TG Therapeutics, Inc. (TGTX) Earnings Call Transcript & Summary

Hi. Good afternoon, everyone, and welcome to the 120 session of the 42nd Annual Goldman Sachs Global Healthcare Conference. My name is Graig Suvannavejh. I cover both U.S. and European biopharma companies here at Goldman Sachs. It's my great pleasure to be hosting TG Therapeutics today in a fireside chat. And with that, let me welcome Company's CEO, Michael Weiss. Michael, how are you? Thanks for joining us.

Thanks for having me, appreciate it.

It's actually your second healthcare conference with us. And for those of you who may have joined last year, Michael, you may remember as well, we did our fireside chat. It was the very last day of the conference in the very last time slot. I was happy to see you again. I was relieved that the conference was done. But you moved up in the conference lineup. So congrats on that. Last year, we didn't cover your company, now we do. But I make light of last year's conference. But in any case, again, it's great to see you.

Yes. We always like moving from the last slot to at least one of the earlier spots. I think we made it -- are we first day. I think we made it to the first day.

The first day as well.

That's pretty good. That's a home run.

So for those of you who might be newer to the TG Therapeutics story, maybe Michael, in an overview, could you just tell us a little bit more about the company. I've been following the company actually since I think it was 2013 and certainly aware of the progress you've been making. But -- and congrats on that progress. But if you give us some insight as to like what you're working on? And what would you consider either your key technologies or your key areas of expertise?

Yes, sure. Thanks. And yes, so the company was founded in 2012, and we met up with you in 2013. So yes, you've been one of the longer folks who've been involved and followed the company. We -- as you -- you'll remember from way back when we were always focused on B-cell diseases. So the company was founded around the principle of looking for best available treatment options for patients with B-cell diseases. And that's always been dual focused on the hematology/oncology side, as well as the autoimmune side. So the hem/onc side, diseases like chronic lymphocytic leukemia, follicular lymphoma, marginal zone lymphoma, all would fit into B-cell diseases or B-cell cancers. And then on the B-cell disease aside autoimmune, MS is the one that we've targeted. But RA, lupus, MG, all things that also could be impacted by aberrant B-cells. So we've maintained a very strong focus in this area. On the oncology side, we took a slightly different approach right from the beginning and we said, we're going to develop combination treatments using novel agents, whether they're small molecules or immune modulating drugs to create these combinations and look for better treatments. It's kind of a RIF on multiple drug. Chemotherapies have worked quite well, but you're giving 3, 4 chemotherapies to get to the best outcome. Can we use 2, 3, 4 novel agents also get to a better outcome but with a better tolerability for the patient and potentially even better outcomes, of course. So that was our initial focus there, and we've worked, I think, well in that area. For marginal zone follicular, we have our first drug approved, which is Ukoniq. Generic name is umbralisib. So folks may remember as umbralisib. Brand name is Ukoniq. And so we got our first approval as a single agent there. Our big effort had always been in CLL, where we're putting together a combination of our glycoengineered CD20 plus Ukoniq. And that study went out positively last year. We filed for approval, and we have a PDUFA date for the combination, which we refer to as U2, that combination, we'll have a PDUFA date in March of next year. So working toward that first doublet combination. And I'm sure as we get into the conversation, we could talk more about some of the triplets and potentially the quads that we're thinking about and working on. And then just to finish the update on the core pieces of the puzzle today. So on the autoimmune side, we have our glycoengineered CD20 ublituximab for multiple sclerosis. Again, we have completed a Phase III -- 2 Phase III trials actually, both have reported out positively, and we are targeting a BLA submission in the third quarter of this year, which ideally would lead to an approval in the third quarter of next year. So by the third quarter of next year, we should -- could, should, we would say could, should, but whatever, have marginal follicular approved and those are late-line treatments in those settings. U2, the combination approved in ideally all lines of CLL. So that's the study we conducted, it was for all lines of CLL. So our hope and expectations that we'd receive a broad label. And then for the treatment of MS with our single agent CD20. So that's -- I'd say that's a core of what we've been working on. We've got a pipeline that's targeted right now, mostly on the hem/onc side, but we're going to be probably pushing forward into some additional autoimmune activity as well.

Okay. Thanks for that fairly comprehensive background to the company. And it seems to me that we've got maybe a couple of big buckets that we can tackle, but maybe just sequentially, why don't we start off with your first product approval, which is for Ukoniq. And I think it's a unique asset in that it is a PI3 kinase delta inhibitor that's perhaps differentiated. But I think for those who know about the class, the class has not seen great successes. So perhaps, can you just walk us through what makes this a differentiated PI3 kinase delta inhibitor?

Yes. So -- interesting. So early on, we always -- the drug's chemistry is very different than the chemistry of the predecessor compounds. So the initial approved to PI3K idelalisib and duvelisib, were very, very similar compounds. So chemistry wise, you look at them, I think they're almost 80% homologous. So these are very similar compounds. So ours is quite different in chemistry. It looked different preclinically. And we always knew something different was going on. There was an -- interesting part of the story was that idelalisib promoted itself as a pure PI3K delta. And duvelisib promoted itself as a PI3K delta/gamma. And so when we start with those agents, autoimmune related toxicities, the common link was delta, so the initial belief was that delta was the cause of the autoimmune-related toxicities. When we got deeper and deeper in this, we said, there's something that doesn't make sense here because we're not seeing it, and we're very much a pure delta. We have very little activity to the other isoforms. We have -- I think we've sort of low teens [indiscernible] potency to delta and something in the order of one micromolar-ish to gamma or maybe even higher, right? So really -- and in terms of drug development, no one would develop a drug, that was 1 micromolar potent, right? Even 2 -- anything that's micromolar potent, doesn't get developed as a drug because it's just not potent enough to have a clinically meaningful effect. The difference, what we realized was that the other compounds, even though they might have had a very nice differential between delta and gamma, they all had low nanomolar potency to gamma simultaneously. So when you have low nanomolar potency to both targets, you're going to have clinically relevant effects on both targets. And so that was, I think, the -- one of the breakthrough discoveries that we had internally, which was like, oh, yes, idelalisib is a delta gamma also. And then we went back and we looked at all of the knockout data, knockout delta, knockout gamma, knockout delta and gamma together. And what you basically see is that if you knockout delta, there's a susceptibility -- it's what they call susceptibility to autoimmune-related toxicities. But it's not really sufficient on its own. Gamma is actually being used -- pure gamma inhibitors are now being used to enhance PD-L1 therapy because they down regulate T-regs. So the combination of down regulating delta and gamma together, we believe, and we think it's supported by the knockout data and by all the [indiscernible] screening, that that's really what's causing the vast majority of the autoimmune related toxicity. So we see much less of it because we're getting less. And the other side of it is we also hit a target called CK1-epsilon. And CK1-epsilon actually has a natural protective effect on T-regs and also probably has some activity in CLL. There's some paper supporting activity of that target. So it's unique and it's very delta specific, but it also hits CK1-epsilon, which none of the other deltas or PI3Ks hit. And we think it's the connection of those 2 targets that creates the profile for Ukoniq.

So you've very nicely elucidated the differences between the existing or prior predecessor compounds and [indiscernible]. And now you're launching Ukoniq, and you just reported first quarter sales for the first time, congrats on that. As it relates to either the perception or what physicians are aware of, are they seeing -- or is it still early to say are they realizing that these are, in fact, different compounds, and perhaps they should be using them differentially? I think the feedback from a high level has been, it's a trouble class. I really want to touch it. I want to try something different and new. So thoughts on that.

Yes. So we've had some really good feedback from the clinicians that we've been talking to. So the team has had great engagement across the community and academic centers. And the feedback we're getting, I mean -- I'd say, look, my marketing people are coming back and telling me they're getting great feedback, is one thing, but my Chief Scientific Officer, Owen O'Connor coming back and saying the same thing consistently that people really are resonating to the clinical profile of the compound. And again, we use a lot of investigators here in the U.S. on our earlier-stage programs and our pivotal programs. So we've got a lot of folks who have touched the drug. And if you use it, which is feel like the [ size sims of ] biotech and educated consumers, our best consumer, we want everyone to try it. And once they try it, they're going to recognize that it's a different agent, and it has a different profile. Again, it's not -- I've said this multiple times, too, it's not the perfect drug. It's significantly better than what's come before it in our view from the data that supports that. But it's also about whether we have 10% to 15% of the patients that come off the drug for some tolerability issues. So there's going to be some percentage of patients that are not going to have a good time on it. But most patients will, the vast majority will. And that's not what you get with the other ones that they have 40%, 50% dropout rates for tolerability issues. I mean, in folks' hands, I mean, that's why you don't want to start someone on a drug when you know half of them are going to come off pretty quickly, and they're going to have some bad side effects. So we want to get as many -- our focus for this year for the sales and marketing effort is get as many people to try the drug. I personally -- we're not making our company on marginal zone follicular lymphoma, right? we're making our company on success in CLL and success in MS. And over time, marginal follicular will be nice contributors. But it will be overshadowed very quickly. We're going to launch in March in CLL. The numbers will be overshaded very quickly by what we're doing in CLL. It's a much bigger market. The label will be broader. We're looking at frontline and relapse in CLL. So the team has to get out there. Their job is to get out there, get engagement with as many folks as possible, make sure people see and understand the profile and get as many people to give it a try. Once they try it, then once we come out with CLL, we'll be in great shape.

That's great to hear you put that into perspective. It seems as if just to kind of recapitulate, it's almost a starting place for Ukoniq in terms of follicular MZL with the greater opportunity perhaps in combination settings. And you've spoken to the opportunity about CLL. CLL, though, is quite a competitive landscape. And so how does U2 fit in kind of the fabric of everything that's happening in CLL right now?

Yes. So the easiest way to think about it, and I try to simplify things as much as I can. So you have BTKs, you have ibrutinib, which is the original and perceived as it's got the most data, and then you've got 2 new ones that have come to market. But in essence, someone is going to pick a BTK. I don't care how many there are. So let's not get bogged down on which BTK they choose. They choose a BTK but they all have an overlapping profile, right? So they all have some level of cardiovascular risk. They all have some level of bleeding risk. They have all some level of drug-drug interactions. So there's commonality amongst when you may not be good candidates for those drugs and when you're coming off those drugs. So for instance, if you've been on ibrutinib for 5 years and you come off because you've now progressed, you're not going on another BTK, right? So U2 is there. If you come off for tolerability issues, debatable whether you consider another BTK before you go to U2, our data shows that you can switch over from the intolerance of BTK, tolerate it well with very few -- I mean, very few overlapping toxicities. I mean it's almost nonexistent, and then -- and have a great outcome. I know acalabrutinib did a similar study, and they weren't as -- it wasn't as easy to switch, right? So that data exists. So while acalabrutinib, on average, has a modestly better overall safety profile, it still carries the same overall baggage. So if we just say, look, let's put all the BTKs together, you've got venetoclax over here, you've got BTK over here, and then you've got chemotherapy and then -- and in between is you U2. So no matter how you sequence, if you're an academic center -- let's make this real simple, if you're an academic center, U2 is third line therapy for the most part, right? If you're in a community where venetoclax isn't used very much, U2 is primarily second line therapy, right? It's going to fit after BTKs and before chemotherapy. We would argue that there are about 20% of patients that are probably poor candidates for BTK therapy upfront. So we think there's a portion of that BTK naive market that belongs with U2. It's not all of it. If we get 10% or 20% of the patients that want to be on a BTK but come in and have some major cardiovascular issue, which is a lot of patients, I mean, you're talking about an elderly population to begin with, patients that need to be on blood thinners also have great risk, there's lots of bleeding associated with all of the BTKs, and then there's a variety of others. I mean headaches on acalabrutinib and there's -- I mean, some of them even have some liver abnormalities. So there's a lot of reasons why you might want to consider something else. And with U2's data, particularly in frontline, I mean, we're talking about close to 40 months of PFS median for the upfront. That PFS is not done yet. We'll update it. My guess is, if I had to guess, it's going to be close to 4 years. It could be more. We just don't know where it's going to land. Because it's not done. But if you have a cardiovascular condition, we think this is a great option for you. So again, we're not trying to take -- U2 is not designed to take the market in CLL. U2 is designed to take the niches that are there and provide patients who fall through the cracks. And with 40 -- 35,000, 40,000 patients seeking new treatments every year, there's a good chunk of them that are not being well served today, again. So it's competitive in that most patients are well served. But unfortunately, there's still a lot of patients who aren't being well served, and that's where U2 is going to fit in. So we think there's a great opportunity there. And then over the longer term, we have really good data with U2 plus venetoclax. So while today, venetoclax is primarily, not exclusive but primarily an academic -- academically used drug, we do think, over time, it will make itself [indiscernible]. It's already found its way to some of the larger centers. So we know that it's getting there. And it will be more broadly used. But we think U2 plus venetoclax as a frontline treatment or a post BTK treatment will become a leading treatment option. The data that we have emerging from those studies looks quite good. I mean, in terms of the first 25 relapsed patients we presented, it's the best data certainly on MRD-negative that's ever been presented. So we think the combination goes well together, opens up a whole another piece of that market. So instead of going in and around the other folks with U2 plus venetoclax, we can really step in both academics and then future in the community into the frontline with that regimen and second line, of course.

Let's stay on you U2, and you've got a PDUFA, as you mentioned, so that you could be on the market by next year. So what are the pre-commercialization activities that you're doing that either are very similar to what you had to do for Ukoniq versus what you're going to do now moving into the CLL space. Is it considerably more work? I mean, different types of target physicians, just can you give us a sense of like how that's going to look? And just really a view around how should we think differently about the uptake curve for U2 relative to any kind of uptake curve for Ukoniq, which, again, is for a different set of patients in a different disease?

Yes. So when I think about it, we've got a sales team out there that's basically explaining Ukoniq as Ukoniq, right? And that's a -- obviously, a super important component of the U2 combination is that small molecule and the small molecule toxicity. So -- and for the most part, the profile in lymphomas is very similar to the profile in CLL. So there's -- if you've learned and understood the Ukoniq profile and marginal zone follicular, you pretty much understand the profile in CLL. They're not exactly [indiscernible], but they're pretty tight. So we have a sales team that's focused on that. We have a medical team that's focused on that. Then we have the CLL data itself. Now that data really can't go through the sales channel. So that's not something our sales team would work on, but our medical team can educate folks with that kind of information. So that's out there. And obviously, there's -- we're working with a lot of KOLs doing [indiscernible], really understanding how they see it and how they think we should position it. And so that's really -- the bigger part of it is really a knowledge-based program to begin with to make sure that we understand how the data will be viewed and how people want to use the drug. I mean we've got a pretty good sense over the years. Again, the niches that we talk about and these unmet medical needs that exist, they've come through years of conversations with the KOLs, right, and community physicians, right? We understand the patients who have already seen BTK and what they're coming on next in the community, we understand how the KOLs think about, how they triage CLL patients in the academic centers, but markets change and you want to make sure you have the most updated market research and information. And so we continue to go out there and pressure test these assumptions that I'm speaking to you about, they're being pressure tested constantly. And again, our goal is to just make sure we understand how to position the drug. But there's only so much you could do in terms of -- you can do a lot of education, obviously, the sales team can't be involved at all.

When we're thinking about these combinations, you alluded to potentially triple and quadruple combinations. I just wanted to quickly switch gears there. And you've mentioned the venetoclax combo, where else could you take U2?

Yes. So we're excited about U2 plus 1701, which is our BTK inhibitor. So again, the BTK class is not going anywhere. It's -- the BTKs and CLL are very similar to CD20s and MS, right? So you're going to be on these drugs for many years. And so what happens over time as you -- from a market standpoint, you're going to continue to stack your patience. So the market grows every year just because you have year-over-year, even if you have no -- if you have flat growth of new starts, but you have 5 years of use, you're going to be stacking for a while. So it's a big market opportunity. We think our BTK has a very attractive profile, the safety and activity looks very good. So we think U2 plus 1701 and 1701 and 1701 may have real opportunities, and we're going to price it right to make it attractive for folks. So we think there's a real opportunity for us with that triple. And then we're also -- I won't say separately, but sort of separately working on our triple immunotherapy. So we have ublituximab, we've got our PD-L1, and we have our CD47, CD19 bispecific. So we have a few of those pieces working in combination right now, and we're going to try to tie them all together at some point into a triple combination, in some cases, with, in some cases, without Ukoniq. In some cases, potentially with 1701 or without 1701. So we have a lot of permutations within that portfolio to mix and match, depending on the disease, that we're going after at the time. So things like -- where we haven't really penetrated as of yet something like diffuse large B-cell or mantle cell, some of these triple therapies maybe more attractive. In mantle cell, adding BTK with some of these mechanisms may be attractive, maybe Ukoniq, more so in diffuse large B cell. So we're going to -- we've got a really nice platform that we've built, a clinical platform where we can do this testing relatively quickly, and we're going to continue to do that. So we think there's some really interesting things in the back. But in the foreground today, you've got U2 plus venetoclax and U2 plus 1701, I think are the leading triples that we're working on today.

And with respect to -- and I'll move over to the MS opportunity in just a second. But as we look at your oncology pipeline and whether it's 1701 or some of the other bispecific compounds that you mentioned, is it best for us to be thinking about these as part of a combination? Or is there a thought to develop these as single agents?

So I think the jury is still out. I think we'll see where the data takes us. We'll see where the commercial opportunities take us. I think it's all subject to that. So we're still -- we're doing a lot of work with 1701 as a single agent. We're doing a lot of work with 1701 in combination with U2. And I imagine, longer term, we'll be looking at 1701-based combinations, as well as additional U2-based combination. So I think there's a lot of ways we can go with it. But the lead for sure, right now, U2 plus 1701, we think, looks quite interesting. 1701 as 1701 looks quite interesting, 1801, which is our CD47 CD19, on average, those have not been single agent compounds across the board. I mean, one would hope to see some level of single-agent activity. But as a longer-term development strategy, CD47 as a single agent has not to date appear to be the path, certainly not the path of least resistance for an approval. So we'll watch as the field evolves. A lot of folks have certainly shown interesting to exciting activity in combination with CD20s. So we'll continue to look at that.

And just lastly briefly on 1501, your PD-L1, how is that differentiated from others?

Yes. So it's a pretty interesting molecule. It's, I think, 1 of 2 PD-L1s that have retained the FC function. So what's interesting about PD-1, PD-L1 is the PD-1s for very good reason engineered out the FC region so that they wouldn't have activity there, right? And that was because PD-1s target T cells, and you don't want to kill the T cells, right? So that was the reason. When they went into the PD-L1 land, which happens to be a tumor target, not at T-cell target, most people continued with the FC engineering. The only other one that did not, was the one that I think was Merck to Pfizer, if I'm recalling correctly. But that one has a very short half-life. It's really kind of strange for an antibody. That one I think it only has like a 3-year -- 3 to 5-day half-life. This one -- so this is the only one that has full FC capabilities with a 2, 3 week, whatever normal antibody half-life. So it's a pretty interesting and relatively unique profile.

Okay. We'll move now to your MS opportunity, which, for some, is even more exciting than your U2 CLL opportunity.

Sure.

You've reported recently very good Phase III data, which actually I thought was almost better than your Phase II data, which you rarely see. Congrats on that, but it [ is in ] CD20. We know that there is another anti-CD20 in the market, who knows, maybe there are others that might be coming as well. But maybe if you can point out the salient kind of characteristics of your glycoengineered anti-CD20?

Yes. So we didn't talk about on the heme side, but it's actually worth noting that -- so this compound is glycoengineered. In our analytical assays, it's the most potent CD20, so more potent in our hands than obinutuzumab and dramatically more potent than Rituxan and OCREVUS, which is the compound that's approved now for MS by Roche. So it's a very, very potent CD20. But what's unique about it is we're able to deliver it in shorter infusion times. So on the oncology side, in CLL, we've given in a 90-minute infusion. So that's actually, I think, even for Rituxan and CLL and for [ obinu ] that's first about a 4-hour infusion. So we may see some very interesting interest in that compound because of that 90-minute infusion and because of its enhanced potency. On the MS side, the enhanced potency may be responsible for the robust activity that you highlighted. So the Phase II looked great. I agree with you. I think the Phase III looked as good, if not better. And we think it's potentially attributable to the high potency. We use a lower dose than our competitor, OCREVUS. And the activity, again, not a head-to-head study, but the activity look quite impressive. So we're very enthusiastic about the profile that's evolving. It's a 1-hour infusion every 6 months. OCREVUS recently received approval for a 2-hour infusion every 6 months. So they've cut down their infusion time from 4 hours to 2 hours, but it's still 2 hours instead of 1-hour. And by my last calculation, I think 1-hour is still better than 2 hours. I also understand that they're looking at higher doses to try to improve their activity profile, which will certainly then push the infusion time longer yet again. So I think we're well positioned. With the 1-hour infusion, the activity profile looks extremely compelling. They reported a -- and it's included in their label, issues around breast cancer -- potential breast cancer liability, which we know that physicians feel obligated to talk about with -- certainly with female patients. So that's something that we won't have to talk about with ublituximab based on the data that we've reported. So we're feeling quite good. The -- so OCREVUS is the other infusion product at CD20. There is Kesimpta, which is a subcu product that's given, I think, 3x subcu in the office and then monthly subcu at home, which had also very nice data, slightly different compound, it's ofatumumab, which some may remember from CLL, which is very potent towards CDC but not very potent in ADCC. So just a different profile in terms of how it approaches the B-cells. I think long term, we've got 2 -- and that drug is being promoted by Novartis. So we have 2 big competitors out there who, I believe, will do everything in their power to make CD20 as the #1 class of agents in the treatment of MS, and that all works to our benefit. So we're going to be one of a class of 3. I don't perceive any additional CD20s coming to the market anytime soon. So it will be a class of 3 for quite some time. Between estimates from our competitors anywhere from 35% to 50% of all MS new starts and switches will go on to CD20s. That's a very large opportunity, and we're going to be, I think, very well positioned to meet the demand of that marketplace.

And how will you -- what's the strategy in terms of being able to compete against those 2 other bigger players? Is it just kind of riding on their coattails and just hopefully, just saying, hey, we're here? Or do you feel like there's some really meaningful blocking and tackling you need to do?

I think it's probably somewhere in between, which is probably a wimpy answer. But I do think there's a lot about riding their coattails, right? So I mean, my gut tells me that the more commercials, they do, the less commercials we need to do. And we don't find in doing any commercial, right? We are -- so we're going to ride their coattails as they build the CD20 market. And then we need to really -- I think our focus will be making sure that the 5,000 physicians that treat 80% of the patients know full well what the value proposition of ublituximab is, right? So we need to get in those offices to make them sure they understand the efficacy profile, the safety profile, the convenience. And one thing that we haven't talked about is price, right? So we want to make sure that we come in at an attractive price. Physicians don't pay for these drugs. But in the MS community, there's a lot of physicians that are upset about how MS drugs have been priced and how the price have risen over the years. But the patients do pace for some proportion of their drugs and the system pays for it. So we think that there's a way in which we can use price to also enhance our position in the marketplace. But yes, we need to get in there with the physicians and make sure that we're getting them to understand that we're there. So that every time a patient walks in the door, who is in line for a CD20, we'll hear about all 3 drugs. And we think if we get a fair showing -- if you decide you want to take an IV every 6 months, we think the 1-hour infusion at a better price is going to be the top choice for you. If you decide you want a subcu, we're out of the game. That's going to be reserved for the other guys. But we think most patients -- from our research, a significant portion of the patients are very happy with the 6-month infusion, for 1 hour, you show up, you get it done. You don't have to deal with monthly getting your infusion, getting into your home first, which requires some paperwork and effort and then putting it into your body yourself, versus just showing up meeting with your doctor, getting your infusion, going home, going back to work. So we think the IV is going to play a significant role and we think that [ ubli ] is going to -- it's going to be a significant player in that market. But yes, that's the key for us, getting in front of those [indiscernible].

You did mention price and a question I have is on the assumption that you've done market research studies with payers, do you already have a sense of what that pricing looks like relative to the brands? In other words, without using the word, but saying the word, it's some sort of discounting or lower price. And I'm trying to get a sense of, obviously, once you have the label, you'll be able to speak more about it. But is there a sensitivity in the community because some of the first MS drugs came out 2 decades ago at $15,000 a year and now they're $80-some-thousand a year and there hasn't -- there's been incremental innovation, of course, but still it's quite price inflation and sticker shocks for these patients?

Yes. So we started on this price thing from the very first advisory where we had when we started to get into MS, where the doctor said that exact same thing. They were just angry. They were literally angry that why would it go from $15,000 to $85,000, it's the same molecule, same drug, and they were upset about it. So we do think there's room there. So -- but the core of the question is, have we done the market research to know exactly where that price needs to be, and the answer is no. We've done market research. We're circling around where we think it is. I mean it doesn't have to be 50%, and I don't think it's going to be 5%, right? I mean, that's not going to get it done. So it's going to be something that's got some teeth, but it's not -- it doesn't have to be crazy. I mean there's a number in there. And again, there might be -- it's almost like a Dutch auction in a way, right? So there's multiple payers, and not everyone is going to have the same price point. And yes, if there's one payer that's down at 50% discount and the rest are at 25%, well, we're going to probably leave that one payer out of the mix. And we meet the demand of the market that clears the vast majority of what we're trying to accomplish. So we're working on it. Like I said, we don't have an exact number, but we know it's not going to be crazy, but it's also not going to be nominal, right? We want to -- it's going to be something that has some real meaning to it.

We've got maybe a minute or 2 left, and I just want to get through maybe some more housekeeping type of questions in terms of where you ended the first quarter with cash? How do you feel about the current cash runway? Certainly, you're launching several products, hopefully, over the next several years as a use of cash, but how are you thinking about that?

So we ended last quarter with about $525-million-ish in cash, so $5.25 billion. I feel like we have cash into 2023 doesn't really account for revenue. So between then, if we have those launches, we should have some revenue. So we're just -- we're feeling good about our position. We're not feeling at all stressed that we have to do anything. We want to execute, and we're heavily focused on building out the commercial and really having a good launch in CLL and MS. And that's going to -- that will change our cash trajectory as much as anything else.

And then maybe 2 quick last questions. One, catalyst, I think we kind of spoke to some of those, but if you could, in your own words, kind of couch the next 6 to 12 months for investors as they see kind of the path for the company? And then my last question is a little bit crystal ball-ish 5 years from now, where would you like TG Therapeutics -- what would you like the company to look like 5 years from now?

Sure. So quick on the catalyst. Step one, let's get our MS filing in, in the third quarter. So let's get that set. That would hopefully set us up for a PDUFA date about 12 months after that. Next up would be ECTRIMS. So some updated information on the Phase III, try to, again, just get in front of as many of those physicians at ECTRIMS as possible with new and fresh information from the Phase IIIs. Then we head into ASH, where we'll be highlighting our U2 plus venetoclax, as well as our U2 plus 1701 and 1701 alone data. Then that leads us into early next year, where we'll have, hopefully, an approval in March for the U2 combination in CLL, which should hopefully lead us a few months later to third quarter for approval in MS. And I think that covers us for about 15 months or so. So pretty big 15 months for us coming up. And we'll build off that. And then going from 15 months to 5 years, we certainly think we can be a significant participant in the CLL market and a significant participant in the MS market. And so as we think about building out the company, we obviously like to see that our drugs are helping patients and being used significantly in those marketplaces and just continue to build off that. I think we have -- we'll have a great CLL franchise, and we've got a lot of compounds that we could put through the channel there and a really nice franchise across all of the lymphomas. So we think there's room for us to continue to grow. And like I said, we have the pipeline to do it. We'll look to beef up our MS offerings. I think we've got even some things potentially within our portfolio that could be moved into MS programs. We've got a great -- also, again, the clinical capabilities of TG, both on the hem/onc side and on the MS side, are really -- are well positioned for us to be able to continue to push and take advantage and drive additional compounds or combos into both those areas, including MS. So I think if you look down the road 5 years, we'll be, what, 3 years into the MS launch, 3.5 years in the MS launch, almost 4 years into a CLL launch. We should be -- at that point, I'd see us moving with some U2 venetoclax potential approvals, some additional triples. So yes, I think just continue to drive the business organically. I mean, we'll look for possible additional opportunities to bring into the company. But I think in terms of the growth, I think it's -- we're set for the next 5 years in terms of how this all rolls out. Now if you want to go about 10 years, it's a longer conversation.

Well, we'll do that next year. All right. Michael, thank you again. Thank you for our viewers for dialing into this fireside chat. Have a great rest of your conference and great rest of the day. Thank you.

Thanks, Graig. Appreciate it.