Sol-Gel Technologies Ltd. Ordinary Shares Investor Day 2026

Yes. So, good morning. Actually, good afternoon.

To our guests that took the trouble to visit us here, and to everyone that is listening to us. And Sol-Gel team that are also watching us in Israel and is our biggest support when we are along this journey. First of all, I would like to thank our great guests the scientists who agreed to speak to you. They will be introduced later, one after the other. And we the team of Sol-Gel and the management team that is here are very excited to talk to you about the prospects that we see in revolutionizing the treatment of golem and introducing such a profound change in the life of golem patients, with our new drug SGT610. So thank you again. I will now start our presentation. Many of our investors are familiar with the presentation because it was in our company deck, but we introduced several changes that were meant to respond to frequently asked questions by you guys over the last month or two. And I hope this presentation will add clarity in those aspects that were maybe not fully clarified until now. So to introduce ourselves, to introduce our sorry, sorry, sorry, sorry, sorry.

Introduce ourselves Sol-Gel is an experienced dermatological company specializes in severe or, if you will, rare diseases in dermatology. SGT610 being the first product that is now approaching approval. This is our team. You see the team. All very serious looking people. And one thing that makes me feel a bit apologetic is that we have only one lady here. And in fact, when I stepped up as the CEO last year, I was concerned about it. And I was asking myself, how can I make a change? But all these people are so talented. So experienced, so diligent. There was no one I could replace. So what slightly corrects the situation is that our VP of clinical and regulatory affairs Dr. Ofra Levy-Haham has two jobs, both of regulatory and clinical. And in reality, I can tell you, she does a job of two executives. Hi, Ofra. And this slightly corrects the imbalance. But we are fully aware that a right company these days should consist of more balanced gender. OK, now again, so just in highlights what we are going to talk about, our drug is, of course, first and foremost, is targeted at golem patients. I'm saying first and foremost because in the future, I believe there will be additional indications maybe even bigger than that.

But right now, we concentrate on golem patients. The mechanism is a well-known mechanism. It's the blocking of the hedgehog signaling pathway. And the development history as we know is that we acquired the drug from Pelopharm. Pelopharm did not fail in the study or did not meet the statistical significance that they expected. We've made a lot of due diligence, a lot of employed several independent statistical teams as well as world experts. And decided that the data that we will review later is really compelling and we are biased as we are we are quite convinced that this drug will be a success. In terms of the designation, it's an orphan drug. And the breakthrough and will be the first drug to treat golem patients after so many years. So we are very excited about this. Now let us start with the data. This is the raw data of Pelopharm phase three, with one addition is that we are showing here only the observed data, namely only patients that completed 12 months treatment. So this was not the data that was submitted to the FDA, but it's the data after we eliminated those people who patients that didn't comply, that didn't show up, that didn't don't have the final data.

I'm making note of it because this was the source of some questions that we've been asked over the past Pelopharm data shows this one. And you show that one. This is the data that our experts has done, our statistical team based on the raw data of Pelopharm. So what did we learn from the Pelopharm study? What observations led us to believe that this is going to be a great drug? So here is the first graph. This is a post-hoc analysis. And show that patients who do not have the PTCH1 mutation do not respond any better than placebo. This is very surprising observation although it makes sense it is still surprising because other studies made on hedgehog inhibitors didn't make this distinction. We know that it is a valid for our drug. And we suspect that it is valid for other topical hedgehog inhibitors if in the future someone will think about developing. But this is very, very important. And makes much of the change in our study. Patients without mutation has a very same response as placebo. Let's go further. I'm custom that someone else does this job for you. So I apologize. And here this is one of the changes that introduced.

In order to overcome this block of 10 BCCs that people feel that this was somehow just a drug for people with 10 BCCs and more. So here is the data. And please listen to the definition. In the post-hoc analysis, a greater number of BCCs at baseline was associated with larger treatment effect favoring pathology over vehicle. Large treatment effect means the separation between the drug and placebo. So what you can see here is, first of two things. First of all, had we patients that have less than 10, 10 onwards, 8 onwards, 6 and up, had the very same efficacy. Very same efficacy as those of 10 and onwards. The same efficacy. And had we used a larger patient selection, namely from 6 BCCs onward, we would have reached the same p-value more or less. So 10 was used for some reasons, maybe for statistical considerations, to increase the likelihood of success in the study. But it is certainly but the drug efficacy the drug's efficacy is equal for two BCCs, for three BCCs, for five, and was 10. The efficacy is equal. Because the more the action is equal we just inhibit the hedgehog system inhibit the transcription factors downside to PTCH.

And the proof is the reduction of the levels of Glee in the tumor. So the drug doesn't know if it's two or 10. It's the same efficacy. What is different is the response of the placebo patients. What we have realized is that while the drug is always the same, patients with a mild disease mild stable disease do not grow new BCCs. And therefore it is impossible for the drug to overcome the placebo and to show its advantage. Because the drug is supposed to prevent BCCs to grow. If the BCCs do not grow in the first place, there is no way for us to show the advantage of the drug. So again, just I would like to hammer this because all baseline BCCs respond to the drug. But the difference is dramatic in placebos. Though the placebo of low BCC number, they simply didn't grow in this particular study. Not in real life. In real life, patients with one or two or three can suddenly experience breakout of BCCs. But in this study, these were mild patients with stable disease. And therefore we were not able to see in that small group of patients the advantage of the drug.

Let's go further. So now on the right is the graph that convinced our management to do the deal with Paty de Gieb and for me and my family to invest a little, a bit, a bit significant bit of additional amounts in order to support the study.

So everything is in this graph. You see, despite the small number of patients that qualify, despite the high standard deviation, despite all this, we show a dramatical difference between the drug and the vehicle. And a statistically significant one. What I would also suggest to take note of is that you see that the graph of the drug is almost leveling off. If we continue this graph for another 3 months or 6 months, it probably will be leveled off at about 3 because it's already asymptotic, as the technical word is. But here the slope is growing, it's growing. So in all likelihood, 3 months from now, it would have been 8 against 3. So it will be— the protective effect will be 5 BCCs. It means 5 more surgeries spared. So this is a very powerful demonstration of how effective is the drug. And it also, you may recall, we may go back to this slide when we talk about again about how many— the patient selection.

You see that 1 year is not enough to capture the full protective effect of this drug. That is the biological process. So a good company, when planning a study, and that is something that the FDA has also suggested, we'll come to it in a moment, has to find the ways, have to find the selections that will be able to reveal the potential of the drug within the limitation of number of patients, this rare disease, and within the limitation of time. In 1 year, we have to show as much as possible. So if we take patients that maybe will take them 2 years to respond because they have a stable disease, these patients are not suitable for that study. So this is the reason with this that convinced us to go on with the product. Let's go. That's— oh, sorry again.

Now this is something interesting that maybe will give some color to the interaction with the FDA and to, as a background to our confidence that the FDA will be forthcoming and agrees to our thinking. So it's so important I will read it with your permission. We recommend, says the FDA, conducting a new adequately powered randomized vehicle control trial to support the efficacy of your product. However, it may be possible to identify study design elements from the completed trial that could be modified in the future trial to increase the power, such as identify more sensitive patients population, among Gorlin patients or including a broader population such as subjects with non-Gorlin high-frequency BCC. What you see here, what we did is precisely what the FDA recommended. We continued— we started a new study with what we believe is the more sensitive patients, the patients that are likely to respond to the drug. And again, I wouldn't say that we are aligned with the FDA because FDA can do whatever they choose, right? But certainly it is something that is in the spirit of the recommendation of the FDA. So this is a summary again of what— of all the improvements that we introduced in the studies. 2 of them refer to patient selections.

We use Facial BCC 3 and above was the previous study and our study was 10 and above. PTCH mutation was not mandatory in the PELAFAM study and it is mandatory in our study. And that's it in terms of operational improvement.

We introduced several important changes that we think will improve the accuracy of the study, reduce false positive or false negative.

And as we already know, has also reduced the number of dropout patients. As a result, you know, every patient that drops out costs dearly to the statisticians.