Jasper Therapeutics, Inc. Common Stock H.C. Wainwright 28th Annual Global Investment Conference

Sure. Thanks, Emily, and thank you for inviting us to join you today. Yes. Recently, Jasper and Kira Pharmaceuticals announced a sign-and-close merger in mid-July of this year. We are pretty excited that this now creates a company with multiple assets in immunology, two of which are in the clinic, and a third one that is close behind. Our lead asset, known as KP104 or venosabef, is a dual-functional inhibitor of the complement cascade. It inhibits both the alternative and terminal parts of the complement cascade, so we think it has a very unique mechanism of action. Kira has published positive phase II data in PNH over the last few years. The lead indication there in PNH, we are looking forward to talking to the FDA next year at the end of phase II meeting about a potential approval pathway.

Furthermore, we have started a renal basket study led by patients with IgA nephropathy, looking to release the first interim data from that study later this year, and then expanding the basket study to include patients with C3G, FSGS, and possibly a few other renal indications as well. We think that the kidney undergoes different types of injury, but complement seems to be a common pathway for many of them. Our second asset, briquilimab, is an aglycosylated IgG1 antibody against the KIT receptor. Previously, we have developed that for mast cell diseases as well as a conditioning agent for patients undergoing stem cell transplantation in a variety of indications. Right now, we are completing some of the work we had agreed with the FDA regarding a potential pathway to approval for patients with SCID, severe combined immunodeficiencies, undergoing re-transplant.

We look to have the analysis done later this year and go to the FDA for a pre-BLA meeting next year, with the potential for a BLA at the end of next year. In SCID for transplant, briquilimab has both orphan and rare pediatric disease designations, so we would expect to be eligible for a priority review voucher if approved. We have also completed a phase II study in a key mast cell indication called chronic spontaneous urticaria. That was a great proof of concept. We think that this is a large market, with further potential to develop briquilimab as a chronic agent. However, with the new company and the different programs that we have and the amount of capital and the competitive landscape in CSU, we have not committed to further development there.

But we will continue to assess the landscape and what we think is a potential large opportunity for briquilimab. The third asset, I am so excited to have so many different assets right now. We have quite a development team, too. The third asset, KP701, is a bifunctional antibody or a bispecific antibody that targets both CD79B and CD32B. CD79B, of course, part of the B cell receptor. CD32B is the FC inhibitory receptor. So by bringing those together, we think we can induce anergy in B cells. We know B cells are really important for a lot of autoantibody diseases, and we have seen great success with depletion programs like Rituxan. But really, for a lot of chronic patients who are on these agents for decades, that comes at a pretty significant cost of immune suppression, long-term immune suppression.

Even if you come off an agent like Rituxan, you are talking months and months and months before your B cell compartment starts to normalize. With this approach, we think that we can provide that type of efficacy that has already been proven by B cell targeting agents, but with a potential for improved safety profile, because again, the B cells are there, they are just more or less put to sleep. So those are the main assets. There are a few others. One of the assets, C5 long-acting program, has been out-licensed to Mirador Therapeutics also as part of this transaction as well, and we do have additional assets deeper in the pipeline.

Yeah. So venosabef, KP104, very unique molecule, we think, in the field of complement. On one end, it is an antibody target C5, similar to Soliris or ULTOMIRIS. We know that targeting C5 will disrupt the memory and attack complex. So it really is the most important step of protection with regards to analytic indications like PNH, but also what we think leads to the damage in the glomeruli. On the other end of the molecule are the actual functional domains of Factor H. So Factor H is a part of the complement cascade that provides regulation on the alternative side. So it is more like modulation, where we can basically fully block the C5 component of the complement cascade on the cell surface, be it a red blood cell or in the glomeruli, and then further enhance the activity with Factor H.

What that brings is the benefits of the upstream inhibition pathways such as Fabhalta, of course, Factor B inhibitor, that allows restoration of hemoglobin in PNH patients. That is the big difference between Soliris, ULTOMIRIS and Fabhalta for PNH patients. We know that Soliris and ULTOMIRIS protect the patients, but you are still transfusion-dependent for a lot of them because we do not see normalization of hemoglobin, but with Fabhalta, you see that normalization of hemoglobin, but you do not have the protection for the breakthrough if that occurs. With venosabef, you have both, and we think that is pretty unique for a disease like PNH. In the kidney space, again, we think this is a way to go directly at the complement that is already activated and sits in the kidneys with the C5 component, but also have the disease control ability from the alternative pathway.

We are pretty excited to see what the data shows in our renal study. We think that these mechanisms may be synergistic or additive, but we will have to see.

Yeah, sure. The PNH phase II is 18 patients, kind of a very strong first step in the development of that indication, where we saw 100% of the patients, all patients got at least a 2 gram per deciliter increase in hemoglobin. 89% of patients restored to normal hemoglobin levels. We think that is early, but indicative of potentially best-in-disease kind of profile. 100% of the patients remain transfusion-free. 94% of the patients had an LDH of below 1.5 upper limit of normal. We do think that data set shows the potential of this dual mechanism of action, where we are seeing everything we would want to see from the molecule in terms of both alternative and terminal inhibition.

We're looking to have our end-of-phase II meeting sometime in the first half of next year. We're completing the CSR study reports for the PNH study and want to make sure that we really nail what's next. The design of the phase III or the phase III trials we think is fairly well set at this point with regards to approval pathways, where we're seeing one study in naive and one study in C5a-experienced or switch patients. That's probably where we would start with the FDA, but we could also understand if the FDA is maybe moved off a little bit. These aren't very large studies. We think we have the development capability to do these studies through their approval.