Bacteria 4D Simulation, Safer Large Gene Insertion, uniQure Roller Coaster

Welcome back to Jen's podcast, Touching Base. I'm your host, Karina Singleman, managing editor of Jen.

Today, I'm joined by a few of our Jen editors. Hey, everyone, I'm Faith Lynn.

Howdy, I'm Alex Filipitas. Hey, everyone, it's Udrak.

So thank you again for joining us for yet another episode of Touching Base.

This week, I'd like to start off by acknowledging that next week is National STEM Week.

The goals of National STEM Week are to engage students and promote the future of STEM in the workforce by encouraging collaboration between educators and industry.

For me, at least, I think that these goals resonate as both a scientist and as a science communicator.

My own story is I got very lucky that even though my parents were not scientists, they really did encourage that interest in me.

So even though they didn't know anything about the industry, they still pushed me to follow my passions and to try to find opportunities.

And so this week for National STEM Week, this is more of a concerted effort by people in STEM and people who value STEM in education and STEM in the workforce to try to get action items happening.

There's legislation that's trying to push the inclusion of more STEM.

So that way, the US does maintain a strong footing for the future of science.

And, you know, I think that this is a good step to encourage future scientists and hopefully will enable more people from a wide variety of backgrounds to become the future researchers that will even cover eventually in Jen.

Should we be lucky enough to be here in in many years to come.

So I think with that this week, I'm going to ask everybody to start the episode by talking about the science.

So Alex, we're going to hold off a little bit on the business news. So thank you for being patient.

This week we do have some really interesting stories, including a 40 modeling of bacteria, a new technique for inserting gene size DNA into the genome and blood biomurgers for dementia.

I'd actually like to start off with Uduak talking about this 40 modeling. What can you tell us?

Sure. Thanks, Karen. So first off, this is a new study that was just published in the journal cell.

And the work is led by scientists at the J Craig Venture Institute, along with collaborators at institutions such as Harvard Medical School and elsewhere, you can get all the details as always in the paper.

So instead of high level, this paper describes efforts to simulate the complete life cycle of a minimal bacterial cell in four dimensions, so covering both space and time.

And this simulation, so computer simulation covers the process from DNA replication through protein translation through metabolism through cell division, all of which takes place over about 100 minutes.

As I said, this is this is work from the Craig Venture Institute. And for this particular simulation, they focused on a modified bacterium that has a very sort of stripped down genome with just the genes needed to replicate its DNA to grow divide and perform most of the functions that generally make life possible.

As I'm sure you can imagine, just creating a simulation of a single cell is so computationally intensive. So this is a much simpler simulation, but still pretty challenging as I'll talk about a little bit briefly.

And then also to note the particular bacterium that was used for this simulation is actually a genetically minimal bacterium that I believe was also developed at JCVI.

It's named JCVI sin 3a and it's derived from a particular subspecies of Michael plasma my coides.

So basically they created a version of this bacterium with a synthetic genome with fewer than 500 genes, all of which reside on a single strand circular strand of DNA.

And they claim this is the most genetically minimal organism that grows and regularly divides independently, like other bacterial cells.

It doesn't have a nucleus. So every molecule that comprises and sustains it is either something from its outer membrane or is transported into it from outside the cell or is assembled within the site of plasma, this particular cell.

So the paper goes into pretty pretty significant detail about what that simulation process was like. And as always, definitely encourage folks who are interested to read the paper for more details.

But just a few high level notes, some aspects were a lot more computationally intensive than others. I mean, as I mentioned earlier, this is already a pretty computationally intensive process.

But some aspects took a little bit longer. So for example, simulating the chromosome replication process nearly doubled the amount of time needed to capture the whole cell cycle.

So to get around that, the researchers got creative and used a dedicated GPU just for that task and then had other tasks running on other, another computational infrastructure.

Another challenging thing which they talk about, it was pretty challenging to simulate cellular events sort of occurring at the same time in different parts of the cell.

They were ultimately, they were able to generate a simulation of the cycle that was accurate to within about two minutes of what it would look like if this were the real life, real world cycle of the cell.

So they were able to do that computationally within about two minutes of the real world cycle.

So for those who are interested, definitely feel free to get more details, something that I thought was really interesting was they do talk about some of the limitations of the study of the work that they did.

There are aspects of the bacterium that they were not able to or they did not simulate for this particular study.

They also go into more detail about the required computational burden. So both time and computational resources needed to simulate a cell in this detail.

So it's it's pretty interesting work definitely encourage folks to check it out.

That sounds absolutely fascinating.

And I'm really just impressed with the computational abilities that we have, you know, I've said this so many times about, you know, the functionality of AI and it's used for drug discovery and analysis, but even just use dedicating an entire CPU for the simulation.

You know, you think, oh, it's just a little cell, but these little cells, they run the world.

This is impressive. Yeah, thank you.

No, absolutely. Definitely an interesting, interesting when you think about how much work and how much is required just for these processes that our cells do.

Every day all day without without our knowledge, it's pretty impressive when it comes when you finally start looking at it in this fine green detail and keep in mind that this isn't even a full cell.

This is just this is a pretty stripped down version and it's a bacterium on top of that. So this is like one of the smallest possible cells we can be talking about.

So imagine doing that on a much grander scale for even bigger cells. It's it's quite impressive.

Yeah, absolutely. I mean, and then, you know, if you consider the scale up implications for simulations for for organs, you know, like the brain or body movements for even a small organism, like a fly.

It's yeah, there's a lot of there's a lot of work and competition going into that.

Absolutely, absolutely. Yeah. Yeah. And to your point also, this is not even all of the genetics and all of the function of a single cell.

Yeah, impressive. I actually would like to keep on this genetics concept actually and pass a ton over to Fay.

Can you tell us a bit about your story?

Yes, Karina. So I'm shifting from AI today to talk about gene editing and this particular story focuses on placing large gene insertions at programmable locations in the genome.

So we're all aware of baby KJ's story who nearly a year ago now became the world's first patient treated with the spoke base editing therapy.

And today KJ is healthy and free from the toxic ammonia buildup caused by his rare genetic metabolic disorder.

At the same time, KJ's disorder stem from a single disease causing mutation that could be precisely targeted. But many genetic disorders are actually caused by dozens or thousands of mutations scattered across the gene.

So a common question that the field has been wrestling with is how are we going to scale these therapies to broader patients where individualized corrections would be way to resource intensive to reach more patients.

And so large gene insertion is proposed to be a generalizable medicine that could treat patients regardless of their underlying disease causing mutations.

So this is a new paper published in nature, which now makes large gene insertions safer for therapeutic applications and the work comes from Ben Klein cyber's group at Massachusetts general hospital.

The technology that they developed is called install and it uses circular single stranded DNA donors that can actually now evade the immune response.

So to put this into context, this install technology is an alternative to double stranded DNA donors that are usually required by recognition by the diverse suite of genome editing enzymes, including recombinases.

The drawback to double stranded DNA is that it's actively recognizes foreign by the immune system and it triggers a toxic immune response.

So now this new technology what's interesting about is that it's still compatible with recombinases.

What they do is they cleverly attach a very short region of double stranded DNA that can go undetected by sea gas, which is a cytosolic DNA sensor in an immune system activator.

So ultimately the results show that in mice that received the circular single stranded DNA, they were able to survive compared to more lethal immune reactions that were shown in mice that received the conventional double stranded DNA molecules.

So the results are exciting because they do show safety.

The ultimate question is how does this translate to the clinic, right? So we know the technology is safe. When looking at efficiency, efficiency shows that less than 1% of mouse liver cells were successful at DNA integration.

So this efficiency is low. It could be beneficial for some diseases, but most disorders would require either single or double digit efficiencies to benefit patients.

And when I spoke to Ben, he highlighted that increasing the efficiency is definitely a future direction of the work.

So for example, the study uses lipid nanoparticles or LMPs that are mostly made to deliver mRNA, but these LMPs could be further optimized for carrying this new circular single stranded DNA donor.

You could also engineer the nucleic acid component by adding modifications that can assist delivery to the nucleus. So there are many other approaches that would be the next step in order to increase the efficiency rates for the technology.

But I would say the other thing that emphasizes that install opens a new non viral and non toxic delivery method using LMPs for large gene insertion.

So the field has traditionally favored viral delivery methods like AV vectors for double stranded DNA because AVs go directly to the nucleus and avoid immune sensing in the cytosol.

There are drawbacks to AVs like high manufacturing costs, restrictions in the cargo size and inability to redo. So having a non viral alternative to AVs has been of high interest.

So we'll see how the technology evolves in the future right now still proof of concept, but very promising to have safer large gene insertion.

Yeah, now that's interesting that there is this promise, you know, and as you said, point proof of concept.

But I do appreciate that they've pointed out a number of pitfalls, but also opportunities of where they can tweak things and make some changes to try to improve the functionality and efficiency.

Because yeah, 1% doesn't seem like it would be quite enough to really be curative, at least not in an adult. I wonder if there would be, I wonder if there would be differences if the treatment in the efficiency of the treatments and the effectiveness of the treatment if it were done in infants and small children like baby KJ had the treatment.

We're in fetal or in fetuses that were impacted. Yeah, because it's just their smaller bodies, their fewer cells. So if the efficiency is going to a few cells and still making an impact, those cells will grow and multiply much more. And so the overall impact might be more beneficial.

It's curious. Yeah, yeah, it's certainly a long-term journey. So the scope of this paper was still right in mice and I believe also primary human cells, but still very much early pre clinical work.

But at the same time, I think it's a great foundation where in talking with a few experts, gene-ending experts in the field, this safety and non-toxic problem to be in response by itself has been a challenge for even getting to the next step of translation.

So to even see mice surviving compared to this fatal immune response, I think within the scope of the safety problem is going to be a valuable advance for for helping to later address efficiency down the road.

This may be too early to ask, but did you did in your conversations with the researcher, the researchers on the paper, did you have, do they have a sense for what kinds of diseases, something like this might be useful for.

Oh, obviously, if we get when we get to clinical, if and when we get to clinical stage, right.

Yeah, yeah. So I think a big hook for large gene insertion as a whole is that broader impact is really the game and having a more generalizable approach for treatment.

So for specific diseases, I think the goal is that there is an all encompassing approach that can treat a wealth of diseases that are beyond right single mutations, but anything that really requires multiple mutations, you can insert a larger chunk of DNA to address that gap.

So, so I think that's that's really the exciting part, the fact that we see a lot of crowding in the space for particular diseases where they're easy to target mutations, but the large gene insertion hopefully will make a broader impact beyond.

So also one thought then, say, is there any insight at this point as to dosing or how much material needs to be a insertion when as this research progresses to the point of a clinical study down around.

Yeah, I think that all wraps into the whole efficiency question and getting those efficiencies at a rate that is going to downstream translate and impact patients.

And so I think what's exciting about particularly developing a more non viral delivery approach is that one of the drawbacks of AV vectors is that it is hard to reduce patients.

And so having a technology that can go to LMP route and have something that can address that that bottleneck is pretty exciting.

But again, this is still a mice will pre clinical studies and I'm sure dosing is will be an active area of investigation once we get farther down the translation pipeline.

I'm actually going to jump back in here and talk a little bit about some more research stepping away a little bit from the genetic side of things moving more towards the blood side of things.

And so this next paper that I'm going to actually talk about is focused on Alzheimer's and and dementia so that that sort of cluster of disorders there.

And this is work led by scientists at University of California San Diego and the paper for those who want to seek it out is published in JAMA network open.

So definitely encourage folks to check it out now the major finding is that there is potentially a blood based biomarker that can predict women's risk of developing dementia as many as 25 years before symptoms start.

And as I'm sure we can all imagine that would definitely be a boon for efforts both to prevent and better track and monitor the disease as it emerges.

So just by way of background, the data that was used in this study came from over 2700 participants in what's called the Women's Health Initiative Memory Study or WIMS.

And this is a large national study that enrolled women aged 65 to 79 years of age back in the late 90s for those of us who are alive then and then followed them for up to 25 years.

And all the women were cognitively unimpaired when they entered the study and blood samples were collected at baseline. So I'm going to come back to that in a second because I need to provide a little bit more background about the study and what specifically they were looking for.

And so specifically they were looking at plasma levels of something called phosphorylated tau to 17 or P tau to 17.

And this is a form of a protein that reflects early brain changes that are associated with Alzheimer's.

And the goal was to kind of study a little bit the association between levels of this particular protein and the development of mild cognitive impairment and dementia among women who were cognitively healthy.

When the study started well before any of the sort of memory or thinking problems were detected.

So back to what I was saying earlier, they collected samples right when the women first entered the study so that provides baseline levels of of P tau.

And they were looking then a P tau to 17, excuse me. And they were so looking at associations, the goals was to look at associations between this protein and the development of cognitive impairment.

But also to determine whether those associations varied by things like age, race or hormone use, or whether the patient in question or the individual in question was a carrier of the APOE for allele.

So more information to keep in mind as I dive into the results. And as I'm sure audience knows what what APOE is APOE for is and the association with Alzheimer's specifically.

So big picture findings.

Scientists in looking at the data found that women who had higher levels of P tau to 17 in their blood at the start of the study were much more likely to develop dementia later on in life.

And in fact, they found that women with the highest levels had the greatest likelihood of developing dementia over the long term.

But it's important to know that this risk was not the same for everyone. So remember, they were also looking at associations between race or age, hormones or a hormone use and so on and so forth.

And one of the findings that reported in the paper is higher P tau to 17 levels were more strongly associated with poorer cognitive outcomes among women who were over the age of 70, for example, then those that were younger than 70 years at baseline.

So when that first sample was collected.

It was more, it was also more strongly associated among those who had the APOE for allele. So perhaps not unexpected, but it's it's good to see that that that association was there. It gives it gives more insight into potentially what's going on with with the women in this in this study.

But he also found that P tau to 17 was more predictive of dementia among women who had been randomized to estrogen plus progestin hormone therapy versus placebo.

So again, seeing another bit of an association there with hormone use. They also found differences in the strength of the association between white and black women.

They also found that combining P tau with age improves dementia predictions similarly in both groups. I'm not explaining this very well. There's a lot of sort of moving parts because we're looking at several different associations here.

But I definitely would encourage if Alzheimer's disease dementia is of interest to you, please do go check out this paper. It's really interesting to see kind of the different associations that emerge.

And I will say this to the researchers do note that while there does seem to be while they are finding these associations, we still need more studies as we say often on this podcast.

There's a lot more studies that are needed to determine if this kind of testing for P tau to 17 because keep in mind again, this is in the plasma. So obviously we're talking about potentially a blood test here.

But much more work is needed to be done to see if this could actually be used in routine clinical care.

And also honestly, whether identifying this the risk earlier can meaningfully change outcomes for the people in question. I mean, if we can figure out it's coming earlier.

One would assume that we hopefully could, but again, obviously just knowing how complex this disease is definitely more work is needed.

And then we'd say there's still more research they know that could be done looking more closely into the associations that are identified.

So how does someone's genetics play a role looking into more detail at that hormone therapies as we know lots of women by that age or typically on some kind of therapy hormone therapy.

So how does that how does that how does that impact their their level so.

And again, looking at this over the course of the person's life, the study started in the 1990s. So it's a great data set for studying how these things are changing over time.

So really interesting study really interesting work definitely encourage folks who are interested in this area to check out the paper.

Thanks, Uduak. I actually have two questions, which I mean you may or may not be able to answer.

Did the authors indicate whether they're continuing to collect data from the same cohort of women. I'm asking because I'm curious if it might be feasible for them to continue testing the blood to see if.

You know, you said that there was a wide range of of women some who were above 70 at the start of this somewhere younger, but if, for example, there was a woman at the start of the study who was above 70 and had a level of X amount, but another woman at the same time was younger.

When she got when the younger woman reached the age of 70.

Is her level were you know a group of the women who at the time 70 are they about the same then at the start baseline level of that initial 70 year old like what is the path for that and is there a difference maybe later on when those women who were younger to start with are older and more equivalent to the

current age of the initial 70 year olds or older than 70 year old woman, you know, what what is that tell us about the changes over time I would be curious to see if they might be considering anything like that.

Yeah, it's an interesting question. I don't believe they go into that on this paper, but I could also be misremembering I don't think so.

But it would be an interesting study interesting question to ask I also I don't want to speak, but I I'm relatively I think the I'm not I think the trial data is still the particular data from the study is still available.

I don't know if the study is still ongoing, so I also don't want to miss speak there, but I would imagine that even if it isn't they still have all this data collected from the early 90s, I believe.

I'm not sure exactly when it started, but definitely the early 90s, so conceivably they could go back and look for signals that would try to get at the question you're asking because obviously the women, as you mentioned, they're aging over time.

So they could definitely look at what was happening when this woman started at 65 and compared to when a different woman start was 65 perhaps when she start like that sort of thing.

So they could definitely make those kinds of comparisons, I would imagine, but yeah, I can't I don't think that was done for this specific study or I can't speak to that for sure.

Okay, yeah, and then my second question also again, he might not be able to to answer it, but did they give any any inclination of possible activities or actions or pre treatments to help prevent the onset of dementia symptoms.

Again, no, I don't, I don't believe so I think this was just looking specifically at associations. I think, and I can actually say, I mean, I already imagine.

This is a complicated disease, imagine complicated disease, and I think I think we're still a long way from fully understanding it, and I think that makes it very difficult some of that can make it difficult to give specific directives on what you can do to kind of prevent it.

I mean, I'm sure there's certain things that you know folks who are, you know, at higher risk, probably in conjunction with their doctors with their physicians.

Talk about, but I think it's it's a difficult it's one of those diseases that I think a lot of folks are working on it trying to understand it, trying to figure out if there's things we can do differently.

But there's still a lot to learn is I think what I feel safe saying, of course. Yeah, I just was curious if they if the researchers themselves had gone into anything based off of the other connections that they had made.

So yeah, super interesting. Thank you. So I'd like to shift gears and round out today's episode with some business updates from Alex.

Thanks. And using a wrestling metaphor to this chart, what a battle royal we had a few days back is Unicure scrapped with the FDA over its gene therapy candidate for Huntington's disease.

Unicure stock rollercoastered plummeting 42% early last week, then flat in the middle of last week and then rebounded at the end of the week, 58%.

Not counting another 51% jump in after hours trading late Friday, once fin a facade resigned as the FDA's chief medical and scientific officer and director of the center for biological evaluation and research or CBER effective at the end of April.

With facade running CBER, the FDA stunned Unicure in November by telling the company that what it called game changing data in September may not be enough to secure approval for AMT 130.

Not even the 75% reported slowing of disease progression three years after treatment with the high dose of the gene therapy.

FDA then stepped up its jaw boning against Unicure last week when it issued what the company called a strong recommendation to conduct a perspective randomized double blind sham surgery controlled study to support future marketing application for AMT 130.

Unicure's chief medical officer, Dr. Walid Abisab, told analysts on the company at quarterly earnings call that during the sham surgery and I quote,

patients would be anesthetized for an extended period of time 10 to 12 hours where you have to cut through the skin and maybe superficially drill a hole on the skull without really going through the bone.

Not so counter to HHS the Department of Health and Human Services defended its FDA by accusing Unicure of distorting the sham surgery patient experience.

Boate, not a shot back Mizzuo securities analyst Hugh air who said the sham surgery would not only be hard to execute, but and I quote potentially unethical.

Then on March 5th, the FDA stepped up its feud with Unicure through an unusual telephone briefing mainly for reporters from national general news outlets.

No, I wasn't invited to that call in which an official insisting an anonymity criticized an earlier placebo controlled clinical trial of Unicure saying as I'm quoting from Reuters that the trial outcome.

Boate was stone cold negative. We have a failed product here. Now that official's name had not been confirmed at deadline, although congressman Jake Ochenklaus, Democrat Massachusetts ID, the man is preside.

While preside supporters on social media complained about the congressman's campaign contributions from donors tied to biopharma.

Yet investors voted with their dollars for Unicure. It shares jumped 18% on March 5th, 34% on March 6th, and another 25 this week as a recording date.

Let's eluce threads to be tied in coming days like who will succeed presided running CBER, which not only reviews gene therapy applications, but vaccine applications.

And that's been a whole other controversy in recent months. Another wrinkle this week, Ron Johnson, Republican Senator from Wisconsin said Tuesday, he's going to hold hearings and investigate the FDA over all those rejections and broad sides against rare disease drug developers like Unicure.

Pass the popcorn, but seriously, let's keep our eyes and ears open the next few weeks. What do you think?

I think I'm going to make some popcorn. I will definitely follow your directive Alex to pass it along. My gosh, yeah, I feel like that's a huge mess and I'm really appreciative of you following and trying to pull all those messy threads apart to explain everything to us.

And last week was tough, but yeah, I had another topic, which I'll get into in a minute as the original kind of main stock watch theme, and then all the Unicure news, not only kept hitting, but hit into late last week and affecting the stock.

So that one, that stock watch took a bit more rewriting than usual.

I bet because that just, you know, the title of your stock watch included roller coaster and that really does feel like a major roller coaster happens.

Yeah.

Yeah.

No.

So what else do you have for us?

Okay. Well, as a sort of tease the second or two ago, the other big item in stock watch and on the business scene concerned Moderna.

We were talking about vaccines a minute ago.

It's bad to be on the hook for up to $2.25 billion, including 950 million of that upfront.

But it could have been much worse for Moderna.

The mRNA vaccine developer faced a much steeper potential settlement of its patent dispute with two other companies over the lipid nanoparticle technology used in its spike wax COVID-19 jabs.

Arbutus biopharma and Genevante sciences, Genevante's subsidiary of Royvan sciences joined Moderna in resolving their five year LNT patent dispute on the eve of a trial at the court of appeals for the federal circuit.

Moderna agreed to pay that upfront 950 million in July to Arbutus and Genevante.

Moderna also agreed to pay up to $1.3 billion if a federal appellate court rules that Genevance and Arbutus claims against Moderna for patent infringement are not barred under

Title 28 of the U.S. Code Section 1498, the exception being doses found to have gone to U.S. government employees.

That's if that ruling is maintained by the U.S. District Court for the District of Delaware, which heard the initial case which stretches back to 2022.

Under the settlement, Moderna also agreed that the court of appeals for the federal circuit should and a judgment of infringement against it and no invalidity for those four Genevante Arbutus patents.

There was let me just try to break it down. One of the patents was an LNP formulation patent that provides apparatus and processes for producing liposomes.

And then there were three molar ratio patents which cover formulation, production, delivering and or administering lipid particles.

The Genevante also agreed to grant Moderna a global non-exclusive license to its LNP delivery technology for infectious disease applications such as COVID.

Investors responded to all this by sending Moderna shares rising 16% on March 4th. Analyst Miles Minter, a William Blair said and I quote,

the settlement value was better than feared. Now, why is that?

Minter says it's because Moderna now knows it'll have the money to carry on with numerous clinical trials in progress now of the cancer vaccine it is co-developing with Merck and Company in Tismaran Auto Gene.

These three trials are set to report data this year on top of a study that in January read out positive median five year interim data.

Now I wondered, where did Roevant agree to the settlement rather than pursue a trial where it potentially stood to gain far more from Moderna?

I've got to pose that question right to Roevant CEO MacLein. He answered that the settlement was an opportunity to and I quote, significantly de-risk our LNP litigation while ensuring a meaningful and immediate financial outcome.

Chichen, he also said the settlement provided certainty and allows Genevante and Arbutus to crystallize the value of this IP.

Now that LNP litigation he referred to was Roevant's still ongoing lawsuit against the other big COVID-19 vaccine developers, actually developers Pfizer and BioNTech, which used the LNP tech and it's in their COVID-19 vaccine community.

Pfizer and BioNTech have racked up 101 billion dollars in sales between 2020 and 2025, which would give them roughly two-thirds of the mRNA-based COVID-19 vaccine market.

Moderna by contrast racked up most of the other third 48 billion bucks in sales for Spike Vax.

Now would that make Roevant less likely to entertain a settlement with Pfizer and BioNTech since more money's involved?

I ask lying that, but he didn't really say. He didn't reply, however, that Roevant's priority is, and I quote, ensuring that our intellectual property is appropriately recognized and that any outcome whether through litigation or a negotiated resolution reflects the value of the foundational technology developed by Genevante and Arbutus.

So unless Pfizer and BioNTech choose this settle as well, and who knows because BioNTech's husband and wife co-founders are leaving the company that came out this past week, then all we can say about BioNTech and Pfizer and Roevant and Arbutus is, see you in court.

You never expect that companies that are so scientifically based would be so dramatic also, where have so much drama around them, the companies themselves are not dramatic.

Like they're justified in their actions of whatever they're doing, but just there's always some big story around some company.

Any big new technology seems to really lead to a whole bunch of legal wrangling over patents. We saw this a decade ago with CRISPR technology and several actually two inner parties review cases that went through the courts.

And that we've seen that with other earlier, you know, technologies, you know, stretching back with your SFM radio or whatever.

So that's, I guess, par for the course, but no surprise to see, you know, fairly, you know, normally buttoned down companies really go at it like gangbusters in the legal papers.

I mean, I guess, you know, humans are going to be humans.

Yeah, everybody wants credit for what they've done.

That's it for this episode of Touching Base. Thanks everyone for joining and thank you for listening.

We have plenty of other episodes for you to enjoy. So please check out our previous episodes to get insights into business news and to hear about interesting science updates.

You may also want to listen to our sister podcast behind the breakthroughs. It's hosted by our colleague Jonathan Grinstein of Inside Precision Medicine.

Both of these podcasts are available on all platforms right now. And for your convenience, we've linked them in the description.

For the entire Gen team, I'm Karen a single man until we touch base again next time. Bye for now.