Good day, thank you for standing by. Welcome to the Addex Therapeutics to announce full year 2022 financial results and provides corporate update conference call. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be the question and answer session. To ask a question during the session, you need to press star one one on your telephone keypad. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. To ask a question via the webcast, please access the Ask a Question tab. Please be advised that today's conference is being recorded. I would now like to hand the conference over to our first speaker today, Tim Dyer. Please go ahead. Hello, everyone. I'd like to thank you all for attending the 2022 full year financial results conference call. I'm here with Robert Lütjens, our Head of Discovery - Biology. I draw your attention to the press release and the financial statements issued earlier today, which are available on our website. I also draw your attention to our disclaimer. We will be making certain forward-looking statements that are based on the knowledge we have today. I will start this conference call by giving a quick overview of our recent achievements before handing over to Robert, who will review our clinical and preclinical pipeline. I will then review our 2022 full year financial results. Following that, we will open the call for Q&A. Our partner, Janssen Pharmaceuticals, continued to make excellent progress in executing their global phase II study in epilepsy patients with ADX71149. Several patients have completed part one of the study and progressed to part two. An independent interim review committee has been established by Janssen to review the data from part one and make a recommendation on the future direction of the study. We expect to announce the recommendation from this independent interim review committee early in Q2 this year. We continue to believe there is value in dipraglurant and have substantially completed our evaluations of future development. We have identified post-stroke recovery and pain as interesting areas for future development in addition to PD-LID. We are currently pursuing collaborative arrangements to advance future development. We continue to be excited by our pre-clinical pipeline, which has made excellent progress with multiple clinical candidates rapidly advancing towards IND-enabling studies. We've selected a drug candidate in our mGluR7 NAM program for stress-related disorders, including post-traumatic stress disorder, are progressing this drug candidate into IND-enabling studies. We expect to start dosing in these studies in the second half of this year. We also continue to progress several backup compounds from differentiated chemical selection candidate selection phase. We have made substantial progress in our collaboration with our partner, Indivior, in advancing several novel GABAB PAM compounds into clinical candidate selection. As a reminder, Indivior's primary interest is in substance use disorder. Under the agreement, we have retained the right to select drug candidates for development in certain exclusive reserved indications, including Charcot-Marie-Tooth 1A neuropathy, chronic cough, and pain. During 2022, we extended our collaboration with Indivior. Indivior agreed to provide us with additional research funding of CHF 1.8 million. We expect Indivior and ourselves to select compounds to advance into IND-enabling studies in early 2024. Our mGluR2 NAM program for mild neurocognitive disorders associated with Alzheimer's disease, Parkinson's disease, and depression ran into some challenges during clinical candidate selection phase, so we've gone back into lead optimization. We're making progress at the end of this week. Last but not least, our M4 PAM program for schizophrenia continues to make rapid progress through lead optimization. M4 PAM is a particularly exciting target for schizophrenia, especially following the recent positive phase 3 data from Karuna. Following the inconclusive data from our blepharospasm clinical study and the termination of dipraglurant's development in PD-LID due to slow recruitment rate attributed to COVID-19 pandemic related constraints, we have completed the close down of the studies and implemented a number of cost-saving measures. These cost-saving measures have significantly reduced our monthly cash burn going forward. As of today, we estimate that our cash reserves provide us with a runway through the end of Q3 2023, and enough time to secure a partnership to strengthen our balance sheet and provide resources to advance our portfolio. I will hand over to Robert, who will give you some more details about our exciting pipeline. Thanks, Tim. I will start with an update on our epilepsy program, which is in phase II, and an update on the rest of our portfolio. Janssen have recently completed recruiting part one of the ADX71149 phase II epilepsy clinical study. As a reminder, 71149 is a metabotropic glutamate receptor, subtype 2 or mGlu2 positive allosteric modulator discovered in partnership with Janssen Pharmaceuticals, a Johnson & Johnson company using Addex's proprietary allosteric modulator platform. Janssen have extensively profiled ADX71149 in preclinical models of epilepsy and have demonstrated both standalone anti-epileptic efficacy and a strong synergistic effect in combination with Keppra. There's a large market opportunity as more than 2 million patients are taking Keppra and many have breakthrough seizures or a suboptimal response. Furthermore, despite several available treatment options and many in research of alternative or improved therapies to treat the seizures. Interestingly, Keppra, while being largely sold as a generic, is still leading the market for antiepileptics, with close to CHF 1 billion sales revenue per year. Janssen have completed an extensive preclinical and clinical package and are currently running both a phase II study and an open label extension study in epilepsy patients. It is important to note we have significant economics in our deal with Janssen. We have pre-launch milestones of EUR 109 million, low double-digit royalties on net sales, and Janssen are responsible for all costs. I would like to show you some of the preclinical data. I mentioned the synergistic effect obtained in pre-clinical models of epilepsy. Here is the compelling data obtained by our Janssen colleagues in the 6 Hz model, a highly predictive model of epilepsy with a combination of 71149 and Keppra, which has been instrumental in the decision taken by Janssen to move this program into epilepsy. The left graph shows how the effect of levetiracetam is dramatically increased in presence of a low dose of 71149, producing a 35-fold shift in efficacy. The right graph shows the result obtained when the paradigm was reversed, where a low dose of Keppra induces a 14-fold increase in efficacy of ADX71149. The take home message here is that we see a strong antiepileptic effect with a combination of low doses of 71149 and Keppra, similar to the one obtained with a full dose of Keppra. This is truly a synergistic effect, not just an additive or pharmacokinetic effect, as demonstrated through isobolographic analysis. If models translate into patients, then our approach could become an important novel treatment for epilepsy patients suffering focal onset seizures. To the phase II study design. This is a phase II double-blind, placebo-controlled proof concept study and is enrolling patients with focal onset seizures who have suboptimal response to treatment with levetiracetam, which I remind is the active substance of Keppra or brivaracetam. Patients will establish a 28-day seizure count over a 56-day baseline period, prior to being randomized to receive either ADX71149 at 50 mg twice a day or matching placebo. The primary endpoint is the time taken to return to their monthly baseline seizure count. The study has two parts, part one being the four-week acute efficacy phase, and part two being an eight-week maintenance of efficacy phase. Part two will include patients who did not reach their baseline seizure count during part one of study, and they will continue on their randomized drug or placebo. Janssen plan to recruit up to three cohorts to test multiple doses of 71149. Today, cohort one of 60 patients has completed part one of the study. Janssen have established an independent interim review committee to look at the data from part one and issue a recommendation for the future conduct of the study in early Q2, 2023. We look forward to sharing their recommendation as soon as it is available. Now on to dipraglurant, our mGlu5 negative allosteric modulator. I'd like to mention that the field of mGlu5 negative allosteric modulators is very active with 2 modules, mavoglurant and basimglurant, which are progressing in clinical trials, demonstrating this mechanism action is safe and well tolerated. Mavoglurant, discovered by Novartis, is being developed by Stalicla in cocaine use disorder with a strong financial and scientific support from the U.S. National Institute on Drug Abuse. Basimglurant, discovered by Roche, is progressed by Noema Pharma in trigeminal neuralgia. While these indications could be interesting for dipraglurant, we believe the differentiated profile of dipraglurant is particularly suitable for dyskinesia associated with Parkinson's disease or PD-LID and post-stroke recovery. We are currently working with key opinion leaders to establish the future development plans in PD-LID and post-stroke recovery. In parallel, we're pursuing collaborative arrangements to implement these future clinical plans. Let me now update you on our preclinical programs. We have made significant progress in advancing our preclinical programs. As a reminder, all our programs were identified in-house from our proprietary allosteric modulation discovery platform. The success of our platform is driven by the combination of our unique small molecule chemical library and tailor-made proprietary biological screening tools and methods, which we deploy to identify the initial hits and support lead optimization. I would like to share with you the progress we have made in four of our most advanced preclinical programs, the GABAB positive allosteric modulator, the mGlu7 negative allosteric modulator, the mGlu2 negative allosteric modulator, and the M4 positive allosteric modulator programs. Our GABAB positive allosteric modulator program, which is partnered with Indivior. The aim of this collaboration is to deliver treatment for substance use disorders. Indivior is supporting the research at Addex and have recently committed additional funding for us to complete clinical candidate selection activities, reaching CHF 13.8 million total funding so far. As a reminder, GABAB's receptor activation has been clinically validated in a number of disease using baclofen, a GABAB allosteric agonist. Baclofen is FDA-approved for treatment of spasticity and is widely used off-label to treat numerous diseases, including alcohol use disorder, chronic cough, Charcot-Marie-Tooth 1A, and various types of pain. However, Baclofen has a short half-life and comes with significant side effects, hampering its wider use. Thus, there is a strong need for a better baclofen. We believe this can be achieved with positive allosteric modulators and their differentiated pharmacology, having the efficacy of Baclofen but longer half-life and improved side effects profile. We are well on our way to meeting this objective with multiple novel drug candidates rapidly advancing through clinical candidate selection phase with the aim to nominate drug candidates for IND-enabling studies in 2024. As part of our agreement with Indivior, we have the right to select drug candidates from the funded research activities for our own independent GABAB positive allosteric modulator program. I will now speak about the indications we plan to pursue. Firstly, Charcot-Marie-Tooth disease type 1A, or CMT1A, which is a type of inherited neurological disorder affecting the peripheral nervous system. It is caused by a duplication of the PMP22 gene, which leads to the production of too much of the PMP22 protein. Excess of this PMP22 protein damages the myelin sheath that surrounds and protects nerve fibers, resulting in slow and progressive damage to the nerves. People with this disease experience weakness and wasting of the muscles of the lower limbs beginning in adolescence. Later, they can also have hand weakness and sensory loss, resulting in a significant reduction in their quality of life. CMT1A is the most common subtype of Charcot-Marie-Tooth disease, accounting for about 70% of cases. There is currently no approved drug to treat CMT1A. However, baclofen has shown beneficial effects in patients. In addition, we have collected robust preclinical data with our GABAB PAM in highly translation models of CMT1A, demonstrating positive effects of chronic treatment on both biomarkers and behavioral measures, suggesting GABAB PAM has the potential to slow or even stop the progression of the disease. There is also a strong rationale for developing GABAB PAMs for chronic cough. Chronic cough is a persistent cough that lasts for more than eight weeks and can be caused by a variety of factors, including respiratory, sorry, infections, asthma, allergies, and acid reflux, but also possibly because of an overactive cough reflex. Support for this approach comes from validation with baclofen used off-label in several categories of chronic cough and from GABAB expression in the neuronal pathway involved in cough. We believe that GABAB PAMs could be an innovative new treatment of chronic cough, offering improved efficacy, fewer non-responder patients, and lack of gustatory side effects in comparison to P2X3 inhibitors. We are currently progressing our proprietary compounds in disease-relevant models of chronic cough. Another indication we're highly interested in is pain. GABAB receptor activation has been well-validated by Baclofen, which has shown efficacy in patients with cancer pain and is used off-label in patients with bladder pain or trigeminal neuralgia. Current medication is largely based on opioids, gabapentin and pregabalin, NSAIDs for bladder pain, or carbamazepine and other anti-epileptic drugs for trigeminal neuralgia. These medications are suboptimal as they leave a significant proportion of patients without adequate or even any benefit and carry a risk of significant side effects. Here again, we strongly believe an approach using a GABAB positive allosteric modulator, which we expect to be highly efficacious without the side effects reported for current medications. Here also, we are working with multiple compounds progressing in late clinical candidate selection phase. We expect to move into IND-enabling studies in 2024 in parallel to delivering compounds for our partner, Indivior. We have made significant progress with our mGlu7 negative allosteric modulator program for stress-related disorders, including post-traumatic stress disorder, as we have now selected a clinical candidate drug to enter IND-enabling studies and have identified several differentiated backup compounds. We have established a wide intellectual property position, ensuring a strong protection for our program. PTSD is a psychiatric disorder affecting approximately 3.5% of the population and may occur in people who have experienced or witnessed traumatic or events such as a serious accident, natural disaster, or war. Current treatments rely mostly on behavioral therapy as most pharmacological treatments such as anxiolytics and antidepressants show insufficient benefit. The rationale for inhibiting mGlu7 receptors as an approach for treating stress-related disorders, including PTSD, is based on a wide body of preclinical evidence from the anxiolytic profile of mGlu7 knockout or knockdown animals to studies using mGlu7 negative allosteric modulators performed at Addex, but as well as in many other groups. We have completed a robust preclinical package with our lead drug candidate and are now moving into IND-enabling studies and expect to enter phase one studies in second half of 2024. Onto our mGlu2 negative allosteric modulator program for mild neurocognitive disorders or MNCD and depression. MNCD is a vague term expected to correspond with decline but not limited to cognitive impairment. Besides being potentially the early sign of Alzheimer's disease, MNCD is also often experienced by patients suffering from depression. Even patients that do respond to antidepressant treatment continue to suffer from MNCD, which significantly affects their quality of life. Developing mGlu2 negative allosteric modulators offers the exciting opportunity to treat cognitive impairment while also addressing symptoms of depression. Both procognitive and antidepressant effects have been demonstrated in relevant preclinical models with our mGlu2 negative allosteric modulator candidate compounds. We're completing lead optimization of our series and expect to begin clinical candidate selection phase with multiple compounds by end of this year, with the aim to start IND-enabling studies in 2024. Finally, a few words about our muscarinic M4 positive allosteric modulator programs for treatment of schizophrenia and other types of psychosis. Psychotic diseases increased with a steady lack of actual options for the last 50 years with limited efficacy and significant tolerability issues, often leading to treatment discontinuation and relapse. The big news in the field came from Karuna Therapeutics, who recently published the positive results of their third phase 3 registrational study of their KarXT compound in schizophrenia patients and who are on track to submit a New Drug Application to FDA by mid-2023. KarXT is a combination of xanomeline, a muscarinic M4 receptor agonist, and trospium, a peripherally restricted muscarinic antagonist. This combination allows to selectively activate muscarinic receptors in the brain while blocking the off-target effects xanomeline has because of its poor selectivity. This is a perfect validation of the M4 receptor target and upon our positive allosteric modulation approach that we are aiming at identifying highly selective and brain penetrant molecules. In summary, our drug discovery engine has achieved great progress with multiple drug candidates advancing towards IND-enabling studies. The renewed commitment of our partner, Indivior, the delivery of a candidate starting IND-enabling studies in the mGlu7 program, and the significant progress achieved in our other preclinical programs are further validation of the quality and productivity of our allosteric modulation platform. This concludes my prepared remarks, and I hand it back to Tim. Thanks, Robert. I'll now switch to an overview of the financials. Starting with the income statement. We recognized CHF 1.4 million of income in 2022, compared to CHF 3.2 million in 2021. The primary source of revenue is research funding from our collaboration with Indivior, which we expect to reduce in 2023 as drug candidates move to late-stage clinical candidate selection and our partner takes over more of the operational execution of the development. In terms of expenses, R&D expenses were CHF 14.7 million in 2022, compared to CHF 12.8 million in 2021. The increase of CHF 1.9 million is primarily due to the increased R&D outsourced activities linked to clinical candidates, so clinical activities that were ongoing in the first half, as well as, to a lesser extent, share-based compensation costs. Given that we have terminated clinical activities in 2022, we expect R&D expenditure to be significantly lower in 2023. GN expenses were CHF 7.3 million in 2022, compared to CHF 5.8 million in 2021. The increase of CHF 1.5 million is due to increased share-based compensation costs. Finance loss of CHF 0.3 million in 2022 relates primarily to exchange gains due to the strengthening of the US dollar over the period. Now to the balance sheet. Our assets are primarily held in cash, and we completed 2022 with CHF 7 million of cash held in Swiss francs and US dollars. Other current assets of CHF 0.9 million primarily relate to receivables from Indivior and R&D prepayments. Current liabilities of CHF 3.3 million as of December 31, 2022, decreased by CHF 0.9 million compared to the end of last year, 2021, primarily relate to R&D payables and accruals. Non-current liabilities of CHF 0.1 million as of December 31, 2022, decreased by CHF 1.4 million compared to December 31, 2021, primarily due to decreased retirement benefit obligations calculated under IAS 19. To the cash flow statement. We started the year with CHF 20.5 million, raised net proceeds of CHF 3.7 million in the offering executed in July of last year. Received CHF 1.1 million research funding from Indivior, consumed CHF 17.6 million in operations. We have a paper profit of CHF 200,000 in Forex when U.S. dollar cash balances are converted to Swiss francs at the end of the year reporting purposes. This results in CHF 7 million of cash at the end of the year. To summarize, the development of ADX71149 in epilepsy is ongoing, and we are looking forward to being able to sort of report very soon the recommendations from the independent interim review committee, which has been established by Janssen to review the data from part one. We continue to believe in the value of dipraglurant in PD-LID and are evaluating its future development in post-stroke recovery and pain. In parallel, we are pursuing collaborative arrangements to advance development and look forward to sharing more information on this subject in the future. Our preclinical programs continue to make solid progress towards delivering drug candidates for future clinical development in important therapeutic areas including stress-related disorders, chronic cough, cognition, and schizophrenia. As a reminder, our portfolio was discovered in-house from our pioneering allosteric modulator drug discovery platform. Consequently, we have a significant intellectual property for our programs. We have a track record of securing partnerships at the pre-clinical stage and supportive top-tier investors. We recognize the 2022 stock performance and current market capitalization is very disappointing. We are having multiple business discussions across our portfolio and strongly believe that if we are successfully in executing our near-term partnering strategy, our stock price should move to recognize the value of our portfolio. This concludes the presentation. We will now open the call for questions. Thank you. Dear participants, as a reminder, to ask a question, you need to press star one one on your telephone keypad and wait for your name to be announced. To withdraw your question, please press star one one again. To ask a question via the webcast, please access the Ask a Question tab. Please stand by, we will compile the Q&A roster. This will take a few moments. We'll go and take our first question. The question comes from the line of Raghuram Selvaraju from H.C. Wainwright & Co. Please ask your question. Thanks very much for taking my questions. Can you hear me? Yes, we can. Firstly, I was wondering if you could frame for us what Janssen might consider an unexpectedly positive outcome from the epilepsy proof of concept study? In what context they might frame it as such, you know, for example, from a competitive perspective, from the standpoint of being able to combine the molecule with other existing anti-epileptic drugs and so forth? Okay. Where do I start? You know, I think we have to remember that when Janssen started this study, they were going to recruit 60 patients, 2- 1 randomized. That was going to be one cohort. They then modified slightly once it started, now they have publicly announced on clinicaltrials.gov that they are going to have up to 3 cohorts. Now because of this, they're not stopping recruitment, therefore that's why they've established this independent interim review committee to look at the data that expectations because it's part one. Remember that as Robert mentioned earlier in the presentation, the endpoint is at the end of part one is how many patients got to the baseline seizure count and how many didn't, and then how that is split between active and placebo. What we know from Janssen is that they're going to report to us a go, no-go decision. We are not going to, and I don't think Janssen are going to get much granularity from the independent interim review committee, as they really don't want to unblind the study as they move other cohorts. Does that answer your question? Sorry, can you hear me? Yes. No, that's very helpful. I think, you know, what we wanted to get a better sense of was, you know, if there's likely to be a sort of upside surprise, as it were, from this clinical study result. You know, let's assume that the baseline is for a positive outcome, what would constitute a positive upside surprise? I think what you've done is frame it quite nicely, so we appreciate that. The second question is in relation to the M4 allosteric modulator in the context of the xanomeline plus trospium data so far. I was hoping that you could clarify a little bit, first of all, how you expect the allosteric modulation approach on the M4 target to potentially present advantages versus xanomeline plus trospium. Because obviously xanomeline as a single agent was not successful. That was the reason why they came up with this combination approach. Secondly, whether you think the xanomeline plus Trospium clinical development programs represent an appropriate template for the future development of your lead candidate, or if your lead candidate is going to follow a somewhat different path, and if so, why? Thank you. Yeah. Yeah. Maybe, Robert, you'd like. Yeah. I'll answer the first question for sure. Yeah, I mean, it's a very good question. I mean, the main, I would say, and first difference between Karuna's approach with xanomeline is that this is a, I would say non-selective. It's an M1, M4 agonist. Its mechanism of action is activating the M4 receptor. Coming with a positive allosteric modulator, we know that we have all sorts of benefits compared to agonists where we are, you know, helping the activation of the receptor, making the receptor more sensitive to its natural ligand acetylcholine, and therefore also respecting the natural rhythm of receptor activation. The, you know, the other difference, with xanomeline of our approach is that we have highly [inaudible] selective that we have, you know, where we demonstrate a high brain penetration. That's, I think in a nutshell, you know, what is differentiating. Going forward, you know, if you, again, comparing an agonist approach versus a positive allosteric modulator approach, with an agonist, as long as the agonist is on board, we will be activating the receptor. We know that this is a receptor that gets desensitized and gets internalized. So with a positive allosteric regulator. This can lead to tolerance. With a positive allosteric modulator, we have demonstrated that, not yet for the, for the M4, but for some of the other positive allosteric modulator programs that we've worked on, that this is not happening. We don't, basically, we, you know, we don't see tolerance appearing when we are chronically testing the compound. Yeah. Regarding the clinical side of things, I think we'll be looking much more closely at Cerevel, because, I mean, they are developing a positive allosteric modulator on the M4 PAM. We'll be watching very carefully what they're gonna be doing in the clinic. Just as a follow on to that, I thought I would ask a somewhat provocative question. It's well documented that PureTech Health, which was one of the original inceptors of the company developing xanomeline plus trospium, has done very well with that investment. My understanding is there is a historical link between PureTech Health and Addex. I was wondering if you could perhaps comment on the degree to which PureTech Health is aware of your activities on the M4 allosteric modulation side, and what their thoughts are as to what has already been demonstrated from a clinical success perspective vis-a-vis xanomeline and trospium. I mean, all I can say is we're having multiple discussions with multiple parties across our portfolio. That includes the M4 PAM. I mean, as you can imagine, you know, as you know, the Karuna data has certainly lit up the field. There's a lot of excitement. There's been a number of deals already done on other M4 PAM programs. I mean, there was Neurocrine acquisition of the Heptares Sosei program. The Vanderbilt program went to Neumora. There are plenty of other CNS-focused pharma that are, you know, watching this space and discussing with us. Thank you. That's all I can say. Thank you. Now we're going to take our next question. Please stand by. The next question comes from the line of [Peter Elliker] from A Consult. Your line is open. Please ask your question. Thank you. I have very simple question. I noticed in the annual report that the compensation for the board has almost tripled from 21 to 22, and for the executive, it has almost doubled in the same time. Can you explain why? This is all linked to some reorganization of the share-based compensation program, so it's all non-cash compensation, and it's driven by the IFRS 2 calculations that are linked to the reorganization of the equity incentive plan. Okay. Thank you. Thank you. Now we're going to take our next question. Just give us a moment. The next question comes from the line of Edouard Riva from ZKB. Your line is open. Please ask your question. Hello. Thank you very much for taking my questions. I would have two of them. The first one being, as I've seen in the slide that you expect 2 IND-enabling studies for the GABAB, the one that Indivior is gonna develop and the one you are gonna develop in 2024. I was wondering why wouldn't this happen earlier? What are the steps that lead to the start of the IND-enabling studies? This program has been extremely successful. It's generated a lot of molecules with different profiles. You may be aware that Astellas has a GABA-B positive allosteric modulator, which is in phase two clinical development for alcohol use disorder. This is the indication of primary interest to Indivior are profiling many, several compounds in parallel and in multiple preclinical models and doing a very thorough job. In fact, a much more thorough job than we expected. If we look back historically over the guidance, we are certainly delayed, and this is for good reason. They are doing a very thorough job to select compound. Now, the way the selection of compounds works is that Indivior needs to select a compound first before Addex is able to select. Now, until Indivior selects, Addex is not able to select. What we are doing is we are now profiling, I would say, at risk, a number of compounds, in some of the indications that we're interested in. You know, we mentioned Charcot-Marie-Tooth, which we have profiled, you know, in the past, but we are now looking very closely at chronic cough, and certain types of pain as well. Again, these are areas where we are getting some significant interest from potential business partners. Because this is carved out of the collaboration with Indivior, once we've selected compounds, we will actually be free to license them to partners should we get interest or d evelop them ourselves. Understand. Thank you very much. My second question would be, regarding ADX71149. Are you already recruiting for the second part of the study, or are you waiting for the independent review committee? Well, as I said, this is an open recruitment, and as they say in clinicaltrials.gov, you know, they're gonna do up to three cohorts. We are able to say that cohort one has completed, and therefore you can assume that, you know, patients that are being randomized are now being randomized into a second cohort. Those three cohort are only for part the second part, not for the first part. Well, the study has a part one and a part two. Cohort one was completed with 60 patients with a 2 to 1 randomization. Those 60 patients have completed part one. Those that didn't hit their baseline seizure count in part one, have now rolled over into part two. The patients who did hit their baseline seizure count have been offered the open label extension study. Okay. I think it answers my question. Thank you very much. Thank you. Thank you. Dear speakers, please be advised at this moment we do not have any more audio questions. We will hand over to the written questions. Now we have the first question from Jelle Broekhuis. Can you tell us how many patients from each group advanced from phase I to phase II in the seizure study? When you say phase I to phase II, you're talking about part one to part two, I assume. The answer is we don't have any information on that. Thank you. Second question. We have also another question from Jelle Broekhuis. Can you state with confidence that J&J will communicate the data with you and then us from the seizure study? Yes, with confidence we will get the data, and we will be able to communicate it. I have no information on timing, though. I can't give you any guidance on when that will be. Thank you. We have another question from Jelle Broekhuis. Please give us a time estimate of the communication of the conclusions of the interim review board of the seizure study. Yeah. The guidance on any recommendation of the independent review committee is early in Q2 of this year. Thank you. Now we have another question from Patrick Macheret. Which part, if any at all, of the EUR 109 million milestone payment from Janssen is coupled to that ADX71149 epilepsy phase II study part one related to go, no-go decision? We're not authorized to disclose any granularity around the EUR 109 million milestone. I'm afraid we're not authorized to disclose the answer to the question. Thank you, dear speakers. Dear participants, as a reminder, if you wish to ask a question over the phone, please press star one one on your telephone keypad. Alternatively, you can submit questions via the webcast. Dear speakers, there are no further questions at this time, and I would like now to hand the conference over to the management team for any closing remarks. Well, thank you very much for attending the conference call, and we look forward to speaking to you on the next call. I wish you all a nice day. That does conclude our conference for today. Thank Thank you for participating. You may now all disconnect. Have a nice day.