Good day, and thank you for standing by. Welcome to the Addex Therapeutics full year 2025 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 then 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 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. Please go ahead. Thank you. Hello, everyone. I would like to thank you all for attending our 2025 full year financial results conference call. I'm here with Mikhail Kalinichev, our Head of Translational Science, who will provide an update on our R&D programs. 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 then hand over to Misha, who will review in more detail our mGlu5 negative allosteric modulator program for brain injury recovery and the GABAB positive allosteric modulator preclinical program for cough. I will then review our 2025 full year financial results. Following that, we will open the call for Q&A. 2025 has seen several important achievements across our pipeline. We made excellent progress in our GABAB PAM chronic cough program as we continue to complete preclinical characterization of our selected compound. We recently announced robust antitussive activity in a non-human primate chronic cough model, as well as solid antitussive activity in an IPF 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. Misha will be sharing some of the data with you later in our presentation. We've also repositioned dipraglurant, our mGlu5 NAM, 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 mGlu5 inhibitors in the brain injury recovery, including stroke and traumatic brain injury. Included in the agreement is a research collaboration under which we are working with Sinntaxis and Lund University to complete preclinical profiling of dipraglurant and are preparing for clinical studies. Misha will also talk more about this program later in the presentation. Following the decision by our partner J&J to terminate development of ADX71149, we have regained the rights to this phase II asset with a high-value data set and significant materials. We are currently evaluating a number of therapeutic indications for future development, and in parallel, we are discussing with potential partners for the asset. Our partner Indivior has selected a compound for development in substance use disorders and has completed IND-enabling studies. As a reminder, under the terms of the agreement, Addex is eligible for payment of up to $330 million on successful achievement of pre-specified regulatory, clinical, and commercial milestones, as well as tiered royalties on the level of net sales from high single digits up to low double digits. In June of 2025, we invested in Stalicla, a private clinical-stage neurodevelopmental disorder-focused company. Stalicla has developed a proprietary precision medicine patient stratification technology platform, which allows the company to select patients based on their biological dysregulation rather than behavioral phenotype. Proof of concept of the platform has been demonstrated by applying the technologies to identify and develop drugs in subpopulations of patients suffering from autism spectrum disorder. Stalicla has made excellent progress in advancing its patient stratification study in autism and preparing its lead asset for a phase III study in cocaine use disorders. We completed the year with CHF 1.6 million cash, which provides us with cash runway through mid-2026. I'd like to highlight that the cash burn has been significantly reduced following the Neurosterix spin-out transaction. However, current cash does not fund the progression of our unpartnered programs into the clinic. Now for a quick review of our pipeline. We continue to believe in dipraglurant and are executing our plans to reposition the development for brain injury recovery and, in particular, post-stroke recovery. As mentioned, our partner Indivior has selected a GABAB PAM drug candidate for development in substance use disorders and completed IND-enabling studies. We are advancing an independent GABAB PAM program for chronic cough and expect to start IND-enabling studies this year, subject to securing financial backing for the program. As a reminder, we spun out our portfolio of neuropsychiatric assets in 2024 to create Neurosterix and raised $65 million from a syndicate of investors led by Perceptive Advisors. We retained a 20% equity interest in Neurosterix. Neurosterix has made excellent progress in advancing its pipeline in 2025, including starting phase I studies with NTX-253, its M4 positive allosteric modulator program, and we are expecting phase I to be completed this quarter. Now, I will hand over to Mikhail Kalinichev, 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 re-building of neuronal connections and sensorimotor recovery. There is a large unmet medical need in post-stroke recovery and rehabilitation. Stroke is among 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, and the number is growing at the annual rate of 12 million. A variety of rehabilitation therapies are used with post-stroke patients, the recovery is slow and often inadequate. There is an urgent need for pharmacological agents that can facilitate the recovery stimulated by rehabilitation therapies. 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 range of neurological disorders, including stroke, where it plays a role of 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 creating of new functional pathways, moving the neural network towards a pre-lesion state. Exciting new evidence recently published in the journal Brain suggests that the negative allosteric modulator of mGlu5, MTEP, administered daily in rats following stroke, results in a sustained and growing improvement in sensorimotor function in comparison to vehicle treatment. Similar improvement in sensorimotor function was observed in animals treated with our mGlu5 NAM, dipraglurant. MRI imaging of the resting state functional connectivity in post-stroke rodents shows 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 tandem 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 facilitational recovery following brain damage would also be seen in traumatic brain injury patients. As part of our agreement with Indivior, Addex has exercised its rights 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 for 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 of 1 mg/kg and ED50 of 6 mg/kg in cough frequency in guinea pigs. No signs of tolerance were seen after subchronic dosing, and more than 60-fold safety margin was demonstrated based on respiratory depression and sedation biomarker. Recently, we also confirmed the antitussive efficacy of compound 1A in the non-human primates. The IND-enabling studies are planned and ready to start subject to receiving funding. 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 maximal doses. The antitussive profile of compound A was similar to that of nalbuphine, aprepitant, baclofen, and codeine. 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. In the same experiment, compound A appeared well-tolerated as there were no marked changes in respiratory rate at up to 60 mg/kg. In contrast, nalbuphine, aprepitant, baclofen, and codeine resulted in robust reductions in respiratory rate at their highest doses, indicative of sedative-like effects. When evaluation of the antitussive efficacy across compounds was done at the respective highest doses, free from respiratory effects, compound A was shown to be superior to nalbuphine, aprepitant, 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 1 head-to-head comparison experiment, acutely administered compound A and a P2X3 inhibitor had similar efficacy and tolerability profiles. 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. There were no changes in the respiratory rate, body temperature, and growth hormone release in animals treated subchronically with compound A. In the model of IPF-related exacerbated chronic cough in guinea pigs, on days 0, animals received a single oropharyngeal administration of bleomycin or were left intact. Bleomycin-exposed animals were then treated with compound A, 10 mgs per kg, or vehicle orally once daily for 28 days. Intact animals received only vehicle. On days, seven,14, 21, and 28, animals were exposed to low concentration of citric acid to stimulate cough. On day 28, at the end of the experiment, the 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. The 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% to 60% efficacy. The latency to first cough showed significant reductions in bleomycin-exposed vehicle-treated animals versus intact controls 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 histopathological 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% of affected lung in comparison to bleomycin-exposed vehicle-treated animals. In the model of citric acid-induced cough in non-human primates, compound A had no effect on the number of coughs at 0.6 and one, while producing significant and more than 60% reductions at 2 mg per kg. In summary, we have selected a clinical candidate for chronic cough with a robust, reproducible antitussive efficacy of 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 a potential to have the best in disease efficacy and tolerability profile and broad application in cough patients. The compound showed a favorable developability profile in non-GLP tox studies performed in rats, dogs, and non-human primates. 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. Recognized CHF 0.2 million of income in 2025 compared to CHF 0.4 million in 2024. The decrease is primarily due to the completion of the funded research phase of our collaboration with Indivior in June of 2024. This has been partially offset by the fair value of the services received from Neurosterix Group at zero cost. R&D expenses of CHF 0.7 million, primarily related to our GABAB PAM program, decreased by CHF 0.2 million in 2025 compared to 2024, mainly due to the completion of the research phase of our collaboration with Indivior. G&A expenses remained stable at CHF 2.3 million in 2024 and 2025 and primarily relate to professional service fees linked to corporate development activities. As a reminder, on April 2, 2024, we received an equity interest of 20% in Neurosterix US Holdings LLC as part of the Neurosterix spin-out transaction. Under IFRS accounting standards, we are required to account for the investment using the equity method of accounting and recognize our share of Neurosterix results in our income statement. For the 12-month period ended December 31, 2025, our share of the net loss of Neurosterix amounted to CHF 4 million, compared to CHF 2.2 million for the period April 2024 through December 2024. The finance net result is close to nil in both 2025 and 2024 and is primarily related to foreign exchange differences on our U.S. cash deposits. Now moving on to the balance sheet. Our assets are primarily held in cash. We completed 2025 with CHF 1.6 million cash held in Swiss francs and US dollars. Our current assets amounted to CHF 41,000, primarily related to decreased prepaid patent costs and retirement benefits. Our non-current assets of CHF 4.6 million as of December primarily relate to our investment in Neurosterix, which has been accounted using the equity method, and the investment in Stalicla of CHF 0.8 million. Current liabilities of CHF 1.2 million at the end of the year, 2025, increased by CHF 0.4 million compared to December of the previous year, 2024, and primarily relate to R&D related accruals and payables. Non-current liabilities of CHF 0.4 million as of December 31, 2025, increased by CHF 0.2 million compared to December 2024, primarily due to an actuarial experience adjustment in the calculation of the defined benefit obligations. To the cash flow statement. On December 31, 2025, the cash balance amounted to CHF 1.6 million and decreased by CHF 1.7 million compared to the beginning of the year. This was primarily due to the cash used in operating operations and investing activities for a combined amount of CHF 2.9 million, which has been partly offset by the sale of treasury shares for a total amount of CHF 1.3 million during the year. To summarize, we've made excellent progress in advancing the 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 positive modulator program on track to complete phase I this quarter. We are very pleased by the progress Stalicla is making at advancing on its business strategy and pipeline, and 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. 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 a question, please press star one and one again. Alternatively, you can submit your questions via the webcast. Once again, if you would like to ask a question, please press star one one. Now we're going to take our first question. It comes to line of Raghuram Selvaraju from HC Wainwright. Your line is open. Please ask your question. Hi, thank you for taking my question. This is Jan Z sitting in for Ram. I have two questions. The first is, which subsets of patients with chronic cough is the GABAB PAM most likely to be aimed at? Would you say it's IPF or gliosis or something else? How large could that total market be if the compound had a broad antitussive label? Yeah. yeah, Misha, would you like to answer? Yes, of course. Well, considering the profile of this compound, which has balanced central peripheral activity profile, we believe that it will be suitable for a broad range of chronic cough patients, especially due to the fact that it has central component, which we believe is very important in reducing central sensitization seen in certain chronic cough patients. These patients do not respond to peripherally restricted P2X3 inhibitors, but can respond to morphine, which we believe is centrally acting. This way the profile is able to address problems in chronic cough circuit that are both peripheral and central. Our initial intention is to confirm the efficacy of the compound in chronic cough patients that come from unexplained or refractory chronic cough category. Once this efficacy is confirmed, we intend to broaden our patient population in subsequent studies. Thank you. Which psychiatric clinical indications might be best suited to address Addex's portfolio of mGlu7 NAM candidates? Ah. Yes. The MGLUR7 candidate is not in Addex. It's sitting in the spinout company, Neurosterix. We're not at liberty to talk in detail about that. You know, in general, maybe Misha you can say what you can say. Absolutely. Absolutely. There are a number of academic studies looking at mGlu7 knockout mice that show quite remarkable and very broad potential for inhibitors as mGlu7 knockouts show reduced anxiety and depression-like reactivity. They show reduced expression of conditioned fear. They show reduced aggressivity and agitation and certain signs of reduced responsiveness to psychostimulants. Even with this data that have been then confirmed in several pharmacological studies, some of those that were published by us show that we can orient the mGlu7 negative modulators towards anxiety and panic, agitation, aggressivity, depression, and perhaps psychosis and mania. Thank you so much. Thank you. Dear participants, as a reminder, if you would like to ask a question, please press star one one, or alternatively, you can submit your questions via the webcast. 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. I'd just like to thank everyone for attending our 2025 conference call and, I wish you all a very nice day, and we look forward to speaking to you again soon. Thank you. This concludes today's conference call. Thank you for participating. You may now all disconnect. Have a nice day.