Hello, everyone. I would like to thank you all for attending our Q1 26 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 activities and achievements before reviewing our pipeline. I will then hand over to Misha who will review in more detail our mGluR5 negative allosteric modulator program for brain injury recovery.

And the GABA B positive modulator program for cough. I will then review our 26 Q1 financial results.

Following that, we will open the call for Q&A. So starting with the highlights, Q1 has seen several important achievements across our pipeline.

We have made excellent progress in our GABAB modulator COF program as we continue to compete preclinical characterization of our selected compound. We recently announced robust antitussive activity in a non human primate cost 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.

Mikael will be sharing some of the data with you later in our presentation. We have repositioned Dipraglurant our mGluR5 negative allosteric modulator with brain injury recovery.

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 to an exclusive life 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 the University of Lund.

In Sweden to complete preclinical profiling of diproglarant 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 preclinical neuropsychiatric assets. In 2024 to create Neurosterix and raise 5 million through syndicative investment led by Percepta.

We retained a 20% equity interest in Neurosterix the value of which is unfortunately not being properly reflected in our current share price. Neurosterics has made excellent progress in advance advancing its pipeline, including its m 4 PAM and mGluR7 NAM programs.

The lead drug candidate in the M4 PAM program NTX-53, is in phase 1, and we expect data in q 3 this year. On the financial side, we completed the quarter with CHF 900 thousand of cash and successfully raised CHF 300 thousand in Q2.

Given that our cash burn is extremely low following the spinout, this provides us with cash runway through into Q4. Of 2026.

On a going concern basis. However, current cash does not fund the progression of our unpartnered programs into the clinic.

So now for a quick review of our pipeline. As mentioned, we continue to believe in Dipraglurant.

And we are executing our plans to reposition the development for brain injury recovery. As a reminder, we have regained the rights to ADX 9 from our partner J and J with a high value data set and significant GMP materials.

We are currently evaluating a number of therapeutic indications for future development. And in parallel, we are discussing the potential with partners for the asset.

For our GABA B PAM collaboration with Indivior, 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 313 million of successful achievement of a 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-digit.

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. Also presented on this slide is the portfolio of spinout company, Neurosterics.

We are expecting Phase 1 data from NTX-53 program in Q3. Backup m 4 PAM compound n t x 9 has been selected for IND enabling studies, which should start shortly.

The mGlu 7 nan program has selected NTX 9, a highly selective first in class compound, which has demonstrated robust preclinical and anti depressant like activity which supports its development as a potential next generation therapy. We expect NTX81 9 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, Timothy. Hello, everyone.

I will start by speaking about Dipraglurant and our plans for development in brain injury recovery. The program is an orally available, highly selective m g l 5 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 the building 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, and 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 therapy. Now 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 mGluR5 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 network towards the pre lesion state.

Now 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 MPEP administered daily in rats following stroke results in a sustained and growing improvement in sensory motor function in comparison to vehicle treatment. In the right hand figure, we can see a similar improvement in sensory motor function that was observed in animals treated with our mGlu5 NAM We are currently working with our collaboration partner, Sinntaxis, to complete the preclinical profile of dipraglurant in this animal model.

In addition to the compelling in vivo data, MRI imaging or the resting state functional kinetic connectivity in post-stroke products show that daily administration of MTEP also stimulates intra and interhemispheric connectivity in the brain disrupt 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 the 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 interhemispheric connectivity in the brain disrupted by stroke.

Now, I would like to update you on our GABAB positive allosteric modulator cough program. As a part of our agreement with Indivior, ADX 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 8 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 at 30 percent of patients or only moderately effective in up to 60 percent of patients.

In addition, the current treatments carry risks of serious side effects. Support for using GABA B PAMs in treatment of chronic cough.

Comes from the clinical evidence that baclofen a GABA B agonist, is used off-label in cough patients and from the anatomical evidence that GABA B receptors are strongly expressed in airways and in the neuronal pathway regulating cough. Therefore, we believe that GABAB PAMs could offer superior efficacy in cough patients.

The pre IND activities, 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 minimal effective dose on 1 mg per kg and ED50 of 6 mg/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, sedation biomarker.

Recently, we confirmed the antitussive efficacy in the nonhuman primates and are now currently evaluating the compound in rabbits. IND enabling studies are planned and ready to start subject to securing financing.

Now 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 dose.

The antitussive profile of compound a was similar to that of nalbuphine, orvepitant, repitant, baclofen and codeine. Now to cough latency.

Compound A increased 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 but without the CNS side effects such as sedation. In the same experiment where 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, orvepitant, repitant, 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, orvepitant, repitant, baclofen, and codeine in both cough number and cough latency measures. In the model of ATP potentiated citric acid in guinea pigs in a head-to-head comparison experiment, acutely administered Compound A and the p 2 x 3 inhibitor had similar efficacy and tolerability profiles.

As a reminder, P2X3 inhibitors antitussive activities peripherally mediated which explains their lack of sedative effects, but also the reason for more than 30 percent of patients do not respond to treatment. In the citric acid induced cough model, subchronic administration of compound A for 7 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 or the temperature and gross 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 0, 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 14, 21, and 28, animals were exposed to low concentrations of citric acid to stimulate the 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 fecal 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 vehicles treated animals versus intact control starting day 14.

Chronic treatment with Compound A reversed the effect of bleomycin throughout the testing period. Returning the latencies to the levels of intact control animals.

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 vehicles. the This suggests that compound A administered over 28 days reduced lung fibrosis.

Now to the nonhuman primate cough data. Similar to what we saw in the guinea pigs, in the model of citric acid induced cough in nonhuman primates, Compound A demonstrated more than 60 percent reductions in number of coughs at 2 mgs 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 PKPD. The compound showed a favorable developability profile in non GLP tox studies performed in rats dogs, and nonhuman primates.

The compound has a potential to have the best-in-class efficacy and tolerability profile and broad application in chronic cough patients. Subjects to raising financing, we are ready to start the IND enabling study.

This concludes our prepared remarks. On the progress of our R&D programs.

Now I hand it back to Timothy.

Thanks, Misha. Now for a view of our Q1 26 financials.

Starting with the income statement. The operating loss amount to 500 thousand in Q1 26 compared to 600 thousand in Q1 25.

The decrease of 100 thousand between both periods is primarily due to reduced outsourced r and d. As a reminder, on 04/02/2024, we received an equity interest of 20% in Neurosterix part of our 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 3 month period ended March 31, 2026, our share of the net loss of Neurosterix amounted to CHF 1.3 million compared to CHF 800 thousand for the 3 month period ended March 31, 2025.

This increase is primarily driven by the move of NTX 3 into clinical development by Neurosterix. The net loss amounted to 1.7 million during the first quarter compared to 1.5 million during the same period.

Ended March 31, 2025. Again, strongly driven by the increase in our share of the Neurosterix results.

Now to the balance sheet. We completed Q1 with 900 thousand of cash held in Swiss francs and, to a lesser extent, US dollars, compared to the 1.6 million held at the end of 25.

The decrease of 800 thousand is primarily due to our operating loss of 500 thousand and an increase net working capital of 300 thousand driven by 1-off annual payments made at the beginning of the year, such as retirement benefit contributions and insurance premiums. Our current assets amounted to 25 thousand Swiss francs, primarily related to increased prepaid retirement benefit our noncurrent assets of 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 investments in SOLICLA. Current liabilities remain steady at 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.

Noncurrent liabilities primarily relate to the retirement benefit obligations calculated in accordance with IAS 19. Amounted to CHF 300 thousand at the end of Q1 compared to CHF 400 thousand at the end of December Now to the cash flow statement.

We started the quarter with 1.6 million. We used 766 thousand for operations, primarily raised R&D and G&A activities.

We received 65 thousand from the sale of treasury shares. And completed the year with 935 thousand.

Sorry. Completed the quarter.

With 935 thousand. As mentioned in the highlights, we have been active with our ATM facilities, both on the NASDAQ and the 6 exchange and raised a very small amount capital in Q2 to strengthen the balance sheet.

While we wait for good news from marketing and Now to summarize, we have made excellent progress in balancing our GABA B PAM program for cough. And our Dipraglurant post stroke recovery program.

Our spinner company, Neurosterix, continues to advance portfolio with their m 4 PAM program on track to complete phase 1 Q3. We are very pleased by the progress Delica is making in advancing 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, and we will now open the call for questions.

Thanks so much for taking our questions. We have 4 of them.

2 of these relate to the chronic cough program. Firstly, I was wondering if you could provide us with some assessment of the relative position of your lead candidate, the GABA B PAM.

against nalbuphine extended-release? And, 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.

And then 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 mg/kg, whereas with nalbuphine, 1 needs to administer 3 in exactly the same model in guinea pigs where COF is stimulated by citric acid inhalation.

And 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 mgs per kg, we see significant reductions in respiratory rate. And it is nicely aligned 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 than the 1 corresponding to the dose we tested in animals.

Even at the efficacy dose, which roughly aligns to 3 to 5 mg per kg in a guinea pig. If we use 75-kilo calculation for a human, body weight.

So based on that, we expect similar efficacy to Nalbuphine but markedly wider therapeutic margin. And 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 you know, once weekly or once monthly. But once daily formula formulation is believed to be achieved with the current simple formulation that we have.

And that contrast with nalbuphine very well, as with nalbuphine even extended release formulation requires twice daily administration. So that shows another advantage of GABAB PAM clinical candidate over nalbuphine.

The And With--there was also a question on intensity. We use plasmography chambers that deliver COF frequency and COF latency.

There is no way of measuring cough intensity with that setup. The cough intensity is even challenging to measure in human patients, but there are some technical advances that may deliver intensity measures, but it is still in development.

Okay.

And then with respect to the Neurosterix equity holding, I was just wondering, maybe, Timothy, you can comment on this, what strategically your outlook is for, long term, management of this equity position, and if you have any, thoughts around how Addex might ultimately, assess the disposition of this. Or potential monetization of it, and how you are thinking about this specifically in the context of the possible future public listing of I was also wondering if from a scientific perspective, you could comment on the complex interplay between muscarinic receptor signaling pathways.

And in particular, if you could talk a little bit about this does not necessarily have to be solely in the context of what Neurosterics is doing, although I presume that is probably the most relevant aspect. But if you could talk specifically about m 1, m 4 receptor modulation, relative to m 4 and m 7 receptor modulation.

And how these aspects might potentially have differing therapeutic applicability within the context of schizophrenia versus depression. Thank you.

Okay. So let me take the first 1 about the equity holding.

And thank you very much for the questions. So yeah, let's just rewind.

I mean, look. We found in Neurosterix really, as a financing vehicle.

For some of our preclinical programs. And 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. And if you run the numbers, you know, the 20% equity interest that ADX received was valued based on the post money valuation of Neurosterics at about 20 million Now, clearly, with a market cap of 8 million today, there seems to be a little bit of a disconnect.

And now what we know about Neurosterix is that Neurosterix has advanced in the last 2 years an m 4 PAM from clinical candidate selection substantially through phase 1. And we are expecting phase 1 to complete very soon with data coming out in Q3.

it is also identified a backup compound in the m 4 PAM program called NTX 9. Which is ready to go into IND enabling studies.

it is 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.

So we believe that you know, our equity holding is not being correctly reflected Now the question is, really, do we try and monetize it today? We have had some inbound interest.

1 strategy could be to monetize the Neurosterics interest and sell it and to then use the proceeds to invest in our COF program. Alternatively, Neurosterix at some point will be executing a series b whether that is in the private arena or whether it is part of a public offering.

You know, I am not in a position on this call in the context of ADX to comment on that. However, we are you know, we are evaluating you know, all opportunities regarding you know, building value for share for our shareholders.

And with that equity position. Now what I would like to do is hand over to Misha who will talk at length because he is very knowledgeable about the muscular space.

Thank you, Timothy.

So we believe that the contribution of m 1 into the antipsychotic efficacy of cobenci which is co administration of zanomeline and trospium is speculative. There is still this is being discussed, there is no robust data that support that m 1 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 m 1, muscarinic m 1 selected compounds for cognitive improvement and all those clinical trials show lack of activity.

Some also showed a range of vascular of muscarinic cholinergic side effects which also brought additional aspect to consider. If we look at animal studies that evaluated antipsychotic like profile of zanomeline in rodents, it was very clear that the main bulk of activity, if not exclusively, in a hyperactivity model is driven by muscarinic m 4 receptor with virtually no contribution from m 1 So and then, of course, we have positive Phase 1b clinical trial with emriclidin.

So putting all together, we believe that having a selective m 4 post modulator will be able to deliver clinical efficacy in schizophrenia, which we see with zanomeline. That was the main question.

Then you mentioned receptor 7. I believe you had in mind mGluR7.

Am I correct? Yes.

mGluR7. The interplay between that and m 1 m 4 systems.

Yes. There well, there is no direct evidence of interaction between muscarinic M4 and mGluR7, there is some evidence of interaction between mGluR7 and mGluR8.

They may create heterodimers. And their co administration can have an impact on the outcome.

But I am not aware of any functional interaction between these 2 receptors. Thank you.

Thank you. And thank you, everyone, for attending this call.

We look forward to, to speaking to you again soon, and, we wish you a very nice end of your day, end of your week. Thank you.

Bye.