Good day, thank you for standing by. Welcome to the Addex Therapeutics first quarter 2026 financial results and corporate update conference call and webcast. 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 hear an automatic message advising your hand is raised. To withdraw your question, please press star one and one again. If you wish to ask a question via the webcast, please use the Q&A box available on the webcast link at any time during the live event. 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, CEO. Please go ahead. Hello, everyone. I would like to thank you all for attending our Q1 2026 financial results conference call. I am here with Mikhail Kalinichev, our Head of Translational Science, who will provide an update on our R&D program. 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 activities and achievements before reviewing our pipeline. I will hand over to Misha, who will review in more detail our mGluR5 Negative Allosteric Modulator program for brain injury recovery and the GABAB positive modulator program for cough. I will review our 2026 Q1 financial results. Following that, we will open the call for Q&A. Starting with the highlights, Q1 has seen several important achievements across our pipeline. We've made excellent progress in our GABAB positive modulator cough program as we continue to complete preclinical characterization of our selected compounds. We recently announced robust antitussive activity in a non-human primate cough model, as well as solid antitussive activity in an idiopathic pulmonary fibrosis model in guinea pigs. These data further demonstrate the potential of our selected compound in this important unmet medical need. In parallel to completing the preclinical profiling, we are working to secure funding to advance the program into the IND-enabling studies. Mikhail will be sharing some of the data with you later in our presentation. We've repositioned dipraglurant our mGluR5 Negative Allosteric Modulator for brain injury recovery, and have made good progress in preparing the program for clinical studies in post-stroke recovery patients. In 2025, we entered into an option agreement giving us access to an exclusive license to intellectual property covering the use of mGluR5 in brain injury recovery, including stroke and TBI. Included in the agreement is a research collaboration under which we are working with Sinntaxis and Lund University in Sweden to complete preclinical profiling of Dipraglurant and prepare for clinical studies. Again, Misha will talk more about this exciting program later in the presentation. As a reminder, we spun out our portfolio of preclinical neuropsychiatric assets in 2024 to create Neurosterix and raised CHF 65 million from a syndicate of investors led by Perceptive Advisors. We retained a 20% equity interest in Neurosterix, the value of which is unfortunately not being properly reflected in our current share price. Neurosterix has made excellent progress in advancing its pipeline, including its M4 PAM and mGluR7 NAM programs. The lead drug candidate in the M4 PAM program, NTX-253, is in phase I, and we expect data in Q3 this year. On the financial side, we completed the quarter with CHF 0.9 million of cash and have successfully raised CHF 0.3 million in Q2. Given that our cash burn is extremely low following the Neurosterix spin-out, this provides us with cash runway through into Q4 of 2026 on a going concern basis. Now for a quick review of our pipeline. As mentioned, we continue to believe in dipraglurant, we are executing our plans to reposition the development for brain injury recovery. As a reminder, we have regained the rights to ADX71149 from our partner J&J with a high-value dataset and significant GMP materials. We're currently evaluating a number of therapeutic indications for future development, in parallel, we are discussing with potential partners for the asset. For our GABAB PAM collaboration with Indivior has selected a compound for development in substance use disorders and has successfully completed IND-enabling studies. As a reminder, under the terms of the agreement, Addex is eligible for payment of up to CHF 330 million on successful achievement of pre-specified regulatory, clinical, commercial milestones, as well as tiered royalties on the level of net sales from high single digit up to low double digits. As mentioned earlier, we are advancing an independent GABAB program for cough and expect to start IND-enabling studies this year subject to securing financing. Presented on this slide is the portfolio of our spin-out company, Neurosterix. We are expecting phase I data from NTX-253 program in Q3. Backup M4 PAM compound, NTX-529, has been selected for IND-enabling studies, which should start shortly. The mGlu7 NAM program has selected NTX-819, a highly selective first-in-class compound, which has demonstrated robust preclinical anxiolytic and antidepressant-like activity, which supports its development as a potential next-generation therapy. We expect NTX-819 to complete IND-enabling studies in the coming months. Now, I will hand over to Misha, who will give you some more details about our exciting portfolio. Thanks, Tim. Hello, everyone. I will start by speaking about dipraglurant and our plans for development in brain injury recovery. Dipraglurant is an orally available, highly selective mGlu5 Negative Allosteric Modulator, which we believe could improve the outcome of rehabilitation for patients suffering from traumatic brain injury or stroke. The mechanism of action of dipraglurant targets neuroplasticity early in rehabilitation to promote rebuilding of neuronal connections and sensorimotor recovery. The unmet medical need and commercial opportunity in post-stroke and TBI recovery is undisputed. Stroke is among the leading causes of chronic, often lifelong disability, as it leads to motor, sensory, cognitive impairment, and multiple comorbidities. There are over 100 million stroke survivors worldwide, the number is growing at the annual rate of 12 million. A variety of rehabilitation therapies are used with post-stroke patients, but the recovery is slow and often inadequate. There is an urgent need for pharmacological agents that can facilitate the recovery stimulated by rehabilitation therapies. To why mGlu5 NAM is such a great target for this indication. mGlu5 receptor is a suitable target to address post-stroke recovery, as it is densely expressed in the brain, involved in neuroplasticity, and modulates excitatory-inhibitory equilibrium. In fact, activation of mGlu5 has been observed in a large range of neurological disorders, including stroke, where it plays a role in so-called maladaptive rewiring of the brain following stroke. Inhibition of mGlu5, on the other hand, can facilitate adaptive rewiring of the brain, promoting neuroplasticity and creation of new functional pathways, moving the neural network towards a pre-lesion state. To the data. I would like to refer you to the left-hand figure, which shows exciting new evidence recently published in the journal Brain. These data show the Negative Allosteric Modulator of mGlu5, MTEP, administered daily in red following stroke, results in a sustained and growing improvement in sensorimotor function in comparison to vehicle treatment. In the right-hand figure, we can see a similar improvement in sensorimotor function that was observed in animals treated with our mGlu5 NAM dipraglurant. We are currently working with our collaboration partner, Sinntaxis, to complete the preclinical profiling of dipraglurant in this animal model. In addition to the compelling in vivo data, MRI imaging of the resting state functional connectivity in post-stroke products show that daily administration of MTEP also stimulates intra and inter-hemispheric connectivity in the brain disrupted by stroke. It is important to note that improvement in brain connectivity after stroke is known to correlate with functional recovery and is observed across species. Dipraglurant is ideally suited to be used in conjunction with rehabilitation therapies in post-stroke patients, as it has a fast onset of action and short half-life. It has shown good tolerability in healthy subjects and in Parkinsonian patients, showing only mild to moderate CNS-related adverse effects. We have a drug product ready and a strong patent position, and believe dipraglurant can become a first-in-class drug to facilitate post-stroke recovery. We can also speculate that Dipraglurant-mediated adaptive rewiring and facilitation of recovery following brain damage would also be seen in traumatic brain injury patients. The next step in clinical development is to perform an imaging study in stroke patients to show the intra and inter-hemispheric connectivity in the brain disrupted by stroke. I would like to update you on our GABAB positive allosteric modulator cough program. As a part of our agreement with Indivior, Addex has exercised its right to select a compound to advance its own independent GABAB PAM program for the treatment of chronic cough. I will now present this exciting opportunity. There is a strong rationale for developing GABAB PAMs for chronic cough. Chronic cough is a persistent cough that lasts more than eight weeks and can be caused by a variety of factors, including respiratory infections, asthma, allergies, and acid reflux, but also possibly by a cough hypersensitivity syndrome. There is a large unmet medical need in novel antitussive drugs as current standards of care are ineffective in 30% of patients, or only moderately effective in up to 60% of patients. In addition, the current treatments carry risks of serious side effects. Support for using GABAB PAMs in treatment of chronic cough comes from the clinical evidence that baclofen, a GABAB agonist, is used off-label in cough patients and from the anatomical evidence that GABAB receptors are strongly expressed in airways and in the neuronal pathway regulating cough. We believe that GABAB PAMs could offer superior efficacy in cough patients. The pre-IND activities, including in vivo proof of concept, non-GLP tox, and CMC, have been completed, and our clinical candidate has shown favorable efficacy, tolerability, and developability profiles. Our clinical candidate has demonstrated a consistent minimum effective dose on one mg per kg and ED50 of six mg per kg in cough frequency in a guinea pig model of cough. No signs of tolerance were seen after subchronic dosing, and more than 60-fold safety margin was demonstrated based on respiratory depression as sedation biomarker. Recently, we confirmed the antitussive efficacy in the non-human primates and now currently evaluating the compound in rabbits. IND-enabling studies are planned and ready to start, subject to securing financing. To the data. In the model of citric acid-induced cough in guinea pigs, acutely administered compound A delivered a robust antitussive efficacy, reducing the cough number dose dependently and achieving 70% reductions at the maximum dosage. The antitussive profile of compound A was similar to that of nalbuphine, or vestipitant, baclofen, and codeine. To cough latency. Compound A increased the latency to first cough dose dependently, thus delaying the onset of cough. The antitussive profile of compound A in delaying cough onset was similar or better than that of reference drugs. As a reminder, our objective in the program is to design a GABAB PAM with the efficacy of reference compounds, but without the CNS side effects such as sedation. In the same experiment where the compound A showed efficacy, we monitored respiratory rate, a biomarker of sedation. As you can see from the slide, compound A was well-tolerated, as there were no marked changes in respiratory rate at up to 60 mg per kg. In contrast, nalbuphine or vestipitant, baclofen, and codeine resulted in robust reductions of respiratory rate at doses required to achieve maximal efficacy, indicative of sedative-like effects. When we evaluated the antitussive efficacy across compounds at the respective highest doses free from respiratory effects, compound A was shown to be superior to nalbuphine or vestipitant, baclofen, and codeine in both cough number and cough latency measures. In the model of ATP-potentiated citric acid cough in guinea pigs in a head-to-head comparison experiment, acutely administered compound A and the P2X3 inhibitor had similar efficacy and tolerability profiles. As a reminder, P2X3 inhibitors' antitussive activity is peripherally mediated, which explains their lack of sedative effects, but also the reason for more than 30% of cough patients who do not respond to treatment. In the citric acid-induced cough model, subchronic administration of compound A for seven days showed no signs of tolerance, neither in cough frequency nor in latency to first cough. Also, there were no changes in the respiratory rate, body temperature, and growth hormone release in animals treated subchronically with compound A. Compound A was also assessed in the IPF-related exacerbated chronic cough model in guinea pigs. Here is the study design. On day zero, animals received a single oropharyngeal administration of bleomycin or were left intact. Bleomycin-exposed animals were then treated with compound A or vehicle orally once daily for 28 days. Intact animals received vehicle. On day seven, 14, 21, and 28, animals were exposed to low concentrations of citric acid to stimulate cough. On day 28, at the end of the experiment, lung tissue was collected for histopathological analysis. The total number of coughs was significantly higher in bleomycin-exposed vehicle-treated animals than in healthy controls. This difference between the groups grew progressively larger over time, indicative of exacerbated cough in IPF-like condition. Chronic treatment with compound A resulted in robust and enduring reductions in the number of coughs with 40%-60% reduction magnitude. The latency to first cough showed significant reductions in bleomycin-exposed vehicle-treated animals versus intact control starting day 14. Chronic treatment with compound A reversed the effects of bleomycin throughout the testing period, returning the latencies to the levels of intact control animals. A histological analysis of the lung tissue collected on day 28 revealed that chronic administration of compound A was associated with markedly lower Ashcroft scores and lower percentage of affected lung in comparison to bleomycin-exposed vehicle-treated animals. This suggests that compound A administered over 28 days reduced lung fibrosis. To the non-human primate cough data. Similar to what we saw in guinea pigs, in the model of citric acid-induced cough in non-human primates, compound A demonstrated a more than 60% reductions in number of coughs at 2 mg per kg. In summary, we have selected a clinical candidate for chronic cough with a robust, reproducible antitussive efficacy at 1 mg per kg and good PK/PD. The compound showed a favorable developability profile in non-GLP tox studies performed in rats, dogs, and non-human primates. The compound has the potential to have the best in disease efficacy and tolerability profile, and broad application in chronic cough patients. Subject to raising financing, we are ready to start the IND-enabling studies. This concludes our prepared remarks on the progress of our R&D programs. I hand it back to Tim. Thanks, Misha. For a view of our Q1 2026 financials. With the income statement. The operating loss amounts to CHF 0.5 million in Q1 2026, compared to CHF 0.6 million in Q1 2025. The decrease of CHF 0.1 million between both periods is primarily due to reduced outsourced R&D. As a reminder, on April 2nd, 2024, we received an equity interest of 20% in Neurosterix as part of our Neurosterix spin-out transaction. Under IFRS, we are required to account for the investment using the equity method of accounting and recognize our share of their results in our income statement. For the three-month period ended 31st of March 2026, our share of the net loss of Neurosterix amounted to CHF 1.3 million, compared to CHF 0.8 million for the three-month period ended March 31, 2025. This increase is primarily driven by the move of NTX-253 into clinical development by Neurosterix. The net loss amounted to CHF 1.7 million during the first quarter, compared to CHF 1.5 million during the same period ended March 31, 2025. It was strongly driven by the increase in our share of the Neurosterix net loss, compensated by a reduction in our own internal net loss, which reduced by 23%. To the balance sheet. We completed Q1 with CHF 0.9 million of cash held in Swiss francs, and to a lesser extent, US dollars, compared to the CHF 1.6 million held at the end of 2025. The decrease of CHF 0.8 million is primarily due to our operating loss of CHF 0.5 million and an increased net working capital of CHF 0.3 million, driven by one-off annual payments made at the beginning of the year, such as retirement benefit contributions and insurance premiums. Our current assets amounted to CHF 25,000, primarily related to increased prepaid retirement benefits. Our non-current assets of CHF 3.5 million at the end of March primarily relate to our investment in Neurosterix accounted for using the equity method, and to a lesser extent, our investment in Stalicla. Current liabilities remained steady at CHF 1.2 million at the end of March compared to December, and primarily relate to accruals and payables from outsourced R&D and professional service activities. Non-current liabilities primarily relate to the retirement benefit obligations calculated in accordance with IAS 19 and amounted to CHF 0.3 million at the end of Q1 compared to CHF 0.4 million at the end of December. To the cash flow statement. We started the quarter with CHF 1.6 million. We used CHF 766,000 for operations, primarily R&D engine activities. We received CHF 65,000 from the sale of treasury shares and completed the year with CHF 935,000 Sorry, completed the quarter with CHF 935,000. As mentioned in the highlights, we have been active with our ATM facilities, both on the Nasdaq and the SIX exchange, and have raised small amounts of capital in Q2 to strengthen the balance sheet while we wait for good news from our spin-out company, Neurosterix. To summarize, we have made excellent progress in advancing our GABAB PAM program for cough and our dipraglurant post-stroke recovery program. Our spin-out company, Neurosterix, continues to advance its portfolio with their M4 PAM program on track to complete Phase I Q3. We are very pleased by the progress Delixia is making in advancing on its business strategy and pipeline. We are looking forward to completing our evaluation of potential indications for our mGlu2 PAM program and securing the financial resources to advance our portfolio into clinical studies. This concludes the presentation. We will now open the call for questions. Thank you so much. Dear participants, as a reminder, if you wish to ask a question, please press star one one on your telephone keypad and wait for your name to be announced. To withdraw your question, please press star one and one again. Alternatively, you can submit your questions via the webcast. Please stand by while we compile the Q&A roster. This will take a few moments. Once again, if you would like to ask a question, please press star one one. Now we are going to take our first question. It comes line of Raghuram Selvaraju from H.C. Wainwright & Co. Your line is open. Please ask the question. Thanks so much for taking our questions. We have four of them. Two of these relate to the chronic cough program. Firstly, I was wondering if you could provide us with some assessment of the relative positioning of your lead candidate, the GABAB PAM, against nalbuphine extended release. Also, I was wondering if you are thinking about potential dosing formulations that may reduce dosing frequency and therefore improve patient convenience as you look towards advancing this into the clinic. The second question on that front is related specifically to the guinea pig model. I was just wondering how you typically measure the cough intensity in that context and to what extent you rely on those measurements relative to the assessment of the lung tissue. Thank you. Yes, happy to answer the question. Let me start with the first, which is comparison of nalbuphine with our candidate compound A. As you saw on the slide that I shared, the overall profile is very similar. Compound A appears to be more potent. We see a minimal effective dose at 1, whereas with nalbuphine, one needs to administer 3 in exactly the same model in guinea pigs, where cough is stimulated by citric acid inhalation. In terms of maximal efficacy, both deliver approximately 70% reduction. The difference comes from the tolerability aspect of nalbuphine versus GABAB PAM. Here, at the top dose, 30 mg per kg, we see significant reductions in the respiratory rate, and it nicely aligns with what we know on the tolerability profile of nalbuphine in clinical trials, where it showed CNS-related side effects, even at the dose which was lower, corresponding dose to the one we tested in animals. Even at the efficacious dose, which roughly aligns to 3-5 mg per kg in a guinea pig, if we use 75 kg calculation for a human body weight. So based on that, we expect similar efficacy to nalbuphine, but markedly wider therapeutic margin. Regarding your second question on the formulation, our current formulation is expected to deliver once daily compound. So there will be no need for extended release unless we will aim for something that is once weekly or once monthly. Once daily formulation is believed to be achieved with the current simple formulation that we have. That contrasts with nalbuphine very well, as with nalbuphine, even extended release formulation requires twice-daily administration. That shows another advantage of GABAB PAM clinical candidate over nalbuphine. With the guinea pig model- Right. Yes. There was also a question on intensity. We use plethysmography chambers that deliver cough frequency and cough latency. There is no way of measuring cough intensity with that setup. The cough intensity is even challenging to measure in human patients. There are some technical advances that may deliver intensity measures, but it's still in development. With respect to the Neurosterix equity holding, I was just wondering, maybe Tim, you can comment on this, what strategically your outlook is for long-term management of this equity position. If you have any thoughts around how Addex might ultimately assess the disposition of this or potential monetization of it. How you're thinking about this specifically in the context of the possible future public listing of Neurosterix. I was also wondering if from a scientific perspective, you could comment on the complex interplay between muscarinic receptor signaling pathways. In particular, if you could talk a little bit about, this doesn't necessarily have to be solely in the context of what Neurosterix is doing, although I presume that is probably the most relevant aspect. If you could talk specifically about M1, M4 receptor modulation relative to M4 and M7 receptor modulation, and how these aspects might potentially have differing therapeutic applicabilities within the context of schizophrenia versus depression. Thank you. Okay. Let me take the first one about the equity holding. Thank you very much for the questions. Let's just rewind. Look, we founded Neurosterix really as a financing vehicle for some of our preclinical programs. If you remember back and you dig into the press releases back in 2024, Neurosterix raised CHF 65 million. Addex received a 20% equity holding. If you run the numbers, the 20% equity interest that Addex received was valued based on the post-money valuation of Neurosterix at about CHF 20 million. Clearly with a market cap of CHF 8 million today, there seems to be a little bit of a disconnect. What we know about Neurosterix is that Neurosterix has advanced in the last two years an M4 PAM from clinical candidate selection substantially through phase I, and we're expecting phase I to complete very soon, with data coming out in Q3. It's also identified a backup compound in the M4 PAM program called NTX-529, which is ready to go into IND-enabling studies. It's advanced the mGluR7, which is a first-in-class compound with a battery of preclinical data showing its potential in neuropsychiatry, in particular the anxiolytic effects and antidepressant effects. We believe that our equity holding is not being correctly reflected. The question is, really do we try and monetize it today? We have had some inbound interest. One strategy could be to monetize the Neurosterix interest and sell it, and to then use the proceeds to invest in our cough program. Alternatively, Neurosterix at some point will be executing a Series B whether that's in the private arena or whether it's part of a public offering. I'm not in a position on this call, in the context of Addex, to comment on that. However, we are evaluating all opportunities regarding building value for our shareholders and with that equity position. What I would like to do is hand over to Misha, who will talk at length because he is very knowledgeable about the muscarinic space. Thank you, Tim. We believe that the contribution of M1 into the antipsychotic efficacy of Cobenfy, which is a co-administration of xanomeline and trospium, is speculative. Still this is being discussed, but there is no robust data that support that M1 component is necessary or is contributing significantly into its efficacy, either in cognition or in psychosis reduction. As you know, there were multiple companies that were developing muscarinic M1 selective compounds for cognitive improvement, and all those clinical trials show a lack of activity. Some also showed a range of muscarinic cholinergic side effects, which also brought additional aspects to consider. If we look at animal studies that evaluated antipsychotic-like profile of xanomeline in rodents, it was very clear that the main bulk of activity, if not exclusively in an amphetamine-induced hyperactivity model, is driven by muscarinic M4 receptor with virtually no contribution from M1. Of course, we have positive phase I-B clinical trial with emraclidine. Putting all together, we believe that having a selective M4 positive modulator will be able to deliver clinical efficacy which we see with xanomeline. That was the main question. You mentioned receptor seven, I believe you had in mind mGluR7. Am I correct? Yes, mGluR7. The interplay between that and M1 and M4 systems. Yes. There is no direct evidence of interaction between muscarinic M4 and mGluR7. There is some evidence of an interaction between mGluR7 and mGluR8. They may create heterodimers, and their co-administration can have an impact on the outcome. I'm not aware of any functional interaction between these two receptors. Thank you. Thank you so much. Dear participants, as a reminder, if you wish to ask a question, please press star one on your telephone keypad and wait for a name to be announced. Alternatively, you can submit your questions via the webcast. Dear speakers, we'll just give a moment to our participants to enter the queue. Dear speakers, there are no further questions for today. Thank you, ladies and gentlemen. This brings the main part of our conference to a close, and I would like to hand back to Tim Dyer for closing remarks. Thank you. Thank you everyone for attending this call. We look forward to speaking to you again soon, and we wish you a very nice end of your day, end of your week. Thank you. Goodbye. This concludes this conference call. Thank you for participating. You may now all disconnect. Have a nice day.