The Best Use for AI in Drug Development: Q&A with Martin Brenner

One of the biggest questions in the pharmaceutical and biotech industry today is: how is AI being used? Over the past several years, the industry embraced the technology and many companies appeared claiming to be AI-pharma companies.

For iBio, however, AI may play a major role in its drug development process, but the company is not an AI-company. Instead, it views itself as biotech that uses AI as a tool that it combines with existing drug development methods to bring new antibody treatments to market.

Martin Brenner, CEO and chief scientific officer, spoke with Pharmaceutical Executive at the BIO 2026 Conference in San Diego. During the conversation, he discussed iBio’s views on how it uses AI, the company’s current pipeline, and how it’s redefined and expanded its business over recent years.

Pharmaceutical Executive: Can you discuss iBio’s AI-driven antibody drug discovery platform?
Martin Brenner: If you're following the AI, we can't call it bubble anymore. It's here to stay. But, there are companies who are very adamant about doing everything in-silico, and antibodies are usually sampled from nature.

That means we took blood from humans, isolated antibodies from those, and got the diversity of what is possible and what evolution is made in antibodies. These antibodies of the more traditional companies are highly developable, so we can make them into drugs.

They're non-immunogenic. They have a lot of features that look like drugs and can actually be developed. On the other hand, the in-silico companies have gotten very far going after very hard to drug targets, but the problem is these antibodies coming out there have yet to pass certain threshold when it comes to developability as medicines.

What we've done at iBio is combine both and basically build a bridge across both. We utilize AI as a tool. It helps us to solve certain things that otherwise were not solvable before. On the other hand, we're still very heavily sampling from evolution, because millions of years of evolution is very hard to compensate for in an AI.

This overlap between both is really helping us make molecules against hard drug targets. Our key program, Activin E, is a great example. That target was discovered by Regeneron, which I consider one of the greatest antibody companies, but more on the traditional side. They were unable to make an antibody.

Because we utilize both the AI part and the native sampling from nature, we were able to make that antibody.

We try to stay away from saying we're an AI company as much as we can. That's a tool. I'm not a fan of saying there's an AI drug. By that definition, we should call every drug in the market today a molecular biology drug, because that's what's changed since we actually did this from plant extracts.

Pharmaceutical Executive: You’re using AI to speed up your processes, but necessarily to anchor to that as a platform, correct?
Martin Brenner: We don't build foundational models, that makes no sense. You are the fastest for about a day, and then somebody else comes and is a few percentage points better. This is just a race to the bottom, that's not worth us doing.

What we do is incorporate these models into our drug discovery process and utilize them where they make sense and avoid utilizing them where they make no sense.

Pharmaceutical Executive: How did iBio build up to its current state?
Martin Brenner: Let me give you a little bit of history as to how we got there with the platform. In September 2022, our board decided to divest the CDMO, and we acquired the assets of a company called RubrYc Therapeutics. They had been working on a platform for about seven years by that time.

We had already in-licensed our first oncology asset from them when we were a CDMO, and we made an offer to acquire the platform and bring over the scientific team and oncology assets. In January 2023, we went to be an oncology company with this platform and try to find platform deals and raise money on oncology.

We were somewhat successful. We signed a research agreement with Eli Lilly at the end of December 2023 that was for a pain CNS molecule that they had been working on for numerous years with very little movement. We did more in eight months than they did in eight years with that asset.

They told us told that they gave us an impossible target to check what the platform could do. We were able to find binders against it.

In February 2024, we sold one of our early assets that we bought from RubrYc to Otsuka. We got $53-and-a-half million in total ($1 million up front, $52-and-a-half in commercial and renting total milestones), and at the time we were at $3 million market cap. We joke around that we tried to push as much as possible.

Then came March 2024. A gentleman by the name of Patrick Crutcher (the CEO of AstralBio) wanted to do a better myostatin. He looked at all the antibody discovery platforms out there and decided that we had a more unique platform.

We signed a discovery collaboration with him for four targets. That was a very unique collaboration, because at the end of the day, we can in-license three of the four assets at either developmental candidate, or we could hand it back over to him, and then at IND ready approval, we can then in-license it for a little bit more nominal fee.

Pharmaceutical Executive: What are the milestones and timeline for the clinical outcomes in the IBIO-600 clinical trials?
Martin Brenner: The molecule is a long-acting anti-myostatin molecule that also hits its GDF level. That's really important, because if you look at the spectrum of activity of pure myostatin molecules, they only hit myostatin.

What we're trying to do is thread the needle. we want to get as close in efficacy to be other drugs, but without LDL increases in diarrhea and other issues that those molecules are carrying.

We believe we have found that way. Ten years ago, GLDF 11 was believed to be helpful for cardiovascular health, but that has all been debunked by now. So, GDF 11 is very clearly something that causes fibrosis in cardiovascular and cardiac fibroblasts. We have seen it's a negative regulator of muscle and it also reduces fat mass, which is really important if you're thinking about using this as a weight loss drug.

What we've seen in non-human primates with this molecule is that the half-life wasabout 50 days. Typically, it's 2-to-14 days in non-human primates that projects a human half-life somewhere between 150 days. That's important because every single time you dose an antibody, it obviously shows up in blood, but then must diffuse into muscle, because the action of myostatin happens on the muscular level.

There's some information that says only 4% of this antibody arrives at the muscular level. That haven’t been a high number of papers written on this, but there are some that say this.

If your antibody concentration goes down after every two- or four-week treatment, there's not enough actually diffusing into muscle every single time. That means you don't block myostatin 100% or 90-plus percent.

What happens is it eats into your efficacy. By having a long acting molecule, we cut out this trough, because the exposure goes down multiple times. That is what we believe gives us better efficacy in these non-human primates. We saw an 8% increase in muscle after a single injection, and we saw 15% decrease in fat. That was unheard of.

Now we've moved to the clinic with this molecule. The safety studies went really well, and we've started dosing. Obviously, in obesity, you have a chance to enroll patients that are healthy but overweight. But I want to highlight phase one, a safety study first.

We do not compromise the safety of our patients. Could we have enrolled heavier people? Absolutely, we could have, but this is the first molecule coming off our platform, and the first that we moved into the clinic. So, we wanted to be 100% sure that we use the right population for that safety study.

If the half-life is really that long, there's always the margin of error when you predict human half-life from non-human primates. Of course, we're going to image these patients. We're not sure yet if imaging, because they're not heavily obese, is yielding in something.

Pharmaceutical Executive: Can you discuss your phase two studies?
Martin Brenner: We have precedent in these phase two studies. Both Regeneron and Lily have shown very nicely how to set up these phase two studies on top of a GLP-1. The whole point of a myostatin is to prevent muscle loss while you are on a weight loss journey.

Initially, when the GLP-1 medications were fresh to the market, it was considered an adaptive process that you lose muscle while you use weight. I fully agree with that statement. The problem is, if you regain body weight, you regain muscle to a much lower degree.

If your weight cycles a couple of times, you start every single time with a lower muscle mass. Ultimately, you're driving yourself into sort of competing obesity. And we know that patients cannot tolerate the standard forever. We have real world data that shows how often they come off.

If you speak with people that are not morbidly obese, but use these drugs for vanity reasons, they weight cycle a lot more. My worry is about those patients, because if you weigh 400 pounds, go on a GLP-1, lose as much weight as you can. If you're slightly overweight and you weight cycle, you might actually cause long term harm.

We're very concerned that this weight cycling actually can lead to a significant loss of muscle, and there's a label on some of these right now that says increased fracture risk that comes from lower bone density, which is driven in part by lower muscle mass.

Pharmaceutical Executive: Can you discuss the financing behind the study?
Martin Brenner: We have cash into the first half of 2028, potentially into the late second half of 2028. We raised up to $100 million in financing in August. We also took out a $26 million private placement in January with Frazier, so we wanted them to be on the cap table.

I want to be clear, myostatin is not our lead asset, but it is our most advanced. Activin A is our lead asset. We have cash for completion of phase one, for activin A, completion of myostatin 600 phase one.

Pharmaceutical Executive: What is the single most important inflection point investors should expect for iBio in the 12-to-24 months?
Martin Brenner: We have a unique opportunity with IBIO-610, Activin E antibody, because it's the only antibody against the target in the world. We have competitors that use SI RNA approaches, which can block the pathway by about 85%. Antibody can literally obliterate the entire pathway.

The reason this is important is that we see the efficacy setting in on the Activin E side when we block it by about 67%. All the action and efficacy happens between 60-and-100% inhibition. So, 85 is, from a percentage wise, not as heavily weighted towards full inhibition as if you start seeing efficacy at 10% inhibition. That pathway needs to be blocked heavily.

Second, obviously, we have an antibody and given the large population that this likely is going to be used for, we have a globally established manufacturing network for antibodies. They're non-linearly scalable. You can go from a 200-liter batch to a 20,000-liters batch.

sRNA is a synthetic product, so you still run into issues in these large populations. You must scale.

Pharmaceutical Executive: Are seeking partners in the pharma space or are you looking to independently advance your lead?
Martin Brener: Our goal is always to drive these assets as far as we can. We're talking about obesity, we're talking about roughly $1 billion in Phase 3 development costs. We are a fully diluted $50 million company, so it would be hubris to think that we can actually run a Phase 3 trial like that.

But that doesn't mean we cannot do something. Obesity will very likely fall into multiple segments. Obesity itself does not kill people. What kills people is cardiovascular disease driven by obesity, its side effects, and comorbidities from metabolic disease, like diabetic kidney disease. That's what kills people.

We are much more focused on whether we can treat the underlying mechanisms. That gives us a much better chance at reimbursement for these drugs, but it also segments the population in a way that allows us to go initially into a smaller segment, which enables us to run a much cheaper and faster Phase 3 trial.

We want to drive this as far as we can, but we are also very realistic. If it's a broad indication, that is something for a large partner that has the money and the infrastructure to run these trials.

Pharmaceutical Executive: What is the biggest misconception of iBio?
Martin Brenner: We've built a very strong reputation and credibility in delivering these assets, and in our research strategy. We were one of the first companies to look beyond the GLP-1s. Our strategy was to find out what the GLP-1s leave open in patient care? I think that has played out very well, but we remain under-recognized and underdeveloped.

I was asked this question a few months back by one of our bankers at a fireside chat, and I'll stick to the answer I gave then: platform, people, persistence.

The market underappreciates our platform and the power we have there. It's not the goal of the company to be a platform company. The way we've integrated it with our wet lab and our people is extremely powerful. In the next six months, we expect to have three first-in-class assets coming from that platform, and our fourth target should be another first-in-class.

Our people make us different. We have some of the hardest-working people in biotech, and they genuinely believe in the culture and the vision and continue to drive things forward. At one point we were a few weeks away from going bankrupt, and they stayed with us and fought through it. We continue to support them with everything possible.