test them in tumors. You have to test them in various different assays. You still have to have a chemist, make the molecule. So that you need good medicinal chemists who can understand, okay, we'll look at the data and say, all right, I made this change to the molecule.
It had this effect. So now I'll make this change and make it even better. So there's always that fundamental chemistry, biology it's there, but a lot of computational chemistry. Proteomics. And that's in that a lot of it is understanding how to design the Protacs to bring together a target protein and the eatery ligase.
So we'll do structural biology. We'll make crystal structures. How do they actually come to actually be able to see in three dimensions? How are those coming together? Because how they come together is really key when it to come to efficiently together. So you get the most efficient ubiquitination in there for the most efficient degradation.
And then if we make a change of the ProTech, how does that change it? Is it making more efficient? So structural biology, being able to see that in three dimensions is really key. Again, supplemental with all the computational power that I mentioned. So that's our stack. We've got the fundamental aspects of biology, medicinal chemistry.
That's always there. But all the other inputs with the various technologies I listed to try to make that process more efficient, method empirical, more, less trial and error so that we again get these drugs to patients into clinical trials faster and faster.
[00:26:29] Grant: Yeah. It seems like the timeline from getting into clinicals and then out of clinicals, it seems to be shortening because of he's accelerating technology.
That's part of,
[00:26:38] Dr. Ian Taylor: yeah, that's part of it. Yeah. Yeah, because I didn't mention like genomics, where we're at, we're finding the true driver mutations, for example, in oncology they're causing to, so that the targeted therapy, that personalized medicine that you've heard about precision oncology, that really helps because you can take a.
Oh, sequence it, sequences DNA, find the mutation or even take somebody's blood. And just to look at the DNA, that's floating around this bit of release from the tumor. That's even easier, than taking a tumor biopsy, just draw some blood and do the sequencing. So being able to identify those driver mutations, designed drugs to them, pick those patients out right in the old, before precision oncology, you'd be testing or, basically all comers.
But maybe your drug only works on the selection of those now being identified, those upfront fewer patients are treated. Trials are quicker. They're cheaper, quite frankly, that helps, and then you can get the clinical trials done much quicker. So what used to be 12 years could be down to three or four.
That's a huge
[00:27:37] Grant: difference. Absolutely. Yeah. If somebody's listening to this today, you could potentially. In the next five years be treated by something we're talking about today. That's just without question. Yeah, it's just fascinating. This podcast is all about going from lab to launch and talking to the innovators in the life science space.
So Ian, this is a fantastic conversation. Thank you so much for coming on the show today and sharing some of the insight behind the scenes of what's happening at Arvinas and just this field of study. I feel excited. I feel. Bright future for what's going on there. Anybody else that's listening, hopefully you feel the same.
I can. You can't really see Ian. I can see him cause I'm talking to him here, but you can just see the passion. And how you're talking about these things. Before we wrap up the episode we close with one question, which is if you Ian could leave a voicemail to every person in your industry or in your field, some advice or some kind of.
Some something to help them continue to advance the field forward and a voicemail that everybody would listen to. What would you say?
[00:28:29] Dr. Ian Taylor: I hate to be repetitive, but I guess I will be, cause it's what I would say. It's the same thing. So it's focused on the patients. The rest will take care of it.
[00:28:37] Grant: Yeah. Sound awesome. Okay. Ian, this is a, again, like I said, this has just been fascinating conversation to have you on the show. Thank you so much. If people wanted to get involved or get in touch with you. I know that at Arvinas, you have a pretty robust partnership program. But if anybody wanna get in touch with you or with our venous work and they go to get.
[00:28:53] Dr. Ian Taylor: Yeah, go to the website or I think there's a, there's definitely some links there that you can get in touch with whether it be investor relations or just a general inbox or they can just email me directly. You've got taylor.com simple.
[00:29:09] Grant: Okay. Awesome. Thank you for offering that. And again, thank you so much for joining the show today.
We wish you all the best looking forward to following what you're doing at Arvinas, you and your team, fascinating technology with real like everyday applications and potential to save lives or extend life, which is something that I think should get everybody's attention and interest. So thank you again so much for joining and wish you all the best.
[00:29:33] Dr. Ian Taylor: Yeah, this was really fun. I really appreciate the opportunity.