Good morning. I'm Eric Joseph, Senior Biotech Analyst with JP Morgan. Our first presenting company this morning is Pliant Therapeutics, and presenting on behalf of the company is CEO Bernard Coulie. There'll be a Q&A session after the presentation. Just raise your hand, and we'll get a mic over to you. And for those tuning in via webcast, you can also submit questions. Just hit the Ask a Question icon. So, with that...
Sorry about that.
No worries. Bernard, thanks.
Thanks, Eric, and first I want to thank Eric and the JP Morgan team for giving us the opportunity to present today. As you know, at Pliant, our mission is to develop novel treatments for rare, high medical need fibrotic diseases. With that mission in mind, we have developed what we consider as the industry-leading fibrosis platform, which is based on small molecule inhibition of integrin-mediated TGF-beta activation. We know that TGF-beta is the main regulator of fibrosis, and we have shown that with our approach, we can generate a strong antifibrotic effect, as well as tolerate or well-tolerated drugs. Bexotegrast is our lead program. Currently, it's in development for both IPF and PSC. We have completed our phase IIa program in IPF and are currently enrolling our phase IIb trial, BEACON-IPF. Our phase IIa program in PSC is ongoing.
We recently reported data on the lower doses between 40 mg and 160 mg . And in both phase IIa programs, we have shown that bexotegrast is well-tolerated in these two quite different patient populations, as well as clear effects on a number of exploratory endpoints and a pivotal endpoint being FVC in IPF. Besides bexotegrast, we have another program, which is in clinical development right now, called PLN-101095. It's a phase I study in patients with advanced or metastatic solid tumors. PLN-101095 is a potential first-in-class, dual-selective alpha V beta 8, alpha V beta 1 inhibitor, meant to overcome resistance against checkpoint inhibitors in these patients that have advanced solid tumors that are resistant, obviously, to checkpoint inhibitors. We have a strong financial position. At the end of the third quarter last year, we had $524 million in cash and cash equivalents.
This allows us to fund our operations well into the second half of 2026. This is our pipeline. Besides our two clinical programs, we have a third program, PLN-101325, which is an allosteric modulator of a muscle integrin called alpha 7 beta 1. Indication is muscular dystrophies, including DMD. We anticipate to have our regulatory filing happening this quarter, allowing to start phase I development. The rest of the presentation, I will focus on bexotegrast as well as PLN-101095. 2024 will be a catalyst-rich year for Pliant. We will have upcoming 320 milligram data in our phase 2a PSC trial called INTEGRIS-PSC.
First quarter, so this quarter, we will have 12-week interim data, and then by mid-year, we will have our 24- and beyond week data from this study at 320 milligrams. PLN-101095, we will have phase I data in patients with solid tumors in the second half of 2024. This will be mainly PK data, safety data, as well as data on a number of biomarkers of biological activity. And as I already mentioned, PLN-101325, we will have regulatory filing happening this quarter. So as you know, our core platform is our integrin-focused small molecule library, which has continued to expand both in terms of the number or the diversity of integrin receptors we can target with our chemistry, as well as the number of indications beyond just fibrosis, as well as potential platform applications that we can cover.
We anticipate that, you know, based on, on-- or with the, with the platform as the basis, that this can lead to additional, agreements, collaborations with pharma based just on the platform. Bexotegrast is a broadly applicable antifibrotic. We know that localized TGF-beta inhibition has the potential of being a backbone antifibrotic. Tissue-specific TGF-beta inhibition avoids systemic toxicity and, at the same time, generates a very strong antifibrotic effect. To date, Bexotegrast has been tested in over 700 participants, with a growing number of patients in two different indications, IPF and PSC, and we have seen that it continues to be well-tolerated. At the same time, it has the potential to treat multiple fibrotic diseases because Bexotegrast continues to show an effect, an antifibrotic effect, on number-- on a number of different exploratory endpoints in two different diseases.
Moreover, bexotegrast can expand into additional indications in lung and liver fibrosis beyond IPF and PSC. If we look at the preferred treatment option in IPF, we did a physician research study asking physicians, prescribing physicians about what they consider as the key attributes for a drug in IPF. Antifibrotic mode of action is the first one. Obviously, bexotegrast targets specifically TGF-beta, which is the master regulator of fibrosis. And we have seen across the multiple endpoints in different patient populations that we have looked at, that it is truly an anti-fibrotic. Second, physicians are looking for treatment that can be combined with standard of care, but it can also be used as monotherapy. And again, we have shown effects on FVC in patients with IPF in both a monotherapy setting as well as in combination therapy.
It's one day- one pill once a day, which is quite different from the current situation with standard of care, which are multiple pills, multiple dosings a day. And then, of course, last but not least, safety and tolerability. We have shown- extensively shown that, our drug is well-tolerated, and we have no GI side effects, which are typical for some of the other drugs. Going back to the basics. So how does it work? Bexotegrast is a dual inhibitor of alpha V, beta 1 and beta 6. These two integrins are expressed, solely expressed in fibrotic tissue, a very low expression or no expression in normal tissue. Alpha V, beta 6 is expressed on epithelial cells. Alpha V, beta 1 is expressed on fibroblasts, and both are responsible for overactivation of latent TGF-beta.
Latent TGF-beta is being tethered or sequestered in the extracellular matrix, and upon binding to these or with these receptors, it will be activated to active TGF-beta. It will bind to its receptor, which will lead to activation of the pro-fibrotic pathway, leading to overexpression of pro-fibrotic genes, and ultimately, leading to excessive production of extracellular matrix proteins, which will lead to fibrosis. So selectively blocking these two receptors with bexotegrast, we basically prevent the conversion of latent TGF-beta to active TGF-beta. And as a consequence, we see an inhibition or a reduction of this overactive pro-fibrotic pathway, which is under control of TGF-beta. And as a consequence, we see obviously all the anti-fibrotic effects that we see in our different patient populations. Note also that this is a safe approach because it's localized TGF-beta inhibition.
We don't touch any systemic TGF-beta, as those receptors are only expressed in fibrotic tissue. Coming back to our phase IIa data, INTEGRIS-IPF, which has been completed, we looked at four different doses, ranging from 40 mg- 320 mg, up to 12 weeks of treatment for all doses, and we went beyond 24 weeks at the highest dose. This study was designed for, you know, with safety in mind, right? Safety is our primary endpoint. The study was not powered to show a significant effect on forced vital capacity, which is a pivotal endpoint for IPF. Still, we did see effects on FVC. So exploratory endpoints included change in forced vital capacity from baseline over 12 weeks and 24 weeks. We looked at lung fibrosis by imaging using Quantitative Lung Fibrosis score, which is a validated imaging score for fibrosis.
We looked at a number of symptoms, including cough, as well as effects on selected biomarkers, and I will show you some of these data. These are the 12-week FVC data, where we basically see, I would argue, starting from 80 mg, a separation of the FVC curve over 12 weeks, where you see a continuous decline of FVC in the placebo-treated patients with a separation or a stabilization of the FVC curve under active. Notably, at 320 mg, we actually see a positive deflection, meaning there is an improvement in FVC. Note that in both the placebo as well as in the treated group, about 80% of these patients were on standard of care, and about 20% are being treated, as you know, in monotherapy setting with bexotegrast.
If you look at the 24-week data, that was only 320 mg- sorry, the 12-week data, looking at the 320 mg, we see that the delta between active and placebo is 140 ml, sorry. If you compare it to selective investigational agents, such as the Boehringer compound, which is a PDE4 inhibitor, as well as BMS compound, which is an LPAR1 antagonist, we see a clear, a better effect, compared to those two drugs, and definitely compared to some of the historical data with the approved agents, Esbriet and Ofev. One of the endpoints, secondary endpoints in our phase IIb study is relative forced vital capacity percent predicted decline of more than 10%.
This is a predictive endpoint in the sense that it's a risk factor for progression. And what we looked at was the proportion of patients that had, over 12 weeks, a relative FVC PP decline of more than 10%. And what we saw was a clear dose response on this categorical endpoint, ranging from 40 mg- 320 mg. I think the key data slide from our IPF study is this one. We have shown that with bexotegrast, we see a durable increase in FVC above baseline. So about 50% of patients in the active group at 12 weeks, actually 56% of patients, had an FVC, a positive FVC, meaning an FVC above baseline.
All of those patients, except one, remained above baseline at week 12 at week 24, while in the placebo group, although small, initially there was some variability, but once you pass 24 weeks, all placebo patients are progressing and have an FVC that's below baseline, and I think this is, this is the key slide. It means that under treatment, we see a continuous separation between active and placebo at 24 weeks, and I think it's safe to assume that that separation will continue to grow as you go up to 52 weeks.
We also looked at the amount of fibrosis using an imaging biomarker called Qualitative Lung Fibrosis score, which is measured by high-resolution CT, and we see that under active, there's actually a stabilization of fibrosis, while under placebo, we see continuous progression over 24 weeks of this specific quantitative lung fibrosis score, which is to be expected because, of course, patients are progressing. Two percent is considered as the MCID. That means any number below that is considered noise, it's variability, but once you go above that, it's true progression of fibrosis. So this brings us to the BEACON-IPF study. This is our phase IIb study that's currently enrolling. It's a placebo-controlled randomized study, of course, looking at two doses, 160 mg and 320 mg in patients with IPF. The primary endpoint is changed from baseline in absolute FVC.
A number of secondary endpoints include time to progression, disease progression, change from baseline and absolute FVC in subpopulations. That means in patients that are on monotherapy or patients that are on standard of care. We will look again at QLF, so we will measure lung fibrosis by means of high-resolution CT. We will look at a number of patient-reported outcomes and, of course, safety and tolerability. This is a 52-week study, and about 70% of patients will be on standard of care. About 30% of patients will be on monotherapy. We anticipate this study to be fully enrolled based on the projections we have right now, probably by or in the third quarter of this year. So this brings us to our PSC program. So the phase IIa in PSC is still ongoing. It's called INTEGRIS-PSC.
This is a pretty unique trial in the sense that this is the first PSC trial that's truly enriched for patients with suspected moderate to severe liver fibrosis, based on a number of inclusion criteria that are listed here on the slide. Again, this is a trial looking primarily at safety and tolerability, but we have a number of exploratory endpoints, including liver fibrosis biomarkers such as ELF and PRO-C3, liver biochemistry, as well as liver imaging. The design of the study is similar to what we did in IPF. Four different doses, ranging from 40 mg- 320 mg, up to 12 weeks for all doses, and then with the highest dose, we go beyond 12 weeks, up to 48 weeks, potentially with a data readout at 24 weeks.
And again, the week 12 data for 320 mg, are upcoming this quarter for... The 24-week data will be mid-year. What I'm going to summarize here are the data for the lower doses. Starting with ELF. ELF is a validated biomarker in PSC and in liver fibrosis in general, and it's predictive of, transplant-free survival. What we have seen here at all doses is that bexotegrast reduces ELF relative to placebo. Note also how ELF increases over 12 weeks in the placebo-treated group, which reflects the fact that we have enriched for active fibrosis. At 160 mg, we reach significance, but actually, every dose is active. Similarly, we saw an effect on PRO-C3.
Relative to placebo, we see a stabilization of fibrosis, while in the placebo group, there is a continuous increase in PRO-C3 , again, reflecting the fact that they are having active liver fibrosis. Much to our surprise, we also saw an effect on alkaline phosphatase. So our drug is an antifibrotic. It's not an anticolestatic, so it's not supposed to do much on alkaline phosphatase. If we look at patients that had an elevated alkaline phosphatase at baseline, we see a reduction of alkaline phosphatase at 12 weeks. We actually included both patients with normal and elevated alkaline phosphatase, assuming that, you know, there wouldn't be an effect. Also, alkaline phosphatase is not a pivotal endpoint in PSC to start with. It kind of reflects, liver function, but not necessarily the stage of fibrosis, and it's not predictive for clinical outcome in PSC.
Still, we did see this effect, and the reason we think this is happening is the following: So we used an MRI approach. Basically, this is MRCP, but combined with a contrast agent called gadoxetate. Gadoxetate is taken up by hepatocytes and then secreted into the bile. The amount of uptake by hepatocytes reflects, I would say, healthy hepatocytes, so hepatic function or hepatocyte function. And so what we saw was, on the left-hand side in this slide, a relative enhancement in terms of uptake of gadoxetate by the liver, reflecting improved hepatocyte function, while in the placebo group, we saw a decrease, again, reflecting, you know, progressive liver disease in PSC patients.
At the same time, as the as gadoxetate is secreted into the bile, you can use it to measure the speed by which it travels through the biliary tree and gives you an idea about the patency of the biliary, basically. And when we look at the time of arrival of the gadoxetate to the common bile duct, we see that there is actually improved bile flow under bexotegrast by reduced times to get there versus placebo, where we saw an increase of almost 100 seconds in terms of, you know, after 12 weeks, the time it needed to get to that common bile duct. And what I think is happening here is the fact that basically, because of its anti-fibrotic effect, we see an opening up of the bile ducts again.
So rather than having strictures and obstruction to outflow of bile, it seems that we are able to restore with bexotegrast bile flow, which is fundamentally addressing what is happening in PSC, the fundamental issue with PSC. So, as I mentioned, 320 mg data are coming up this quarter at 12 weeks, and then at 24 weeks mid-year. For the rest of the presentation, I will briefly touch upon PLN-101095. It's a potential first-in-class dual inhibitor of both alpha V beta 8 and alpha V beta 1. It's really designed to reprogram the immune-suppressive tumor microenvironment of solid tumors by resensitizing the solid tumor to checkpoint inhibitors. The compound itself is orally administered based on our initial phase I data, even at the lowest dose.
Right now, we get above IC 90 concentrations, which means there is a high oral bioavailability. The compound itself is highly potent, has shown activity in a number of different tumor models in mice that are anti-PD-1 resistant. We saw actually a greater reduction with our compound compared to the alpha V beta 8 monoclonal antibodies that's in development, as well as a TGF-beta monoclonal antibody. We also see a significant reduction in tumor fibrogenesis, and the reason for that is related to the fact that the drug also hits alpha V beta 1. So what is happening? From a gene signature perspective, we are basically rebalancing the tumor in terms of going from a high TGF-beta gene signature to a high interferon gamma gene signature.
Rebalancing means pushing the tumor from non-responsiveness to a checkpoint inhibitor to become more responsive or sensitized to a checkpoint inhibitor. And that's shown in the next slide, where we basically looked at a pancreatic cancer model that is resistant to anti-PD-1. And when we combine the anti-PD-1 with PLN-101095, on the left-hand side, you see a reduction or an inhibition of tumor growth, which is also reflected in terms of its mechanism. We see a reduction in TGF-beta signaling as measured by p-SMAD over SMAD, as well as an increased infiltration of CD8-positive cytotoxic T cells into the tumor. This is the phase I study. This is the design of the phase I study. Right now, we're going through the different cohorts. Of course, safety and PK are key.
We have a number of PD markers of activity that we are looking at, and this is in patients with advanced or metastatic solid tumors that have failed therapy with pembro. And again, we anticipate data by the second half of 2024. So this concludes my presentation. Thanks for attending. Thanks for your attention, and happy to take any questions. Thank you.
Well, thanks, Bernard. And again, for those who have questions, we can make a... Excuse me. We'll bring the mic over to you. Just wait for that. But just to kick things off, Bernard, I guess with the BEACON study now underway for the last six months or so, can- maybe you can just kinda update us on how enrollment has been progressing, yeah, how the pace of enrollment in that trial has kind of looked relative to expectations?
Yeah, I think... I mean, based on our projections, enrollment is going well. And so again, as I mentioned, we anticipate to have the study fully enrolled by, you know, or in the third quarter, under the current protocol.
Okay. It's funny, in recent discussions, actually, you know, yesterday at the conference, speaking with another company in the also in the lung function space, there is a thought that, you know, the agency, FDA, might be open to CT densitometry as a possible approvable endpoint, kind of with the thinking that perhaps FEV or spirometry is kind of outmoded. I'm curious to know whether that's something you've explored or expect to explore a little more deeply with the BEACON study, and or whether, you know, developments in the field you might be tracking that may further validate that endpoint, perhaps as something to leverage in a phase III trial.
Yeah, I think, I mean, we have multiple interactions with the pulmonary division at the FDA, and I can tell you FVC is still the pivotal endpoint to be approved on, and mortality, which of course, can be done after approval. Right now, we didn't, at least we didn't hear any inclination to replace FVC by a surrogate. I mean, FVC itself is a surrogate to start with. I think we need way more validation and, you know, on a number of different endpoints, both circulating biomarkers, and that's something we are including in our phase IIb. We have included in our phase IIa, including, for example, PRO-C3 can be used in liver in lung as well, although it's not as well-validated as it is in liver.
As you know, we have looked at circulating beta 6, which turns out to be also correlated with progression of disease. And of course, we are doing QLF, so we are looking at lung fibrosis with this kind of validated surrogate of lung fibrosis, sorry, using high-resolution CT. But again, I mean, those are secondaries. Forced vital capacity remains the primary for a pivotal endpoint, and that I don't think will change soon. So, but yes, we do take a whole bunch of additional biomarkers as secondary or exploratory endpoints, just to kind of continue validation of some alternative endpoints beyond FVC.
With BEACON, I don't believe this is the case, that you have incorporated an interim analysis. Maybe just confirm that that is the case and perhaps sort of the thinking as to whether or not to include an interim or...
Yeah.
Or not.
It's a good point, Eric. I mean, I forgot to mention, but actually, the Phase 2b is designed to be potentially be a pivotal, from a power perspective, and to show a significant effect on overall change in FVC from baseline, which means that an interim analysis is going to kind of weaken that possibility. So we don't have an interim analysis scheduled in this Phase 2b, just to preserve the integrity of the trial and, you know, giving it the possibility of being a pivotal trial, so.
Okay. And you know, you still have some flexibility or... look, you're evaluating two different doses in BEACON. Is the purpose behind that ultimately to kind of still pick a winner that you might advance into a phase III trial? Or would you still expect to ultimately conduct the phase III with an eye towards approval with both dose strengths available for patients? And maybe just talk a little about the rationale really for continuing to explore a two-dose regimen here in BEACON IPF.
Yeah, the Phase IIb is truly a dose-finding study, right? And it's meant to understand what's the optimal dose from both an efficacy and safety perspective. But the ultimate goal is to pick a winner. And so a confirmatory Phase III will be with one of the two doses. We don't plan to continue both doses. It's something that we know, we are aware of, that some of our competitors are doing. They are running Phase III trials with two doses. I think part of that is, by, I think, request from the FDA, because they only tested one dose in Phase IIa, which is not something we did.
As you know, we tested four different doses, which has allowed us to kind of narrow it down to the two higher doses to be tested in phase IIb. But again, to your point, we are going to test one, going to move forward with one dose once we get to phase III.
In one of your slides, you kind of lay out the competitive landscape, both, you know, the two existing commercial products and some of the developing regimens. Maybe just from a mechanism, perhaps standpoint, I guess, how do you look at bexotegrast, how do you look at the positioning of bexotegrast relative to, um, those, you know, developing or approved-
Yeah
... alternatives and perhaps their ability to, you know, combine, like-
Yeah.
I mean-
Before. Yeah. I think, I mean, right now, they are at the same stage or a little bit further ahead compared to us. There are, I would say, three programs going. One is BMS, which is the LPAR1 antagonist, one is Boehringer Ingelheim, which is a PDE4 inhibitor, and a third one is actually United Therapeutics, where they are looking at an approved product, their prostaglandin agonist, Tyvaso, to see if they can also position it in ILD or in IPF, which is an inhaled. But both BMS and Boehringer are oral drugs like ours. From a drug, from a combination perspective, we don't have drug-drug interaction liabilities at all, so we can potentially combine our drug with the BMS drug or the BI drug.
From a mechanism perspective, I don't think it would, you know, it makes sense. I mean, these are complementary mechanisms, and could potentially lead to even a better effect. I think from a side effect profile, there are some issues with both, and notably, anti-PD-1 has a diarrhea liability. And we are only aware of the 18-milligram data in Phase IIa that were published in the New England Journal of Medicine. We are aware that Boehringer is also evaluating 9 mg, if I'm correct, so they had to half the dose, probably to mitigate a little bit of the diarrhea risk, because as you know, nintedanib, so Ofev, their own approved drug, has the same issue. And so we've seen in the Phase IIa that combining both drugs is even worsening the diarrhea and kind of increasing the dropout rate.
BMS LPAR1 antagonist is, I think, an antifibrotic. It's a mechanism that definitely has an antifibrotic mode of action. The effect that they saw in their phase IIb study that they published on at ATS was relatively moderate in terms of additional improvement on top, on top of standard of care in IPF. I think you saw my slides. It's somewhere in 20+ ml versus what we saw with 140 ml. And actually, in their phase III, they have doubled the dose as well, so probably to kind of increase chances for success from an efficacy perspective. But again, to your question, we can combine with both.
But, you know, comparing at least based on phase II data, our drug seems to be more efficacious on FVC, compared to the Boehringer or the BMS drug, so yeah.
Shifting to PSC and the upcoming 12-week readout at 320 mg, maybe you can just share some of your expectations or help frame investor expectations for that readout. The data that you've presented through 160 mg to date shows a pattern more of one of stabilization, I think, on some key endpoints of PRO-C3 and ALP. Is it possible that we might see sort of reductions on those endpoints as you go higher in dose?
Our expectations are relatively conservative, I would argue. I think what we anticipate to see is, with 320 mg, a confirmation of what we saw at the lower doses. I think it's noteworthy that, notably on ELF and PRO-C3, 40, 80, and 160 almost are equiafficacious, or, you know, have similar effect size, reaching significance at 160 mg, which suggests there is a little bit more activity. The reason that we see, already at these very low doses, activity in PSC, and we didn't see that in IPF, probably is related to, tissue distribution. We know that concentration in the liver, at least in preclinical tissue distribution studies, is about three times higher than in the lung, so that may explain that shift in dose response or lower dose.
With 320, I'm not sure if we're going to push this even further. But of course, thinking about the future, thinking about longer-term studies, you want to optimize your chances for success, and if we can show that 320 is safe in this patient population, then definitely it would be a dose that we would consider for further development, you know, for example, together with 160. Kind of a comparable approach to what we have done in IPF. So again, we are quite, I would say, conservative in terms of expectations. If 320 would push it even further, that's great, but, you know, based on what we have seen so far at the lower doses, I don't anticipate that to be the case.
And I guess just thinking about next steps within PSC, I guess yeah, I'm just trying to think of, like, the, you know, the type of signal that, in your view, would be compelling to move forward enough into next stages of development, and perhaps there's also a sort of a regulatory, some regulatory feedback that's sought in the process. So I guess, maybe just kind of, share with us, share with us, you know, your view on sort of what a a registration study might look like in terms of endpoint selection and just and the opportunity which with where you might, you know, be able to get feedback from regulators on that.
Yeah
... design.
Absolutely. So the next steps for us is once we have the 12-week 320 data, and actually, we are already preparing for submission to kind of basically have a conversation with the regulators, notably the FDA, in terms of a proposed Phase III design or at least pivotal trial design. And so we kind of will plug in the 320 data, 12-week data, submission will be made, and we anticipate to kind of have that interaction with the FDA somewhere mid-year, just accounting for the regulatory submission timelines and what have you.
Our anticipation is that the FDA is not going to move away from histology, right, as a primary endpoint, but we want to get a better understanding in terms of the use of certain biomarkers on top of histology, also trying to understand how they think about duration. I think we have precedent based on the Gilead phase III design on how the FDA thinks, but at the same time, we want to kind of explore potential, you know, venues to potentially, you know, look at shorter trials or improve chances for success using certain biomarkers. But again, we don't think histology will move away. And based on what we have seen in our phase IIa study, we anticipate being a strong antifibrotic, that we also will see effect on histology, so using liver biopsies.
So that's ongoing. That process basically has started, and once we have the 3 20 data, we will kind of submit and have the conversation. We think we can go straight into a phase 3, and probably duration of treatment is probably 24 months, and that's, again, based on precedent from Gilead. But before that, before we engage in a pivotal program, registrational program for PSC, we want to make sure that, you know, we have the necessary means to do so. So it's not just FDA, it's also access, I mean, additional capital, whether that's non-dilutive or dilutive, that we want to have before we start a phase 3 program in PSC. We have been very clear about that. Right now, the focus is BEACON-IPF.
We need to get that enrolled, and all resources are basically spent on BEACON-IPF in order to kind of get on time to great data. For PSC, we can start a study that's part of, you know, our budget, and when we project our cash runway in terms of second half of 2026, that includes a start in PSC, but we wouldn't be able to finish a phase III 24-month program under the current cash, so we need more. And then, I think that's basically kind of part of the equation as well.
I didn't mention it during my presentation, but obviously, we are looking to partner our earlier-stage programs, both the oncology program, once we have phase I data, as well as the DMD program, and those conversations are ongoing and can generate additional non-dilutive cash that could be deployed towards the PSC program, so.
Okay. Any questions from the floor? All right, well, I think we'll leave it there for time. Thanks very much, Bernard.
Sorry.
Yeah.
Thank you so much.