NovaBridge Biosciences American Depositary Shares H.C. Wainwright 28th Annual Global Investment Conference

Thank you and welcome. Andres, thank you so much for having me.

Thanks for the question, and thank you everyone for joining us. The value proposition of NovaBridge is to combine three things. One is preferential and differential sourcing, predominantly in Asia, on assets that are later stage, that have been tested in phase I, phase II studies, with a clinical development team in the U.S., and a company that's Nasdaq listed, and a capital allocation framework that brings flexibility, so that every asset that becomes a therapeutic for patients follows the best pathway for that to become a therapeutic for patients. Our two lead programs we're using to demonstrate this story, one is givastomig, which is a claudin 18.2 4-1BB conditional activation bispecific being developed for frontline gastric cancer. The second is a program that's within Visara, but the lead program is VIS-101, which is also a bispecific VEGF Ang2, which is being developed for neovascular AMD.

We're trying to do with NovaBridge is say we have access to assets that can become differential therapeutics for patients around the world. We have a clinical team that can help continue to advance and de-risk them, and we want to do this repeatedly, over and over again. We're focusing right now on givastomig and VIS-101, but our model is that we'll do this again and again as we continue to engage with companies that are in later stages with their programs.

Givastomig, as I mentioned, is a bispecific claudin 18.2 4-1BB, which is conditionally activated in the tumor setting. What's really interesting about this molecule is that it actually has the ability to work on low expressers of claudin. A lot of people in the claudin space are chasing the high claudin expressers, but the 4-1BB with the affinity of givastomig, helps it conditionally activate within a very localized tumor setting. We could access, in our phase I trial, we've seen that there's activity with givastomig at claudin levels down to one with a CPS score of one. We're, in some ways, thinking about being able to be relevant in an addressable market that's twice as much as what the claudin molecules that are in market are today.

The givastomig story is very fascinating from the standpoint of its clinical development. We had phase I data that we took with 17 patients, that came out at ESMO GI about a year ago, July 2025. We took that data to the FDA to discuss the programs to move forward to phase II, and get any feedback from them. We were pleasantly surprised that the FDA said that we actually could be on track for running a phase III program. The phase I program is run on two doses, both 8 and 12 milligrams. To your question, we actually see activity at both 8 and 12 milligrams in terms of both response rate as well as improvements in median PFS compared to standard of care.

As we move forward and we finalize with the FDA for dose selection, I think we're going to be balancing a handful of factors. Efficacy is obviously only one of them. Safety, tolerability are going to be the other pieces of that. As the data continues to mature, we're in conversations with the FDA, and we'll narrow down on the dosing for the phase III.

Sure. As I mentioned, by design, this bispecific has one head that's claudin 18.2 binding and the other which is the 4-1BB conditional activation. We don't actually see a lot of the toxicity that you normally see with 4-1BB because it's only conditionally activated when the 18.2 is also binding. But the combination of those two acting within the tumor where there is immune infiltrate, activates the standard of care, which includes the checkpoint inhibitor and the chemotherapy, and you see a very localized response within the tumor setting. The binding site now, the claudin 18.2, we think is what drives us our ability to get to claudin levels that are much, much lower than the standards out there. I think the current standards are 74% and higher, and we can actually see activity in the low claudin between 1% and 74%.

We actually saw in our monotherapy study that was done prior to the phase I activity, that was 11 plus, in terms of claudin levels. With that, we are probably able to, in HER2 negative patients, we are probably talking about doubling the number of addressable patients with the low claudin expressers.