AB Science S.A. (AB.PA) Earnings Call Transcript & Summary

Ladies and gentlemen, welcome to the AB Science web conference. I will now hand over to Alain Moussy, Co-Founder and CEO of AB Science. Sir, please go ahead.

Thank you. Welcome to our web conference. My name is Alain Moussy. I'm the CEO of AB Science. The topic of today is to present our new platform focused on microtubule destabilizer agent, MDA. Next slide, please. Along with me, there is a team made of experts from AB Science, namely Professor Olivier Hermine, who is also Co-Founder of AB Science, the Chairman of the Scientific Committee and an expert in Hematology in the Hematology Department of Hospital Necker in Paris. Also with me is Professor Christian Auclair who is Co-Founder as well and member of the Scientific Committee and expert in Onco-pharmacology and Ecole headed CNRS, which is a well-known research center in [ France ] of excellence. And with me also Laurent Gros, who is our Head of Drug Discovery. Next slide, please. So as you know, for the ones who have an interest in AB Science, we have a known platform based on masitinib where we developed masitinib in 3 main therapeutic areas and the primary one being CNS, but it's not the topic of today. The topic of today is to present our new platform. So the MDA, microtubule destabilizer agents with 2 compounds, one into clinical in Phase I called 8939, which is an intravenous administration form and another one that we'll not present today, which is XXXX coded and will be developed not in hematology but in oncology. Next slide, please. So from this section of the presentation, the experts will explain you this platform and this new compound. At the end of the presentation, we'll take over and open the discussion for your questions, of course, and we'll try to answer that. Olivier?

Thank you, Alain. More or less, first as a quick look to the mechanism of action of our AB8939 compound. This compound was identified during significant screening as microtubule destabilizer [indiscernible] major targets in immuno-oncology today. But let's shift to the picture. In normal sense, you have 2 states for the cells and kind of different states that cell are dividing and cell dividing follow cycle in which we call this the cell cycle, which is divided in several phases, G1 and G2/M basically. But microtubule are critical for this to achieve this cycle for this proper cell division. And if you target this particular cellular process, you can stop and kill the highly dividing cells and namely the cancer cells. Okay. Let's have a quick look. If you apply the 8939 compounds to counter fare, you can see that you will disrupt totally the shape of the cell. If you have a look to the picture at the bottom of the slide, you see on the left, normal cells with the [indiscernible], which is in red -- in the red point and the cell treated with the compound this beautiful network totally disappeared, totally disrupted. And this is transacted in a block in the cell cycle and this block in cell cycle and just a massive cell death because this mechanism of action is not new because some very, very successful component in the clinic use the same kind of mechanism of action by targeting namely the [indiscernible]. Next slide, please. Okay. Okay. Look, our compound differs strongly from the clinical compound actually in clinic namely as the vinca-alkaloids and taxane compounds, which is derived from a natural product. Vinca-alcaloides was discovered in the late 1950s and taxane in later 1970s. And our component is a small chemical compound of flow molecular wide. Natural compound has a huge limit in therapeutic applications, which is due to the occurrence of resistance. There is several mechanisms of resistance. So this compound could be transported outside the cells by some efflux pump, which is a phenomenon. It's called multi-drug-resistance, phenotype. You can also have some several [indiscernible] from vinca-alcaloides with some online, myeloperoxydase is one example, for example. Then you can also have some aberrant expression of [indiscernible] is a form of distributing, which is a basic component of [indiscernible], which is a target of the drugs. But remarkably, AB8939 is able to overcome all these mechanism of resistence. This compound is not a substrate of the efflux pump, as you can see on the curve at the bottom of the slide. On the first part on the right, you can see some normal cell, which are highly sensitive to all drugs, including AB8939, doxorubicin, which is common chemotherapy and vincristine, which tubulin-targeting agent. As this [indiscernible] the express the MDR phenotype, you can see that the resist to the doxorubicin and vincristine compound, but they remain fairly sensitive to AB8939. Next slide, please. Next slide. Okay. Okay. After the characterization of the component of potent and multi-tubular agent able to overcome of the no mechanism of resistance. We evaluate this compound against some blast derived from AML patients in ex vivo. And we select a panel of 99 different samples, and then we test them. And you can see in the A part of the slide at the bottom of that almost approximately 70% of the blast isolated from these patients are sensitive to our compound. By comparison, if you consider right bottom part of the A panel, you see that conventional chemotherapy used in the clinic for the 3 parts of AML, which is called cytarabine. Most of the patients ready to register. There were only 1/3 of the patient with a sensitive to Ara-cytarabine. Okay. It's very interesting because our compound is able to overcome the resistance of the some [indiscernible] from patients. On the other hand, we have selected some naive patients in the B panel. You can see 33 samples, and we test them with multi-tubuline agent, which is used in the treatment of leukemia, which is vincristine. And we can see that most of the patients are refractory to this kind of therapy since only 1/3 of samples response to the vinca drug. By contrast, we have still 70% of the patient, which responded to our AB8939 compound. And we have the same proportion of response, if we consider refractory our [indiscernible] sample, 70% of the patients respond to the drug. Based on this ex vivo data, we move to in vivo experiments. Next slide, please. And we test a number of different patient derived xenograft model. The first one is very, very aggressive acute megakaryocytic leukemia, which was graft on a [indiscernible] mice. And we treat this mice with our compound at different dose. As you can see in the right path, you can see 2 mices, 1 mice is untreated mice, and the color is -- represents the amount of cancer cells to the mice. You can see that after the treatment cancer sell almost disappeared totally from the mice, we can see -- we can consider that the cancer is eradicate from the treated mice. And if we analyze the bone marrow of this mice, we can see that in the center that the compound acts against the cancer cell into the bone marrow of the animals. And this is a critical point to be successful into clinic. And we have several other models, including [indiscernible] models and so on. And each time, it's very important to understand that we have a big success and each time we analyze our complex models, blood, bone marrow, spleen, we totally eradicate the cancer cells from this compartment. And we have a great improvement in terms of therapeutics and better so we have a strong impact in terms of survival in the mice. Okay. We can move to the next slide, please. This might just exemplify the previous one on the last part, you have [indiscernible] conventional chemotherapy resistance model delayed from patients, which was graft on of mice. And you can see that the control of mice on the bottom of the picture. You have a lot of colors that they are blue and green. This means that there is a lot of cancer cells in this mice. If you consider the Ara-cytarabine, which is called [indiscernible] green in the picture, there is no effect because it's a Azacytidine [indiscernible]. And if you see -- have a look to the 8939 -- our 8939 in combination with Ara-cytarabine in mice, you see that the cancer cell disappear. And when we analyze the blood of this mice of the bone marrow, we have almost complete response in terms of eradication of the cancer cell. Okay. This means that this compound works very well in the [ preclinical model ]. On the left part, we have another model, which is used azacitidine, which is another kind of agent, which is used in older patient because it's less toxic [indiscernible] So it's important to check if our compound could work in the with [indiscernible] with kind of conventional chemotherapy. And what you can see is that 8939 and azacitidine, which is called Vidaza, works in the same way, exactly in the same way. And when you combine both, you have a better effect purely. But the interesting point is that when you had our compound to the Vidaza, you don't see increase the toxicity of the treatment, this is critical point because one of the biggest limitation in the usage of chemotherapy is toxicity from the patient. Okay. Next slide, please.

Thank you, Laurent, for very technical but informative description of the [indiscernible] mice data. And now Olivier is going to take over to describe the proof of concept we did in dogs first.

So thank you very much. So as we know, mice model and physics model are what we call [indiscernible] the to assess the effect of drugs, and we showed that AB8939 was very nicely working in this mice model. But the [ real malignancy ] and here is the dog, which is a very nice model of leukemia. And we know that in dogs drugs are very difficult to give to dog because it's highly toxic. And you can see here, a dog with acute lymphoblastic leukemia with cytopenia as expected because was now [indiscernible] this blast. And upon treatment, that's only one cycle at low dose of 0.5 milligram per kilogram for 5 days, you can see that the dog improve his bone marrow function because you can see that the neutrophil count increase significantly complete to almost the normal value. And we do see the same thing for platelets count and the hemoglobin was stable in the dog. So it means that dog was able to increase the normal bone marrow and because the [indiscernible] didn't one that we check the bone marrow onto dog, we didn't check blood reduction. But to see such effect, it means that we are clear at least some part of the bone marrow allow the bone marrow to work again. So based on this preclinical studies and also on the dog model next slide, we wanted to put AB8939 in acute leukemia. So here, I will recall you the landscape of acute leukemia. And we split in 2 parts. The first part is the patients who are eligible to high-dose chemotherapy Anthracyclines, Ara-C [indiscernible] and the second part is patient ineligible to high-dose chemotherapy because they're [indiscernible] to receive the dose and usually up to 75 [indiscernible] we do not provide high-dose chemotherapy. So for patients eligible for high-dose chemotherapy, the first line is usually high-dose chemotherapy and then the Anthracyclines and high dose Ara-C and patient dealing some mutations like FLT3, we may add some effective FLT3 kinase inhibitor for this patient. And in the second line for the patient in case of [indiscernible], usually, we treat these patients with LO translocation and before they receive either high-dose chemotherapy or the combination of [indiscernible] disease and when they took that. There is no drug approved to treat this patient. For elderly patient ineligible for high-dose chemotherapies, the standard of care today is, agent azacitidine, hypomethylating in combination with venetoclax, which is an [indiscernible] drug by routine [indiscernible]. In second line therapy and third line therapy, there is no registered drug in this patient. So you can see here, we have a high unmet medical need for patient with acute leukemia because [indiscernible] 60% of the patients overall will relapse after the first- or second-line therapy. So we did this in next slide, to go in Phase I study based on the [indiscernible] obtained in mice model. So it's a practical Phase I study for acute leukemia. So we did include patients who are refractory or in relapse of AML in second- or third-line therapy receiving not high-dose chemotherapy in first-line therapy. We do also include with patients with refractory high-risk myelodysplastic syndrome and the patients are not eligible for [indiscernible] translocation at the time of inclusion. So the step 1 of the 2 was to increase the dose for 3 days of treatment from 0.9 milligrams per meter square, 3 patients at each dose. And in case of no toxicity, we move to dose 2, 3, 4, 5, 6 and 7, 1.8, 3.6, 6, 9, 12 and 16 milligrams per meter square. The second step of the study is to increase the length of treatment to -- from 3 days to 14 days, and we'll start at the day 5 MTD dose in the step 1, dosed before. And then we move to the second dose at the MTD of the 3-day treatment. And then we will move to the day 3, depending on what we found in the [indiscernible] Phase II in combination with other study, which is standard of care of leukemia today is patients not eligible for the chemotherapy. And we do the combination for 14 days. And also, we will do the treatment for 28 days in case of a good response and good tolerability in the step 2 of the study. So next slide. So here, which is unusual to show you some data in early Phase I and we think that we do observe it's quite a high [indiscernible] in this group of patients. So yes, it is one of the first case patient at the low dose of 0.9 milligrams per meter square. This patient is an AML patient of 81 years old with the de novo acute myelogenous leukemia, which we call intermediate risk prognosis, refractory to a 3 line of treatment, azacitidine, venetoclax, and high-dose Ara-C. So these patients enter the Phase I study. And very interestingly, after the first cycle of [indiscernible] we do see a reduction of blast in bone from 15% to 8%, which we call partial response. So we did the second cycle of treatment to these patients. But what was the most spectacular here is that we do see that the number of neutrophils increased upon treatment as well as the number of platelets. And don't forget that this patients [indiscernible] not only of the blast in the bone marrow, but mostly on the bone marrow failure as a consequence of [indiscernible] that we do see a reduction of blast and improvement of the bone marrow activity and no adverse events were seen in this patient overall. The second case report is also very interesting that the set of 1.8 milligrams per square for the patient with secondary AML, which are very poor progress of AML. And as expected, in secondary AML to have some [indiscernible] 1 gene, which usually does affect to refractoriness to any kind of treatment. And as expected, this patient was refractory to adaptive treatment and very interestingly, after 2 cycle of 3 days x 20 days interval, we do see this patient a drastic decrease of blast in the bone marrow after 1 sector from 55% to 5% which is a limit of the complex response in terms of blood reduction. And after the second cycle, the blast remained stable at around 10%. And very interesting here, we do see also an increase of the neutrophil count from 200 to 500 per microliter, which is a number sufficient to don't get any [indiscernible]. And also, we will see an increase of platelet count from 3,000 to 12,000 per microliter. And also here, we have no adverse event of the disease for the treatment. Next slide, please. So if we can summarize what we do see at the very early stage of this Phase I study. First, we do see no drug qualitative at their reaction superior to 2 in this patient today. And we have so far no toxicity. And interestingly, we do observe 40% of patients with stable disease or that to response by increasing the blast counts and as a consequence, investigators asked for more cycle of treatment of this patient. We do see also which is very high 70% of the patients had an increase of the platelet number and more [indiscernible] 90% of the patients increase their neutrophil count. Meaning that the drug is able to reduce the blast count, while it would not have any toxicity on the bone marrow and hematopoiesis. So over to the next slide, I can say at this moment that we have no extra hematological toxicity -- no hematological toxicity and with even an improvement of the bone narrow figure with an increase of [indiscernible], which is very unusual in leukemia treatment. And we have also -- we do observe 3 dose of significant contradiction of the stability of the blood comp in this group of stations even in patient with high-risk acute leukemia, usually refractory to any treatment like everyone AML. So this data, although they are early, means that we can envision the treatment eventually, as a chronic treatment if we do not see any kind of toxicity because we can control the blast number. And also, we can improve the bone marrow figure, which allows to have a normal quality of life for this patient. However, we cannot rule out that's when we see an increase of the dose, we'll be able that we have observed in dogs and mice to kill all blast and to see a normal bone marrow recovery and the full cure of these patients. And probably based on the early results, we may focus in the future to treat AML with poor prognoses karyotype or molecular events like everyone [indiscernible] because in this proposition, there is a very unmet techniques with no efficient treatment. And also, as we have seen in micro that combination with adaptive disease also increase further the [indiscernible] in the product with drug.

Thank you, Olivier, for the discussion of this preliminary results of our clinical study. And as you have seen, it's only the step 1 with 3 days of treatment or as the protocol will continue, of course. And after we define maximum therapeutic dose will move to 14 days. And after it moved -- we form the NTD 14 days, it will move to 28 days. And also in parallel, 14 days in convention with [indiscernible] because we saw in mice a synergistic in fact -- effect with [indiscernible] So the ultimate goal of the Phase I is not only to reach the MTD, but also to see our, I would say, what's the best treatment in combination or not in combination. But here, it's extremely preliminary data at 3 days of treatment, 3 days only. And we measure the efficacy by doing bone marrow sample at 28 days. So 3 days of treatment and nothing, 28-day bone marrow. And that's it. And then an extension of another 3 days, but only 3 days. So the very reason why we did this call is that as a company, we and the investigators, of course, even before us, they did not expect any sign of efficacy, any sign of efficacy before , that's what we had in mind to mimic the, by the way, that we are within for not related, but how many days, Laurent, it was ?

Probably 5 days.

5 days and sometimes more, but it was unexpected and this very little dose first and very few number of days of treatment. So it was surprising, very surprising for us. Having said that, we move to the -- so yes, -- thank you, Laurent. So to the next slide, which is the patent protection. So it's a new platform. So we have a new patent, of course, covering the composition of matter of this compound and we are protected until we -- the compound is protected until 2036, and the patent has been delivered. And completely new chemistry which does not infringe no patents or nothing. We compete nobody. Then we have on the results that we have acquired so far on the -- what you call MTD1 or [indiscernible], which is a special rare arrangement, special genetic of patients, we're filing new patents. And this is very important because, as you know, FDA and the agencies are extremely keen in oncology to develop and accelerate the approval of treatment, which is based on genetics because it makes a lot of sense for them. So if we can prove that this compound is fitted for MECOM that an additional discovery unexpected because MECOM refractory to all kind of chemotherapy, so it's publicly new and innovative and patentable. And then we can, of course, develop in this specific population. Then there is another protection, which is the open drug sectors that we have at the ABA level and that protects order. So the patent strategy is strong. Then let's move to the next slide, Laurent. So the -- what's the next step? So the next step is to continue the Phase I because we're only on step 1, and we have to move to step 2, 3 and 4. But we can still think of the strategy further. So how much time would be needed to complete Phase 1? Obviously, with these good preliminary results, there is a line of patients waiting to be enrolled. And we are literally back-to-back with the investigators who are fighting to enter patients included in the study. So good news because it can be done rather quickly, of course. It attracts the attention of everybody. So we think we can initiate the Phase II before the end of the year. We had planned a Phase I/II with a mini-Phase II in the Phase I. But in view of these results -- encouraging results, we might actually change a little bit the Phase II and be more -- I would say, maybe more -- actually not spend time on this mini-Phase II but engage into a larger Phase II because we think we can do it. And in this Phase II, we could ambition to have different ones. But one option is to focus on [indiscernible] for the best and where the unmet medical need is the highest, which would be today, the makeup that we might discover new genetic situation where the product could be very effective. But suppose we have the MECOM and only the MECOM we could envisage a Phase II focused on MECOM and [indiscernible] MECOM, where if we can reproduce the case report that we have met public today and before in the press release. If we have a single arm, not controlled and with less than hundreds of patients, and let's say, we can have around 30% of response like this type of response that we have seen, let's say, sustainable for some time, a couple of months, not -- then we could fit -- anyway, we'll discuss that further at the proper time with the agencies. But it would fit the criteria for, in case of success, of course, of an accelerated approval. So there is accelerated approval guideline at the FDA level, which are accessible for drugs in development in AML provided the type of response that we can do. So with a positive Phase II that we could finish by the end of 2024, ideally, of course, ideally, then we could have a package where we could discuss accelerated approval. But of course, we would be guided by the agency. We discuss step-by-step with the agency what would be the best development to do. And in fact, for promising drugs like that, there are actually systems so that the agency and the sponsor work hand in hand to try to have the most adequate development plan. So it's too early, of course, to do that today. We have to complete the Phase I. But the preliminary data are very encouraging and actually confirm what we have seen in human. So for one time, the transition in humans work or seems to work, which is encouraging. And so we wanted to share that with you because we know that you're are stakeholders or potential stakeholders in AB Science. So that's the message we wanted to convey. We spent already at 30 minutes for that, and we can now open the right for your questions.

[Operator Instructions] It seems that we have no question for the moment by phone.

Maybe to give time to the audience to prepare their questions, we could ask Christian Auclair, a distinguished experts in onco-pharmacology, to give his opinion. Likewise, Mr. Olivier Hermine, because he has a vast experience of multiple compounds, not only at AB Science, in this field. Christian, would you like to give your opinion?

Sure. So I would like to make some comments in terms of pharmacology. In fact, in a previous slide, it was a collection on pharmacology and molecular oncology. And during my career, I have had the opportunity to study many, many new compounds designed for treatment of cancer. And honestly, just to throw it up, AC BioScience is quite different of the other one, I would say, very, very. In fact, when we started to study such compounds, we would like to compare this molecule to other ones which are well known. And the first experiment we did is to compare with doxorubicin. Doxorubicin is an anthracycline many use for the treatment of cancer, including leukemia. And when we performed this experiment, we have been very, very surprised. Why? Because it is announced that molecules have a 104 higher efficacy compared to doxorubicin. So it's very, very unusual. The second example to focus on specificity of this molecule is the efficacy on blast coming from patients has been already mentioned but is a very important focus because we have tested this molecule of many blasts coming from patients, but we have refractory leukemia and were known to have the worst clinical outcome in the case. For instance, the people who have the so-called monosomy 7, that is to say the loss of chromosome -- loss of a part of the chromosome 5 mom and also the transformation of neurologic syndrome into leukemia. And this pathology are quite resistant to any treatment. And in fact, the blast coming from those patients are really killed by the AB Science molecule. The third example, and it has been presented by Laurent is the efficiency of the molecule to acute myeloid leukemia. This leukemia is adult leukemia, and very worse also clinical outcome. The people who have this leukemia is living only 1 year. And you have seen that this molecule is quite efficient on this kind of resistant leukemia. And the last point, and not the least, and I've spent 1 year looking at this, is the absence, total absence of hematological toxicology. And it's a key point for the use of this molecule in the clinics. You know that the [indiscernible] is not exactly the molecule of the same -- similar family, resulting in the strong hematological toxicity is the limiting factor of the use of this molecule. And the AB Science molecule don't display toxicity. And so we are very confident for the future, and we are absolutely sure that this new molecule will result in the improvement of the treatment of the patients.

Thank you, Christian. Any question by writing maybe?

Yes, we received a few questions regarding AB8939. So let's start with the question related to the market potential for this indication. Olivier, if you want to give us some flavor about the prevalence of acute myeloid leukemia and the MECOM maybe, which is the highlight so far?

Within patient with -- that we call non-eligible for high-dose chemotherapy, usually, this patient has a condition we call complex karyotype. And among this complex karyotype and genetic abnormalities make up, for example, like 10% of the patients. And we know even in first-line therapy patients, there is a high unmet medical need because either chemotherapy cannot work. And combination of Vidaza and venetoclax and you saw like [ 24 ] [indiscernible], which is not that long usually. So even in first-line therapy, patients has a real unmet medical need. And for younger patients, which kind of receive high-dose chemotherapy and [indiscernible] in the case of poor prognosis biological marker, this patient 40% to 50% or 60% of them, depending on the molecular abnormalities will relapse. So there is the half of the patients in the younger patients would need some treatment in case of relapse. And today, the new drug that shows some efficacy to cure patients are quite low, even in patient in which we use, for example, immunotherapy like [indiscernible]. We know there's a lot of complications, a lot of toxicity in this patient. So here that we do see a drug, which is able to increase the number of white blood cells, platelet number and decreasing the number of blasts without any toxicity, which may open a new avenue to treat patients with AML. And currently, we may say it may represent 50% of the market of leukemia.

Thank you, Olivier. So the positioning of the product would be, as we see on this slide, at this time, it can change, of course, refractory after multiple lines of chemotherapy, in particular in patients who are older and so cannot take those high dose of chemotherapy or in special-focused genetic group, which would be even better because it could accelerate the development of the compound. But we can do both at the same time in time, like 1 Phase II in MECOM and another 1 outside of MECOM. So we will see, and it's too premature, of course, to decide, but there are different options. Laurent?

I'll take another question regarding the data. Is it not too early to publish the data?

Well, classically, that we have to publish that to the statistic report. We can't publish it on to the case report. But obviously, we have to finished the Phase I study. But depending on what we will find at the end of the Phase I -- step 1, sorry, we may [indiscernible], depending on the result maybe to report in the scientific journal the result of the step 1. And if the results are mitigated, we can -- we shall do a step 2 or step 3. So we have to follow the rule of scientific good conduct, I should say, and wait to have more data and finish at least the step 1 to publish in the journal the data.

I would add that at the request of the investigator, not at our request, but the request of the investigator is to do a case report, scientific, not as we do today. Today is just information for stakeholders of AB Science so that they are aware of what we do in this platform and the value potentially of this platform. That's, I would say, corporate communication, which has nothing to do with the scientific communication. However, you have to know that at the request of the investigator, we treated these patients in Spain, he wants to do a case report. Now that, it's he who wants to do a case report. And then Olivier said, we will see if we do certifications. But abstracts, it may be more -- a case report is more appropriate. But definitely, it's important to inform people about that preliminary data [indiscernible] was important. They didn't wait the end of study to report some case report because it was a game changer. Now we would see with this compound. Too premature to say, of course, but it was important, according to [indiscernible], to inform you. Yes, Christian.

Yes. Just maybe to go back to the market. I think that this kind of treatment, which is the degree of toxicity can expand the market of leukemia because instead of proposed to the patients primarily a palliative treatment, maybe this patient may benefit to the new strategy. So it's very important to include this one.

About 60% of the patients went -- ask for a second cycle of treatment after a measure at 28 days, what happened with the other 50% of patients?

They progressed.

As most of the Phase 1 after the first dose -- after the first cycle, if there is no response what we usually do, we exit the patient from the study, and they are treated by other drug because most of the case there's no drug to provide to these patients. Unfortunately, the outcome is quite poor for this patient when do not receive any treatment. Because as you see, we will treat patients with previous line of chemotherapy and in most of these patients and again, the patients they could not receive anything and usually there so [indiscernible] quite rapidly. The thing is totally different for patients who are responding, which is very unusual at a very low dose in a Phase I study. You can see here, good 44% patient response. So legitimately, the investigator asks to do another cycle for this patient, and we are still moving during this Phase I, which is the classical way to progress in Phase I studies.

Another question. If everything goes well with the Phase II, when can we expect to have the product commercially available in the U.S., and what is the addressable market in the U.S.?

It's way too premature because we are just at the beginning. So we cannot answer this question. But just iteratively, in the best scenario, you have a Phase II, which is positive, you have an accelerated approval and then the drug is accessible to the patient. But after the Phase II, probably it's positive and then discussion with the authorities. Of course, there is always the possibility, as you know, to have access to compassionate use. But regulation differs across countries. So it's country by country.

I don't know if we have questions over the phone now.

Yes. We have a question by phone from [ Mr. Robert Vitkine ], a private investor.

First, I would like to thank you for informing us at this very early stage. You did not have to inform us, and its very kind and we appreciate it. It would be great if we had the same level of information for masitinib, your other product, and to know what is going on with masitinib? My question is regard financing. How are you going to finance the research set that you described for AB?

Robert, we could not hear you very well, but we understood your question. How we finance the program? We finance the program by raising money in the market as usual. So we do that for a long time now. And this -- but more specifically, we are very early stage, Robert, of this program, and we're not in Phase III with 1,000 patients in the Phase III. So this program, of course, requires more limited resources than others. However, it has -- it could potentially have a high impact. So to some extent, it's a highly, I would say, rewarding program for a biotech, and it's a plus-plus in the agenda for all of us. And I hope you would agree with us. So we are putting maximum priority on this program.

Are you going to 40% priority to masitinib?

Sorry, no, there is no -- there is no classification like that. We have 2 platforms, and it's important that we have 2 platforms because it diversify and derisk the company. So it's good that AB Science have this second platform. And by the way, the second platform is also not a mono product one because we have seen that there is a second product behind, which would be indicated in another indication. So it opens more options. But important to know, the mechanism of action is the same. It's microtubulin. Microtubulin is effective and demonstrated by some chemotherapy like Taxol, Taxotere. And it's not developable only in acute myeloid leukemia. It can be developed in breast cancer, it can be developed in very refractory cancers or in other indications. So it's not the topic of the day, but it -- we can create value with this platform with different compounds. Laurent, no more questions by right now?

Yes. No more question by phone.

So we hope that this presentation has given you a proper level of information to see what's going on here. So now as a conclusion, so the key message is we have a second platform. This platform is oncology and hemato-oncology-driven where the readout is quick and quicker than for the other program. As you can see, we treat with different cycles, but we measure the blast and the bone marrow after 28 days. And so it's rather quick. So it's ideal, of course, in terms of design. It opens strategies with Phase II maybe uncontrolled, to be discussed with the agencies, of course, to see if they would accept that. Definitely for us, we have in mind -- we have to finish the Phase I, reach the [ NCD ], have some proof of concept of activities, I would say, and then define with the agency proper design for Phase II that could get accelerated approval. So that's the strategy. That's what we have in mind. And we're trying to reach this point by the end -- discuss with the agency by the end of the year and deliver the Phase II by the end of next year. That would be the objective of the company. So we'll report to you for further, I would say, further data or further magnitude. But thank you for your attention, and I hope it has been informative for all of you. Thank you. Good evening or good morning -- no, good afternoon or good evening for the audience. Thanks.

Ladies and gentlemen, this concludes the web conference. Thank you all for your participation. You may now disconnect.