Addex Therapeutics Ltd (ADXN) 2011 Q4 法說會逐字稿

Ladies and gentlemen, good afternoon. Welcome to the Addex Pharmaceuticals Full Year 2011 Financial Results Conference Call. I am Goren, the Chorus Call operator. I would like to remind you that all participants will be in listen-only mode, and the conference is being recorded. After the presentation, there will be a Q&A session.

(Operator Instructions)

The conference must not be recorded for fabrication or broadcast. At this time, it's my pleasure to hand over to Mr. Chris Maggos. Please go ahead, sir.

Thanks, Goren. Today our President and CEO, Dr. Bharatt Chowrira, will give a corporate update, followed by Mr. Tim Dyer, our CFO, who will discuss the highlights of the 2011 financial results before we open the call for your questions.

Bharatt, the floor is yours.

Thank you, Chris. Hello, everyone. First, let me say that it is indeed a privilege to address you in this first teleconference and webcast since I was appointed CEO just a few months ago in August 2011. As you know, 2011 was a year of significant progress and breakthrough for Addex.

We were delighted to see two of our orally active allosteric modulators enter Phase IIa testing during the first half of 2011. In addition, excellent progress was made in several clinical -- sorry, excuse me, preclinical and discovery programs for diseases with major unmet medical need, including CNS, inflammatory and metabolic indications.

Today I'd like to discuss our achievements in 2011, which include the completion of enrollment in the Dipraglurant IR Phase IIa PD-LID trial, the initiation of Phase IIa schizophrenia trial by our partner Janssen Pharmaceuticals, clinical candidate selection for a GABA-B receptor PAM, the pipeline prioritization, the expansion of our allosteric modulator discovery technology platform, and finally, our restructuring and operational efficiency efforts.

As many of you know, dipraglurant, or dipra as we like to call it, is a novel oral small molecule which inhibits the metabotropic glutamate receptor type 5, or mGluR5. Dipra has broad potential to be used in combination with levodopa, or dopamine agonists, for treatment of Parkinson's disease, or PD. Our initial focus is on testing dipra for treatment of levodopa-induced dyskinesia, or PD-LID.

Together with a partner, we hope to study dipraglurant's potential for treatment of non-motor symptoms of PD. This includes co-morbid anxiety, depression or impulse control disorders, and effects on the underlying motor symptoms of PD, as well as for the treatment of non-Parkinsonian dystonia.

Towards the end of March this year we expect to communicate top line data from our ongoing Phase IIa trial, which we will hope will show how dipraglurant can benefit patients with PD-LID. In this double-blind, placebo-controlled EU and US run trial, the primary objective is to demonstrate safety and tolerability in PD-LID patients.

In addition, the trial was designed to evaluate exploratory efficacy as a secondary objective. Efficacy is being measured using the modified Abnormal Involuntary Movement scale, or AIMS. Patient diaries documenting on-time, with or without dyskinesia, as well as off-time and sleep time. In addition, the Unified Parkinson's Disease Rating Scale, the Clinicians and Patient Global Impression of Change and, finally, an evaluation of the patient's mood using the Hospital Anxiety and Depression Score.

We believe a successful treatment for PD-LID will change the way Parkinson's disease is treated by enabling physicians to use the most effective drug for Parkinson's disease, levodopa, earlier and more aggressively. In addition, based on robust preclinical data, potential label expansions for dipraglurant can include PD motor symptoms and/or non-motor symptoms like co-morbid anxiety and depression as well as non-parkinsonian dystonia.

An extended release formulation of dipraglurant is also in development. The choice of two formulations offers the flexibility to tailor treatment to individual patients and their particular problems. It also offers the possibility of an extensive product range and comprehensive lifecycle management.

While dipraglurant has broad potential for treating Parkinson's and other diseases, the most direct path to the market is treatment of PD-LID. No drug is approved for PD-LID and dyskinesia has been identified by the regulatory authorities, patient advocacy groups such as Michael J. Fox Foundation and key opinion leaders as a very important unmet medical need. The potential market opportunity for dipra in Parkinson's disease is well in excess of $1 billion.

Further label expansion outside of Parkinson's disease could more than double the peak sales potential for dipraglurant. As a result, we think that dipraglurant is a compelling partnering opportunity. We are seeking a partner with the vision, expertise and capability to fully exploit dipraglurant's attractive commercial potential.

After we announce the Phase IIa data, we plan to engage in partnership discussions with a view towards having a partner for dipraglurant on board before the end of 2012.

Now let me tell you about another exciting Phase IIa clinical program being developed in collaboration with our partner, Janssen Pharmaceuticals. In 2011, our partner Janssen initiated a 105-patient Phase IIa study of ADX71149 for the treatment of schizophrenia. This mGluR2 positive allosteric modulator, or PAM, was discovered and developed in collaboration with Janssen, and has the potential to be the first oral non-dopaminergic drug that may address both the positive and the negative symptoms of schizophrenia.

In addition, it can be used for potentially treating other indications such as anxiety. ADX71149 is differentiated from marketed antipsychotics in that it may show efficacy not only on the positive symptoms, but also on the negative symptoms such as depression, anxiety and cognitive dysfunction.

And also it has the potential to avoid compliance limiting side effects like weight gain and tardive dyskinesia, which are associated with the use of dopamine antagonists. We hope to share with you top line data for this program during the second half of 2012. In addition, a separate Phase IIa trial in anxiety is planned to start in 2012.

We couldn't be more pleased with the progress that Janssen is making on this program and we are proud to be their partner. Under the terms of this partnership, Janssen is responsible for all the cost of advancing this program through commercialization. We are eligible to receive development milestones totaling up to EUR112 million and low double digit royalties on product sales.

In 2011, we also made significant progress towards advancing several discovery and preclinical stage programs. In our GABA-B receptor PAM program, we selected the clinical candidate and earlier this year we initiated IND enabling studies. This novel, first-in-class, oral small molecule GABA-B receptor PAM has demonstrated excellent preclinical efficacy and tolerability in several rodent models of pain and overactive bladder, or OAB.

Therefore, we are profiling this program for the treatment of chronic osteoarthritis pain and overactive bladder. Chronic osteoarthritis pain represents a significant unmet medical need and a blockbuster potential opportunity for GABA-B receptor PAM.

As many of you know, when NSAIDs are no longer effective, the most widely used alternative for OA pain is opioid drugs. Although effective, opioids have poor tolerability and side effects often include drowsiness, nausea, respiratory depression and constipation. In addition, opiates are under-utilized because of their euphoric and addictive properties. A long acting, well tolerated oral drug without abuse liability would represent a major advancement in pain management and a large market opportunity.

Overactive bladder, also known as urge urinary incontinence, represents another significant opportunity for GABA-B receptor PAM. It's estimated that 11 million to 16 million US women suffer from OAB, according to the US Department of Health and Human Services. Some estimates indicate that an equal number of men experience OAB as well.

Overactive bladder is currently treated with anticholinergic, also known as antimuscarinic drugs, like oxybutynin. But limited efficacy and side effects like dry mouth, constipation, blurred vision and tachycardia significantly limit their usage. In addition, there is growing awareness that anticholinergic OAB drugs can cause adverse CNS effects, ranging from cognitive impairment to episodes of psychosis.

A long acting oral drug without antimuscarinic liabilities would represent a major advancement in OAB treatment and another large market opportunity. Having recently selected the GABA-B receptor PAM clinical candidate, we are on track to submit in late 2012 an application for clinical testing.

In addition, in 2011 we prioritized the pipeline to focus our efforts on the following discovery programs. mGluR4 positive allosteric modulator for Parkinson's and other neurodegenerative diseases, TrkB PAM for neurodegenerative diseases, TNFR1 negative allosteric modulator for inflammatory diseases such as rheumatoid arthritis, and GLP-1 receptor PAM for type 2 diabetes.

We are very excited about these programs and believe that each will have the potential to generate high value drug candidates with markedly differentiated product profiles. We plan to nominate at least one new clinical candidate by the end of 2012.

Underlying our robust pipeline is our industry leading proprietary allosteric modulator discovery technology platform. Over the last 10 years, we have been investing significant resources and time in building the infrastructure and developing the expertise for discovering and developing highly selective oral small molecule allosteric modulators.

Our platform allows industrial scale high throughput screening and can be adapted for a broad range of target, including targets considered undruggable using conventional approaches.

Already we have succeeded in selectively targeting GPCRs such as the glutamate receptors and the GLP-1 receptor with potent oral small molecules. More recently, our platform has been successful with new types of targets such as receptor tyrosine kinases, RTKs, like TrkB, and other single pass transmembrane receptors such as cytokine receptor TNFR1. Our technology platform can also be used effectively to target enzymes in a very selective manner such as epigenetic enzymes, kinases and bacterial enzymes.

These targets span a broad range of therapeutic areas, including CNS, inflammation, metabolic oncology and other indications. In 2011, we continued to enhance our allosteric modulator discovery technology platform capabilities via both investment in novel proprietary screening tools and expansion of our allostery-biased chemical library. In short, we are expanding the realm of druggable targets with our technologies, while discovering oral small molecule allosteric modulators.

In 2011, we continued to expand our dominant intellectual property portfolio with the filing of 21 new patent applications covering NCEs and proprietary discovery technologies. In addition, four new patents were issued.

Finally, in 2011 we fine-tuned our strategy, refocused on our core strengths, and took measures to enhance operational efficiency going forward. The reduction in headcount taken together with the pipeline prioritization significantly reduced our spending and provides cash to fund operations into the third quarter of 2013, without, of course, taking into account any new revenues from new or existing partnerships.

As a result, the company is now on a much stronger footing and well positioned to achieve our near and medium term objectives. Our operational strategy going forward will be to focus internally on our core competencies and do what we do best, discovery and development of oral small molecule allosteric modulators for undruggable targets.

In 2012, we look forward to achieving several major R&D milestones, including announcing top line data from Phase IIa studies with dipraglurant and ADX71149. Filing an application for clinical testing of GABA-B receptor PAM, as well as starting Phase I clinical trial testing for the extended release formulation of dipraglurant. In addition, we are looking to close at least one partnership deal before the end of the year.

Now, I'd like to turn the call over to Tim Dyer, our CFO, for a discussion of our 2011 financial results. Tim?

Thanks, Bharatt, and good afternoon, ladies and gentlemen, and good morning for those who are on the other side of the pond. Before going through the details of our 2011 financial results, let me give you the highlights.

We are pleased to report that our restructuring and operational efficiency initiatives started to pay off in quarter four of last year. This resulted in our 2011 cash utilization of $27.7 million coming in at the low end of guidance, which we had set following the restructuring in July at $28 million to $32 million.

We finished the year with a stronger than expected balance sheet with $36.1 million of cash. We reported income of $3.7 million and an overall net loss of $31.1 million, which is down by 7% primarily due to our reduced headcount. As previously discussed, we fine-tuned our strategy, refocused on our core strengths. These measures resulted in a 29% reduction in our headcount to 81.2 full-time equivalents at the end of the year.

So moving on to the balance sheet, we finished the year with $36.1 million of cash, which should see us through until quarter three 2013, one and a half years from now. On the liability side of the balance sheet, I would just like to point out that all costs linked to the restructuring have been either paid during the year or to a lesser extent, accrued at the yearend.

So moving on to the income statement, 2011 income amounted to $3.7 million, compared to the $4 million in 2010. This amount includes the CHF2.6 million milestone received from Janssen Pharmaceuticals for the start of the Phase II testing of ADX71149 in schizophrenia.

Also recognized income for 2011 is CHF0.7 million of grant from the Michael J. Fox Foundation. This is part of the $900,000 grant we received from the Michael J. Fox Foundation to support our dipraglurant Phase II trial in Parkinson's disease levodopa-induced dyskinesia.

On the expense side, R&D expenses decreased by 10% to $28 million in 2011 compared to $31.2 million in 2010, primarily due to our lower headcount, while G&A expenses slightly increased by 5% to $6.7 million from $6.4 million. This was primarily due to the net effect of our reduced headcount, which was offset by certain one-off restructuring costs. We expect both R&D and G&A expenses to be significantly reduced in 2012, as we see the cost savings from last year's restructuring feed-through.

Moving on to the cash flow statement, 2011 cash utilization of 27.1 -- sorry, $27.7 million is mainly comprised of $29.1 million used in operations, compensated by the CHF2.6 million milestone received from Janssen. If we strip out the cash received in 2010 from our capital increase, we see that cash used in ongoing operations has decreased by 15%. We expect this trend to continue in 2012 as we continue to reap the cost savings from the 2011 restructuring.

And to complete my prepared remarks of the financial outlook, during 2012 we expect to maintain our headcount at around 80 to 85 FTEs and to complete the dipraglurant Phase IIa PD-LID trial. Other 2012 cost drivers will include advancing dipraglurant extended release form through Phase I, and our GABA-B PAM clinical candidate to IND enabling studies. We also plan to progress our focused discovery portfolio toward the clinic and make selective investments in our allosteric modulator discovery platform.

On the basis of these activities, we expect cash utilization for 2012 to be CHF23 million to CHF25 million, and cash reach through Q3 2013. It is important to note that this guidance does not include any cash inflows from new or existing partnerships, which we certainly hope will not be the case.

So, on that note, I thank you for your attention, and now will hand back to Bharatt.

Thank you, Tim. As you have heard today, we are committed to building significant value for our shareholders through a combination of pipeline execution, generating non-dilutive funding through partnerships and improving operational efficiency. We believe 2012 will be a seminal year, indeed a transformational year for Addex.

We have a robust pipeline with important near term milestones, cutting edge science, a strong balance sheet, and high caliber investors who support our overall strategy of building a strong and successful company focused on discovery and development of innovative oral small molecule drugs for treatment of diseases and conditions with large unmet medical needs.

Finally, I'd to acknowledge and thank all our employees for their hard work, dedication, loyalty and perseverance through all the recent changes. We look forward to working together to bring innovative therapies to patients and building shareholder value.

Also, I'd like to thank our shareholders for your continued support of the Company during the past 10 years.

Operator, please open the call for questions.

We will now begin the question and answer session.

(Operator Instructions)

The first question is from Ms. Philippa Gardner from Jefferies. Please go ahead, madam.

Oh, thank you, and good afternoon. I just had one question, which I'm not sure how much you'll be able to answer it. But I guess it's just in relation to the dipraglurant potential partnership. You say you're going to start discussions post the Phase IIa data.

And assuming those are positive, I mean how confident can you be that you can actually sign a partnership this year? And when you say sort of start discussions, are you already talking to a number of potential partners and what has that kind of feedback been so far?

Thanks for the question. so, we have been in discussions with a number of companies in the past couple of months. And our process that we have outlined earlier this year is to bring as many partners who are interested in dipraglurant to get them to complete their diligence.

We have set up an electronic data room so that they can complete diligence on all the material that we have to-date so that they can be ready ahead of the data. And then once data comes out, then we'll run a process involving those partners who completed the diligence and with a view towards completing a deal hopefully before the end of this year.

So, I think it is definitely possible to accomplish that. So, there has been significant interest in this program.

And can I ask -- is the sort of feedback that you've had so far been, I guess, fairly positive, if you're confident in signing a deal?

Well, so, look, it's not a guidance, of course. I mean, we hope to have a deal by the end of the year and that's certainly the plan. We have a lot of interest in this program because, as you can imagine, this dipraglurant presents a significant market opportunity not only for the treatment -- acute treatment of PD-LID as an indication, but also broadly for the treatment paradigm of Parkinson's disease.

And not to mention beyond Parkinson's disease, as we mentioned, we have significant product opportunities in indications such as non-Parkinsonian dystonia. I mean, dystonia, for example, is currently being served only through injectable Botox, and that also is not very well served. So, there is significant market opportunity for dipraglurant in Parkinson's and non-Parkinsonian indications. So, people are quite interested in the broad opportunity that is presented by this program.

That's great. Thank you.

The next question is from Mr. Olav Zilian from Helvea. Please go ahead.

Yes, hi, there. Thank you for taking my question. Obviously dipraglurant is an important value driver for Addex. However, a lot of people still seem to think that dyskinesia is less of a problem these days because of the use of dopamine agonists or other drugs like MAO-B inhibitors or then also lower doses of levodopa. So why do you think that your compound can actually achieve blockbuster status?

Thanks, Olav, for the question. So, I'll hand this question over to Dr. Charlotte Keywood, who's our Chief Medical Officer, who can elaborate on this question.

Thanks, Bharatt. Yes, hi, Olav. That's a good question, in fact. The dopamine agonists and MAO-B inhibitors are used early on in the management of Parkinson's disease for people who are either very young or have got mild Parkinson's disease because they're simply not terribly effective. By far the most effective treatment for good control of motor symptoms is levodopa. So, the MAO-Bs tend to be used early in the disease, and the dopamine agonists.

Now the problem, particularly coming forward with the dopamine agonists, apart from their limited efficacy, then entailing, of course, an add-on therapy with levodopa, is the emergence and increasing recognition of impulse control disorders as a side effect of the dopamine agonists.

And the impulse control disorders, these sort of compulsive behaviors like compulsive shopping or gambling or sex addiction. Although these things sound sort of quite amusing, in fact they can even be a medical emergency, and you have to submit people to hospital to take them off their dopamine agonists and take them away from their credit card. So this is really emerging as a problem with these compounds.

And what we're hearing from our physicians, and this is very much echoed, of course, by the Michael J. Fox Foundation, is that what they really want to do is be able to use levodopa more effectively. And the reason why they're not using levodopa as effectively as they can, i.e. using these low doses of levodopa that you're talking about, is because of the fear of dyskinesia.

And they've all told us that "if only we had an effective antidyskinetic agent, then we'd be free to use levodopa much more freely. We could use it earlier in the disease process. We could use it more aggressively." So the whole market for levodopa would open up. And this is why -- and this is based upon our market research, and is actually supported by the findings of the Michael J. Fox Foundation -- that this is really a very big unmet medical need in Parkinson's disease with a very large market potential.

And the physicians are walking a tightrope at the moment of holding back on levodopa, but compromising patients' quality of life and motor function. If they had a good antidyskinetic agent, they wouldn't have to do that. And the whole -- I mean, physicians have told us that the whole management of Parkinson's disease would be transformed. So, that's why we believe it has a very significant market potential that, of course, has been supported by our Datamonitor market research.

And to further expand on that, so, when we talk to KOLs and the patient advocacy groups, they would like to find a way for the physicians to pair levodopa with an effective antidyskinetic agent so that -- because levodopa is the most effective anti-Parkinsonian drug out there, that they would prefer to pair something like that with an antidyskinetic agent so that it can either delay, stop or treat dyskinesia even -- when they arise, as opposed to continue to treat the patients with dopamine agonists and MAO-B's, so --. To be sure, we see this as a huge market opportunity.

Another point that I would like to make here is that patient advocacy groups like the Michael J. Fox Foundation, they've made it a priority to really educate people about the problems -- the growing problem of dyskinesia out there. And that's evidenced by their large investment in research and development for finding a treatment for dyskinesia. And so they this as a major, major issue in the years to come with respect to Parkinson's treatment and disease management.

Thank you very much for your detailed answers. So, obviously, this area of mGluR5 NAM has been becoming very competitive. And maybe one of your most important competitors is Novartis.

And they have shown statistically significant efficacy in three Phase II studies with their proprietary mGluR5 inhibitor AFQ056. So, surprisingly, however, they had trouble getting the majority of their patients up the effective dose due to side effects. And that was reported last June at the Movement Disorder Society meeting.

So my question is, do you expect to have similar issues in getting patients to tolerate an effective dose of dipraglurant?

So, the short answer is no. I'll let Charlotte elaborate on that. So we feel that dipraglurant is a much more effective and more potent drug and without -- and we haven't seen, and again, the study is still blinded so we can't comment on the ongoing study, but we haven't seen any safety signal that would give us a pause at this stage.

Charlotte?

Yes, thanks, Bharatt. Yes, there's a couple of important differences between the dipraglurant and the AFQ056. And the first one is the potency, but -- and the second one is the kinetics. And the third one is the way we're actually dosing the compound to treat dyskinesia that's very different. And that's related to kinetics.

The pharmacokinetics of the dipraglurant IR formulation are almost identical to that of levodopa so that the two PK curves overlie each other. And what that means is that when you co-administer dipraglurant with levodopa, you get your maximum plasma concentration of dipraglurant when you've got your maximum plasma concentration of levodopa. And that's when you get the dyskinesia.

So the majority of levodopa-induced dyskinesia occur at peak plasma concentration. So typically, between sort of one and two hours after dosing is when you get your worst dyskinesia. Because dipraglurant also goes to its maximum plasma concentration at that time, you can treat the dyskinesia when you need to.

Now, of course, when the levodopa wears off, you don't have dyskinesia anymore because you go into off. Likewise, then, the dipraglurant also wears off. So what you have is by overlying the two curves, you're delivering drug exactly when you need it and not when you don't. Because when it's worn off, you don't need plasma concentration of mGluR5 antagonist floating around in your system.

And that's a big difference with the Novartis compound because what they're doing is they're just giving a fixed twice daily dosing regimen and they're not respecting the kinetics of levodopa so they're not giving it in conjunction with levodopa to acutely treat dyskinesia.

So in order to try and prevent the dyskinesia breaking through when levodopa is given in this sort of pulsatile fashion, they have to try and drive the plasma concentration very high and keep it high throughout the day so they've got enough on board when the levodopa is given.

And, of course, that means you have a much greater exposure to the mGluR5 NAM and then a much greater risk of adverse effects. And so, we believe that by giving our drug that's more potent and has better kinetics alongside the levodopa, we can avoid the problem that Novartis appear to see with narrow therapeutic margin. And, of course, that will all be revealed when we report this out from our study towards the end of March.

So, actually, what were these side effects Novartis has seen?

Well, they're sort of typical, like dizziness or CNS type side effects that they've seen that were kind of dose limiting and not very well tolerated. So the patients had to -- patients in the study were allowed to deescalate. And, in fact, most of them from the 100 mg dose group did deescalate back towards 50 mg and 25 mg.

And it was most likely -- I mean, they haven't specifically reported -- there's a summary of the adverse events, but they haven't specifically given reasons what were the actual adverse events that caused the patients to deescalate. But one can imagine looking at the profile that they would be CNS type adverse events.

Okay. So, although the study you conduct is still blinded, if you follow your patients closely when they take the pill, do you see any evidence for side effects on the back of the uptake of the pill?

I mean, that's difficult to comment on because, of course, this is a placebo-controlled, double-blinded trial. So you see events occurring, but you've no idea which treatment group they're in. And it would be incorrect of me to give you any kind of guidance on this at this stage while the data are all blinded. But all I can say that we have been satisfied with the progress of the study.

And in terms of efficacy, that is still -- that is dyskinesia in a good fraction of the patients?

I can't give you any guidance on it, I'm afraid, but you don't have very long to wait before we all find out.

Okay, thank you. Okay, I'll go back into the queue. Thank you.

Thanks, Olav.

The next question is from Mr. Robin Davison from Edison Investment Research. Please go ahead, sir.

Hi, a follow-up. I'm also, of course, interested in dipraglurant and the potential for partnering. I wondered if you get the impression that your potential partners with whom you're obviously sort of talking at this point -- sort of agree with the thesis of the potential indications outside of sort of PD-LID obviously first and symptomatic PD and even other CNS indications. I mean, do you get the impression that they're interested in those other areas as well?

Oh, yes. Thanks, Robin. Absolutely. And that's why I think -- I'm really excited about this program because it presents not only a large market opportunity in PD, but outside of Parkinson's disease as well. And that's another reason why we are developing the extended release formulation that could be quite useful for non-Parkinsonian indications such as non-Parkinsonian dystonia.

There are about 15 or 16 different types of dystonia that are currently not being very well served. Like I said earlier, the only treatment out there is injectable Botox, again, which can only be given locally in a focal manner, not necessarily through -- in a central way. So, there is a huge unmet medical need there for an oral small molecule that can potentially treat indications like dyskinesia.

And as we have reported in the past, based on our preclinical data in non-human primates, we -- our molecule seems to be the only drug out there that's an mGluR5 negative allosteric modulator that actually treats not only the chorea component of dyskinesia, but also the dystonia component of dyskinesia.

So, we feel very confident that this drug can be used much broader than the PD-LID. And partners actually recognize that, and so agree with us in terms of the broad market opportunity.

Okay, good. On the 71149, obviously you've indicated that your partner is likely to start a phase -- well, in the next -- another study in anxiety this year. I know you've never liked talking on behalf of partners, but is that to be sort of a typical Phase II study? Or, would they be able to go ahead sort of later perhaps because of the Phase II that's going on in schizophrenia giving sort of more preexisting patient exposure, that sort of thing?

Yes, unfortunately, as I said, I cannot really comment on the design that Janssen is going to put forward for that trial. I mean, the only thing that we can say is it's going to start sometime in 2012.

Right. Okay.

-- going to be a Phase II trial.

Yes, exactly. I just wonder, on the GABA-B PAM, it just occurred to me you said you've done rodent models in both OA pain and overactive bladder. And I was just actually wondering, curious really, whether the same dose would be likely to be used in both of those two indications.

Well, I mean -- so, we are still doing the IND enabling studies here. And so, in the animal models that we have tested so far, we see a pretty nice therapeutic window for our compound. And so, we won't be able to arrive at the actual dose that we want to use in Phase II until a little later, but we are working through those.

Okay. Thanks very --

But yes, they look very good in terms of -- and it's a long-acting oral small molecule, so got a pretty good profile.

Right. Excellent. Okay, thanks very much.

The next question is from Ms. Victoria English from MedNous. Please, go ahead.

Thank you for taking my question. I have a couple of questions. The first one is clarification. You say you're talking with a partner about studying dipraglurant's potential for the treatment of non-motor symptoms of Parkinson's disease. Would this be as a combination therapy as well?

Well, so -- I mean, I can't go into a lot of details, but we're in discussions with companies who are interested in different aspects of the mGluR2 NAM in addition to Parkinson's disease levodopa and dyskinesia, as well as the comorbid indications. So, I mean it'll all depend on how broadly and how extensively the partner wants to pursue those indications. It's too premature to talk about that.

Okay. And the second question concerns your comments at the end of your presentation about the other applications for the allosteric platform. And you mentioned briefly, among other things, epigenetic enzymes, targeting, that is. How far along are you in establishing the proof of principle of some of these new targets?

Well, so, I'll say this. We aren't publicly talk about those programs. So, allosteric modulation platform is fairly unique and from that perspective and what Addex -- how Addex approaches that. And so we can -- we have a platform that involves a library that is focused on allosteric modulators.

And then we have a complementary set of high throughput screening assays that we designed for different classes of targets. So, we are in the process of designing some of these really high sensitive assays for enzymes such as the epigenetic enzymes and kinases and such that are going to be very, very effective in selectively targeting these allosteric modulators to these specific enzymes.

And we have -- we are looking at a number of these epigenetic enzymes that -- and I think we are really excited about that program.

Thank you.

(Operator Instructions)

Ladies and gentlemen, there are no more questions at this time.

All right, thank you, everyone, for participating on this call. And we look forward to keeping you all updated in the coming weeks and months. Thank you again.

Ladies and gentlemen, the conference is now over. Thank you for choosing the Chorus Call facility, and thank you for participating in the conference. You may now disconnect your lines. Goodbye.