Adagene Inc. American Depositary Shares Chardan's 10th Annual Healthcare Conference

Thanks for having me. Michael, yeah.

Sure. Adagene is a company focused on masking antibodies. Our lead program is called ADG-126, or muzastotug, masked anti-CTLA-4, for which we have an ongoing randomized phase II trial for Project Optimus. You should expect data in the first half of next year for that. We are testing two relevant doses of ADG-126 in combination with pembrolizumab. You mentioned also neoadjuvant. We have an ongoing IST from Singapore, evaluating a similar regimen, different dosing schedule in neoadjuvant CLs.

It's a little bit of both, but given the mechanism of action of ADG-126, which ultimately leads to unmasking in the tumor microenvironment, we end up as a result, we believe, more Treg depletion, but it doesn't mean that there's no priming of the immune system. I'd say a bit more of a Treg depletion and then some priming as well.

Sure. Thanks to our SAFEbody platform, we believe that we have this very, very high masking efficiency. We also need high expression of the target CTLA-4 to have activation of the molecule. We have those patients in combination with PD-1 at a dose level up to 20 mg/kg, which is really a tour de force in my opinion, when you keep in mind that the ipilimumab of the world are traditionally given between 1 and 3 MPK in combination with Nivo. Importantly, our discontinuation rate due to adverse event in the context of a phase I-B, is below 10%.

It's about the masking efficiency. Masking efficiency, by that I mean when the mask is present, you're not going to bind to the target, and when you have cleavage of the masking peptide, you don't prevent the binding to the target. We're very happy with that when we would compare ourselves versus the other masking technology. Number two, something that I just mentioned, we also need high concentration of the target CTLA-4, which is very, very highly expressed on Tregs, among others.

We need these two conditions to be activated. I will also mention that the binder itself, which is called ADG-116, by the way, is differentiated in the sense that we bind to a different epitope compared to the Nivo or the, sorry, to the ipilimumab and tremelimumab of the world, which ultimately leads to this much stronger ADCC, 10x higher versus ipilimumab, which, by the way, is something that has been replicated by some pharma partners.

Number one, keep in mind that PD-1 single agent doesn't really have activity in MSS CRC, be it in patients with or without liver metastasis, right? It's basically close to 0%. That's number one. Number two, we have looked extensively at the baseline characteristic of the patients across the different cohorts. There are some differences, but we believe that the main driver behind it is dose. That's really the most important in our opinion.