Omeros Corporation (OMER) Earnings Call Transcript & Summary

Hi, everyone. Welcome to day 2 of the Virtual Napa Conference here at Bank of America. I'm Greg Harrison, one of the analysts on the biotech team. And on behalf of myself and Geoff Meacham, we'd like to welcome Greg Demopulos, CEO of Omeros. We'll jump into Q&A in a moment, but Greg, if you want to make any opening comments, please do so now.

Yes. Thanks, Greg, to you and Geoff and the rest of the team at BofA. We're appreciative of the opportunity to join you folks today. So thanks.

Great. So your lead program is a complement inhibitor targeting MASP-2 in lectin pathway. Maybe you can just give an overview of the advantages that you see from your end, looking upstream within complement as opposed to other assets that target later in the cascade like C2 or -- sorry, C3 or C5.

Yes, sure. I mean you already identified one of the major advantages as we see it is that -- is upstream, and we're talking about MASP-2 here just to make sure that I'm...

That's right.

Okay. Yes. No, I mean, MASP-2 is, as you know, the effector enzyme of the lectin pathway. It sits at the neck of the funnel of the recognition molecules, and it's really the key enzyme, the effector enzyme of lectin pathway. So if you shut that down, you shut down the lectin pathway. The importance of it being upstream is that it leaves the classical pathway untouched. So meaning the inhibition of MASP-2 by narsoplimab leaves the functioning of the adaptive immune response of the classical pathway entirely untapped. So obviously, that has significant advantages with respect to infection or avoiding infections, which is why we don't vaccinate any of the patients in any of the clinical trials for narsoplimab. There's really no need to vaccinate. That is different than the C3 and C5 inhibitors that you mentioned, which do affect the classical pathway and therefore, do carry infection risk.

So the big news recently was your PDUFA date for narsoplimab in TMA was pushed back by 3 months. I'm not sure how much you can share, but if there's anything you can share as far as the request that led to the extension of the PDUFA and then what further action is planned as far as interactions with the FDA and next steps heading into the new PDUFA in October?

Sure. Sure. As you might imagine, we don't comment on specific data that are provided FDA in response to the information request. But what I can say is that it really is part of a BLA review process. We've received a number of information requests from FDA, and those traverse clinical, nonclinical CMC. As you know information requests are a routine as part of a BLA review process. And with narsoplimab having been given a priority review, the FDA was under some time pressure to complete that review. So we responded to an information request with a good amount of data and FDA designated a major amendment. This, as you pointed out, adds 3 months to the FDA review period. And that moved the PDUFA data out, as you said, to October 17. Importantly, that maintains first-cycle review status So the purpose of a major amendment is really to afford FDA the time necessary to complete its review. And the objective of that is the approval of the application. It's kind of interesting. We took a look at the number of major amendments that have been issued recently. And the data that we pulled were congressional data and like many other government databases, that lags by 2 years. But what we were able to pull was then between 2016 and 2019 inclusive. And in that time period, there were 17 major amendments. 16 of those products were approved on first cycle on the 1 remaining product, an Amgen product, I think, was approved on second cycle. So I think that kind of makes the case that the objective, certainly, in a major amendment is to reach an approval. So the next steps for us are just to continue to work closely with FDA, address any other questions that they might have, information requests with our objective of getting this drug approved by October 17 or perhaps even earlier if FDA sees its way clear to do that and make it available to patients. There's no treatment for TA-TMA. That is a bad disorder. The mortality rate in severe cases is high, reportedly is north of 90%. So I think it's a drug that's needed. I think the data are clear and looking forward to getting it out there.

Great. So what is the status of the launch preparations? I imagine you're pretty well prepared, given that the PDUFA -- original PDUFA is coming up pretty soon. Where are you at in terms of creating awareness that there's finally going to be a treatment for TMA, educating physicians, getting reimbursement in line and all those other things that need to be addressed before an approval?

Yes, you're right. We've been working hard. I'm proud of the progress the team's made with launch readiness. I think we recently shared that we received a new ICD-10 diagnosis code for TA-TMA. We also received 2 ICD-10 procedural codes for administration. And those all become effective October 1, which will just predate the -- our current PDUFA date. The work that's been done has been focused. It's been hard, meaning hard work, folks have been putting in. We have been really advancing an engagement plan with top transplanters, both U.S. and internationally. And the importance of that is, I think that we've been able to establish Omeros really as a trusted partner in the transplant market, which I think will serve us well going forward. You, I think, have seen the educational disease awareness campaign. That's been out both digitally and in print internationally. And that's proving to be highly successful as well. We've also put in place a disease education speakers bureau, and that's gearing up for this summer. And then, obviously, when you think about the payers and the providers. We've been focused on building a value framework that demonstrates the clinical and financial value of narsoplimab. And I think also that, that is a robust case that we've made. Within the organization as well, there's been a big push to become launch-ready. We have our heads of National Sales, the medical science liaisons, advocacy, all are in place as well as a field marketing team, and we've already initiated the U.S. sales force hiring process. So on the manufacturing side, we have long-term commercial manufacturing agreements in place, and we have sufficient supply to support the launch. So I think the bottom line is we expect when and hopefully, if the approval comes, we'll be fully prepared for the launch.

Greg, it's Geoff. I wanted to maybe just follow up on that. And that is, what impact do you think would some sort of treatment guidelines have? I'm just trying to think of ways to raise physician awareness and give them some sort of guardrails for how to use narsoplimab in the setting. And then the other question is from a payer perspective, are there rigorous pharmacoeconomic data that you could generate over time or that you've kind of gotten part of the way there to help with that avenue of the launch?

Good questions. With respect to the first, it's interesting that to date, there really hasn't been a single universally accepted set of criteria for the diagnosis of TA-TMA, which in part is probably why it is thought to be and likely is pretty meaningfully underdiagnosed. Now there is a group of physicians, transplanters, key opinion leaders, thought leaders in the U.S. and Europe who have come together to put together those criteria for diagnosis. And as I understand it, that could be out later this year or early next. And as part of that, again, that will help to drive, I think, consensus around not just the diagnosis, but also the treatment of TA-TMA. So I think that will be helpful. With respect to the health economics and outcomes research that you're referencing, sure, we've been working diligently to put the strong value case together around narsoplimab. And I think that the case that we've created is compelling. And I think that payers will respond favorably to that.

Okay. That's helpful. Greg?

So we've seen a second complementary inhibitor approved recently, and it ended up taking a relatively high price relative to Soliris, Ultomiris. And this is obviously in PMA, it's a much different indication. But wanted to get your thinking in general on pricing. Does this impact your strategy? And if you could just talk a little bit about the overall strategy. I know you're not going to tell us the actual price, but just how you're thinking about that, especially given that you will be potentially competing in some of the same indications like aHUS.

Sure, sure. Look, we've been working on our pricing strategy for a while now and through market research and advisory boards and other information and input of stakeholders that we've collected. The focus is to identify the optimal intersection between really first the strong value proposition of efficacy that we were just discussing, meaning the significant response rates, coupled with the significant improvement in 100-day survival and safety. So when you look at narsoplimab, we have not seen a safety signal of concern. And the drug has been well tolerated, not only in the very sick population of TA-TMA patients that we've treated, but across all of our indications, IgA, COVID as well, aHUS, and none of those have we seen a safety signal of concern. So we're looking for that point of intersection between the efficacy and safety of narsoplimab and then really what stakeholders are willing to pay for what we see, and I believe what they see or at least that's the indication of the really strong value proposition of narsoplimab. And the focus of that, again, is to minimize patient access to barriers at the time of launch so that patients and physicians can access this right out of the gate. As you mentioned, we have looked at and are analyzing the pricing strategies of the other complement inhibitors that are on the market. As you know, none of those are indicated for TA-TMA. But to get a reference point, we do look at the total treatment cost for off-label use in TA-TMA. And that gives us a reasonable, I think, a reasonable guidepost.

That makes sense. So you mentioned COVID. Wanted to get your take on the strategy in that indication. You've shown a couple of small readouts of very impressive data in pretty small numbers of patients. But wanted to see how that fits in with your plan? And what is the level of prioritization there, especially just given the different epidemiology and trends in the pandemic since you initiated the program last year, last summer or so.

So I think first, I heard a couple of questions in there. So with respect to our strategic plans on COVID. I agree that the data that we have generated there, I think -- I don't know if you'll be able to find data as good. I know you won't be able to find data better in critically ill patients than what we've been able to generate with narsoplimab. And we didn't develop narsoplimab for COVID-19. It just turns out that the pathophysiology of COVID-19, the endothelial injury and hypercoagulation, which are really key drivers in the disease, that pathophysiology just appears to dovetail about as well as could be imagined with the mechanism of action of our supplement. So we've tried to do what we can do to help critically ill COVID-19 patients, and we've done that through the research at our University of Cambridge facilities and also through compassionate use, both in the U.S. and abroad, really, in Italy. But the issue there is that our drug supply of narsoplimab is almost entirely spoken for by the anticipated launch needs in TA-TMA as well as by our clinical trial requirements. So we've publicly been pretty open that we're in discussions with both the U.S. and foreign governments to access funding or larger-scale manufacturing and also really for clinical trial support. Should we be successful, I think that COVID could well become an important part of our narsoplimab strategy for the foreseeable future. And I think, unfortunately, that could be some number of years because I expect that SARS-CoV-2 and its variance will be with us for quite a while. I think the second part of your question was about just, I think, Greg, remind me, it was about prioritization of COVID?

Yes, exactly.

Okay. Yes. I mean, I think, look, we have the I-SPY trial underway, and we're a part of that. They keep us at arm's length, as you know. So even with respect to number of patients enrolled, we really don't have any idea about that. I hear somewhat circuitously that, that enrollment is moving along and things are going well. But other than that, I don't have any specifics. So let's assume the data there are positive. In that setting, we would move pretty quickly to obtain an EUA or possibly even a regular approval from FDA. I also expect that government funding and support for manufacturing, which I said we need and we do need, would become more readily available. There's still a good number of COVID patients dying. Those are at too high numbers. So we push ahead aggressively. I mean I think in that setting, COVID would become a high priority. But that doesn't diminish then the priorities of the other programs. So TA-TMA is also, as I mentioned, associated with high mortality, IgA nephropathy is debilitating. So we would need to maintain those priorities as well.

And what sort of impact do you think an EUA or an approval in COVID would have on the rest of the business as far as there would be, I'd imagine, some pressure to have brought access and maybe a lower price point than you would have in a rare disease like PMA? How do you see that strategy or that playing out? Is there a possibility for a 2-tiered pricing? Or just trying to understand the impacts to the core business and complement.

That's a good question. And you're right. I mean the pricing could be different, right, in a large population disease such as COVID-19 versus the ultra-orphan population or indication of TA-TMA. So we're looking at that, right? We have to consider a number of scenarios and those have been faced before with launches in differing populations and differing indications. We're weighing those carefully. But I can tell you the focus for now is to demonstrate and demonstrate convincingly that narsoplimab efficacy really can be a game changer, given the devastating impact of COVID-19. So we need to access that manufacturing funding. We need to access the support. Once we get through that, I think we'll be able to find -- we'll be able to navigate some path through the pricing. But it's -- as you pointed out, it would be a challenge.

Got it. Let's move on to some of the other indications for narsoplimab. You have the Phase III trial in IgA nephropathy. Can you give us an update on enrollment and time lines of when we could see that data?

Sure. The ARTEMIS-IGAN trials currently enrolling. I think as we've said publicly, we have over now 120 activated sites globally, and we're adding additional sites to help accelerate enrollment. One of the areas of focus for us is China. The prevalence of IgA nephropathy is high there. I think that as I understand it, 1 in every 4 patients on dialysis in China has IgA nephropathy. So there's no lack of patients there. We need to be able to access them. And with respect to timing, our objective is to release data next year.

Great. So is a Phase III trial you're running, it has some differences from what you had in Phase II in terms of enrollment criteria, et cetera? Can you maybe give us a rundown of how those differences could lead to a better outcome in Phase III?

Okay. Well, first, I'll tell you that I think the Phase II trial was successful on a number of fronts. I mean the patients treated with narsoplimab pretty consistently and markedly dropped their proteinuria levels by 60%, 70% or more. So I think the outcome in that trial were clear. I know there was some confusion which you're referencing around that early time point in the second sub study. But that second sub study also taught us a lot about the need for repeat dosing in very sick patients with comorbidities in long-standing disease. I think the median time from diagnosis to entry in the study was about 17 years, and particularly, there was a misbalance between the control of the placebo group and the treated group. The treated group had patients out to 20, 20-some years from time of diagnosis to entry in the study. And I think the median time between those 2 groups was even markedly different, 17 for the narsoplimab group and 7 years for the control. But the knowledge there that we got from that Phase II trial really helped us design the Phase III ARTEMIS-IGAN trial and really to design it for success. So first, with respect to the differences, I think you asked about, it has a run-in period. The Phase III has a run-in period to better ensure that when patients enter the trial, there's no meaningful imbalance between groups with respect to RAS blockade. The Phase II did not include a run-in period. We intentionally did not put a run-in period on that because we were trying to generate proof-of-concept data as quickly as possible. Also, the ARTEMIS trial is a large placebo-controlled trial. And that greatly reduces, as you know, the impact of rare outlier patients like we saw in the smaller Phase II study. And again, I mentioned balance and imbalance earlier. The treatment groups should be certainly in a large study like we're running should be better balanced. And that's better balanced across all of the factors that could potentially confound the trial. So prior treatment, age, duration of disease, that sort of thing. So I think the Phase II trial or Phase II program really set us pretty -- set us up pretty well for the Phase III program and trial.

Greg, it's Geoff. Just a follow-up on that. I just wanted to ask you so many. There's a big diversity of patients from time from diagnosis to comorbidities to disease severity. How do you weed through some of that? And just from an endpoint perspective, proteinuria in the past has been a somewhat controversial endpoint at FDA, but it doesn't seem to be as much so. Are there other measures beyond proteinuria that you can look at to help capture the real clinical benefit?

Sure. That's, again, a good question. We have, look, first, size of the study, right, the end, the population of the patients we're enrolling helps to take care of the imbalances that might occur in a smaller trial. So I guess that's the first answer to your question. With respect to the endpoint, you're right, the endpoint is proteinuria. FDA is now comfortable with proteinuria as a surrogate for renal function, really as a surrogate for eGFR for estimated glomerular filtration rate. And that's in large part due to the data that Dr. Lesley Inker put out from her group and Boston University showing that there is a direct correlation between reduction in proteinuria and slowing in the rate of decline of eGFR, which is really the key to this, right? I mean proteinuria is an endpoint that everybody is now using. But the objective is, can you delay the onset to end-stage kidney disease? And that's -- can you flatten the slope of deterioration of eGFR so that you put off potentially possibly for the life of the patient, the need for dialysis. So I think what we're looking at is proteinuria. We're looking at it in 2 subsets, 2 subsets of patients in the Phase III trial. I think we are the only drug -- narsoplimab is the only drug that can gain regular approval on proteinuria alone. I think the rest of the drugs in development for IgA can obtain accelerated approval and then the confirmatory data needs to come through their eGFR data, which can take 2 to 3 years for that part of the trial to complete to get the subsequent regular approval. So narsoplimab is the only drug with breakthrough therapy designation in IgA. It's also the only drug that can get full approval. So in terms of the endpoint, we were structured to collect eGFR data as well. So let's assume that for some reason, we didn't show the same magnitude or roughly the same magnitude of reduction that we showed in the Phase II. I would -- again, my hope is that we do. There's nothing that tells me we shouldn't. That would result in a regular approval. If we somehow fell short of that, but still had similar to what others are having sort of in that mid-20s proteinuria reduction, the expectation is that would be an accelerated approval for which we would need to then show the eGFR stabilization. And that's already built into the ARTEMIS-IGAN trial. So we don't expect that we'd need to run another trial in that case to get regular approval. So I think we're looking at the right things. I think the studies set up well. And in fact, FDA has had a keen interest in IgA patients who have baseline proteinuria values of at least 2 grams per day. And that is the subset of high-protein fillers that we're looking at in the ARTEMIS-IGAN trial. And FDA has also indicated that it could grant approval based on narsoplimab showing a significant effect in just that subset of patients. So we really -- when you look at it, we have 4 ways to be successful in the trial. Accelerated or regular approval in the overall population, which is greater than 1 gram per day of proteinuria or those same options accelerated in regular approval in that high-protein pillar or greater than 2 grams per day subset of patients.

Okay. Perfect.

Greg, so where do you see narsoplimab fitting into the landscape in IgA nephropathy. I've heard a lot of talk that this could be a combo type of environment. Would you see narsoplimab having maybe the potential for enough efficacy to be a monotherapy? Or do you view it as more of a combo? And then also just that there's the opportunity for another company to reach the market first. So how does that impact your strategy with respect to combos?

Sure. I mean, first, I think that how docs will use, how physicians will use the treatment for IgA nephropathy, there's a good likelihood they're going to use things in combination. That's not a requirement, though, for narsoplimab. I mean, I think that when you look at the proteinuria data that have been generated to date, right, and you look across the drugs in development for IgA nephropathy. So you look at the Factor B inhibitors, you look at the gut-targeting steroids. The reduction in proteinuria there is in the mid-20s, then you look at narsoplimab. And across all of the work that we've done, it's a multiple of that. So our expectation is that, if and when approved, that narsoplimab would really be used very early on in the disease. I mean the role of MASP-2 and the lectin pathway in IgA nephropathy is unique. I mean the lectin pathway plays a key role, not just at the glomerulus, which is -- you can think of as sort of the early stage of the disease, right, the inflammatory stage of the disease. But it plays a key role as well in longer-standing disease. And that is the data are increasingly supporting is due to lectin pathway activation in the tubular interstitial and that's mediated through collectin-11, which is one of the recognition molecules for the lectin pathway. And that's what drives disease progression. So really, unlike other drugs in development for IgA, which we've talked about. And narsoplimab appears to inhibit both the glomerular and the tubular interstitial disease. No other drug has the same mechanism of action of narsoplimab. And we talked about just how the response is so much appears to be so much stronger with narsoplimab. So I think when physicians have these options, what they're going to want to do is as early as they can following diagnosis, you want to minimize the proteinuria. And there is an absolute consensus that elevation in proteinuria is really highly correlated with rapidity of disease of progression. And that, as we talked about earlier, has on end-stage renal disease and dialysis. So I would see narsoplimab as being a first line in the treatment of IgA nephropathy, meaning getting it on early. You're going to want us to optimize your RAS blockade, but that doesn't get you to where you need to be. And I think that the data are, again, increasingly showing that the more you can knock down proteinuria, that correlates directly with the slope of that decay of your eGFR or the true measure, the gold standard of measuring your renal function. And you want that as low as possible. I would certainly want that as low as possible if I were suffering from this disease. And so I'd want narsoplimab on, and I'd want it on pretty regularly.

Great. That's helpful. So just to wrap up on narsoplimab and before we move on to the rest of your portfolio, where would you see narsoplimab fitting in aHUS? How do you kind of view the strategy of gaining a foothold in the market where there's a strong entrenched competitor there?

Yes, that's a good question as well. Look, assuming a good trial outcome, which I do with narsoplimab in aHUS. And I think there's clear scientific evidence showing that it should work well there. It's another TMA. I think that narsoplimab would hold a significant place among the therapeutics for aHUS, which are right now, eculizumab and ravulizumab. But this program in aHUS for us really has a lower priority than the other narsoplimab indications. And that's primarily because we see aHUS as a contracting market. I mean if you look, and I'm sure you folks have, an increasing number of physicians in the U.S. and Europe are treating aHUS now episodically, really focusing on the flares rather than dosing chronically. So that has an effect on the overall market of aHUS. And then I think when you overlay that with the expectation that a C5 biosimilar will make it to the market in the not-too-distant future, I think that even further would be expected to contract the aHUS market. So while we're looking at it, while we're in it, while we have the Phase III program running, that's not a solid priority for us as the other indications.

Yes. That makes sense. So looking at one of your other targets, which is MASP-3, what is the likely development plan there? I know you've called out PNH as a potential indication. But what's your priority there as far as taking on something like PNH, which also has competition or focusing in other indications where MASP-3 could play a role?

Right. I think our current plans, as you just pointed out, are to prioritize, I think, the clinical testing in PNH, right? It's an established disease. There are good benchmarks. And I think that would help us to dial in the use of the drug. We clearly expect that 906, our MASP-3 inhibitor will affect positively, both the intravascular and extravascular hemolysis. I think 906 would prevent both of those. Now that's different than a C5 inhibitor, where actually C5 inhibition increases the potential or really almost causes the extravascular hemolysis. C3 inhibition has been shown to affect both, but when you look at the dosing there, that's twice weekly subcu. There are also the safety issues associated or potential safety issues associated with both C3 and C5 inhibition. We have shown in the data we recently put out from our Phase I trial in 906, we're really expecting once monthly subcutaneous dosing. And I think that's going to be a major differentiator. We also have to see how inhibition of MASP-3 provides any other really kind of biologic favorability or favorable attributes that the other treatments don't. And again, that will just be borne out with additional clinical data. But we're looking at other indications as well. I mean I think MASP-3 is the key activator of the alternative pathway. So I think you need to look across the entire pantheon of alternative pathway indications and understand or at least, I think, acknowledge that MASP-3 inhibition, specifically OMS906 could have an important role to play in any or all of them.

Greg, just on that note, when you look at where eculizumab, they had discussed taking it new indications and then -- but not going there, such as, I think, dense deposit was one disease, also dry eye. Is there sort of a road map of some indications that lectin that could be involved here that you could run? I think an orphan, I don't want to call it a basket study, but that's essentially it. Or is there not enough statistical power in having a very low end and some of those to really -- to have that serve to be an effective strategy?

No, I think you're right. I think the basket trial strategy can work. It, of course, depends on the magnitude of the signal, right? But we've used it effectively. I mean we used it for IgA. That -- the initial work we did in IgA nephropathy was a basket trial. And out of that, what we found was that we got certainly a very strong signal in IgA and in lupus nephritis as well. If you remember, the initial patients we treated, I think the median reduction in proteinuria and lupus nephritis was a little over 70%, which, again, is a multiple of what anybody else has shown. So I think a basket trial is an effective strategy, assuming that the -- as an initial approach, of course. But I think if you expect the signal to be good, it can help you. I think you've got to follow the signs as you're pointing out. And there are a number of indications where either one of these MASP-2 inhibitor, narsoplimab or MASP-3 inhibitor 906 can be utilized. And we're looking at all of those. You mentioned the eye. If you look upstream from VEGF, it is MASP-2. It's the lectin pathway that's upstream of VEGF. So boy, that opens up some pretty interesting ideas around, for example, macular degeneration. Now a lot of -- really the treatments for that are limited to intravitreal. But interestingly, MASP-2 is wholly generated in the liver. It's hepatically generated only. So by taking out MASP-2 systemically, I could imagine that, that would have a pretty good impact on macular degeneration, wet macular degeneration. And interestingly, our preclinical data, animal data strongly support that. You look at 906 and you start thinking about geographic atrophy or dry AMD. And there, again, I think there are opportunities. So yes, I think you're right. I mean basket trial is good. We are obviously very focused on looking at a broad range of indications, looking at the market competition and see what we can do that they can't do and what we have as specific characteristics or attributes of our molecules. That will make them better, whether that be safety or efficacy or both. And I think the results of that survey are very encouraging for us.

That's right. Okay.

So Greg, we've talked a lot about complement, and that's obviously a very exciting part of your business, but we can't let you go without asking about your commercial business. I wanted to get a sense of how people should be thinking about the OMIDRIA franchise. Should it be kind of viewed as almost an annuity or a stable source of cash to fund some of the other programs? Or are there opportunities where you could see another leg of growth for that asset?

I think the answer to that is both. I mean, I think, certainly, with the achievement of separate payment in the ASCs recently, which CMS awarded to us in December, December of last year, 2020. That's very important for us. But I mean that means that we really no longer have to go and keep asking for separate payment every year. We're covered now under the existing policy, which is one of exclusion from packaged payment. So OMIDRIA is part of that. And it would require CMS really to change its policy, which it's had in place consistently since 2019. It would require CMS to change that policy for us to have a different reimbursement scenario in the ASCs. So that's important. That has given our customers now a sense -- a better sense of consistency, which was understandably a bit in question, right? We went through pass-through, then we came off pass-through. We had a 9-month hiatus and then Congress restored pass-through for us for 2 years. Then we went off -- then we -- that pass-through period expired for us on October 1 of last year, and we had another hiatus which ran until really December and frankly, until late in January when the MAX finally posted CMS' decision. So this affords now stability, I think, and a perception of stability and reimbursement, that's very helpful. And I think it's going to be long-standing. The additional component of this is the NOPAIN Act, which is gaining substantial momentum in both chambers of Congress now bipartisan. I think there are 26 or more Senate cosponsors, and that's really split right down the middle between B&R houses. It's now recently introduced, and that's growing in support, I would expect, ultimately, you're going to see 70, 80 or more bipartisan cosponsors. So I think the likelihood that, that gets through, I think, is reasonable. I mean as much as anybody can predict in sort of the ranker that's currently going on in D.C. I would expect gee, this is something that people regardless of what side of the aisle they are can get behind and support. And we're seeing that happen. This is really being driven by voices for nonopioid choices. But every week, I'm seeing a new op-ed supporting it. So I think that's going to -- that would expand reimbursement or separate payment from the ASCs to include the HOPDs, and I think that would further boost growth. So I think we're going to see continued growth in OMIDRIA. And I think as you pointed out, it is also -- it's a revenue-generating machine for us. It largely precludes the need for -- or plans equity financings. And at some point here, that's going to grow to a level I expect where it's not just shedding positive cash flow from that program to the rest of the company, but that could actually cover the cost of our R&D. And I think that's not unrealistic. I don't think the time line for that is that far in the future. But we have to see a few things fall into place. Again, I think the NOPAIN Act would help. And we'll see the continued growth. But the product is well accepted and that utilization is growing, not just within facilities, but we're growing the base. So new facilities coming up, which I think is the key to driving that growth overall.

Great. That makes a lot of sense. So with that, we're about out of time here. So I'd like to thank you, Greg, for joining us today for an interesting conversation and everyone out there watching, and we'll see you all in Napa next year.

Thank you, both, very much. Looking forward to that being live.

Sounds good.

Thank you, Greg.

Thanks, guys. Take care. Thank you very much. Have a good evening.

You too.