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 and Chairman of the Scientific Committee and an expert in hematology, heading the Hematology Department of Hôpital Necker in Paris. Also with me, Professor Christian Auclair, who is Co-founder as well and member of the Scientific Committee and expert in oncopharmacology. He co-headed CNRS, which is a well-known research center in France of excellence. With me also, Laurent Guy, who is our Head of Drug Discovery. Next slide, please.
As you know, for the ones who have an interest in AB Science, we have a known platform based on masitinib, where we develop masitinib in three 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. The MDA, microtubule destabilizer agent, with two compounds, one into clinical in phase I called AB8939, which is an intravenous administration form. Another one that we'll not present today, which is XXX coded, and will be developed not in hematology, but in oncology. Next slide, please. 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 them. Laurent.
Okay.
Please.
Thank you, Alain. Well, let's first have a quick look to the mechanism of action of our AB 8939 compound. This compound was identified during a phenotypic screening as a microtubule destabilizer. Microtubule are major target in oncology today. Let's shift to the picture. Like, in normal cells, you have two states for the cells. The quiescent state is cell are normal, not dividing. Cell dividing follow a cycle which we call it the cell cycle, which is dividing several phases: G1 , S, G2 , and M, basically. Microtubule are critical for this to achieve this cycle for the cell, proper cell division.
If you target this particular cellular process, you can stop and kill the highly dividing cells, and namely the cancer cells. Let's have a quick look. If you apply the AB8939 compound to a cancer cell, you can see that you will disrupt totally the shape of the cells. If you have a look to the picture with at the bottom of the slide, you see on the left normal cells with a beautiful network of microtubule, which is in the red on the left side. The cell treated with the compound, this beautiful network totally disappears, totally disrupted. This is translated in a block in the cell cycle, and this block in cell cycle induce a massive cell death.
Okay, this mechanism of action is not new because some very, very successful compounds in the clinic use the same kind of mechanism of action by targeting tubulin, namely the vinca alkaloid and the taxane derivative. The next slide, please. Okay. Okay. Our compound differ strongly from the chemical compound actually in clinic, like namely the vinca alkaloid and taxane compounds, which derive from a natural product. Vinca alkaloid was discovered in the late 1950s and taxane in the late 1970s. Our compound is a small chemical compound of low molecular weight. Natural compound have huge limit in their therapeutic application, which is due to the occurrence of resistance. There is several mechanism of resistance. Some, it's an...
This compound could be transported outside the cell by some efflux pump, which is this phenomena. It's called multidrug resistance phenotype. You can also have some enzymatic deactivation of several drugs from the vinca alkaloid with some enzyme. Myeloperoxidase is one example. You can also have some aberrant expression of several isoform of the tubulin, which is a basic component of microtubules, which is the target of the drugs. Remarkably, AB8939 is able to overcome all these mechanisms of resistance. 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 cells which are highly sensitive to all drugs, including AB8939, doxorubicin, which are common chemotherapy, and vincristine, which is tubulin targeting agent. If these cells express the MDR phenotype, you can see that they resist the doxorubicin or vincristine compound, but they remain highly sensitive to AB8939. Next slide, please. Next slide. After the characterization of the compound as a potent and multidrug agent able to overcome all the known mechanisms 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 we test them.
You can see in the A part of the slide at the bottom that, almost, approximately 70% of the blast isolated from this patient are sensitive to our compound. By comparison, if you consider the bottom part of the A panel, you see that conventional chemotherapy used into clinic for the treatment of AML, which is called cytarabinoside. Most of the patients resist this therapy. We have only one-third of the patients which are sensitive to our cytarabinoside. Okay. It's very interesting because our compound is able to overcome the resistance of the sample 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 a multidrug agent which is used in the treatment of leukemia, which is vincristine.
We can see that most of the patients are refractory to this kind of therapy, since only one-third of the samples respond to the vinca alkaloid drug. By contrast, we have still 70% of the patients which respond to our AB8939 compound. We have the same proportion of response if we consider refractory or relapse sample. 70% of the patients respond to the drug. Based on this ex vivo data, we move to in vivo experiments. Next slide, please. We test a number of different patient-derived xenograft model. The first one is a very aggressive acute megakaryocytic leukemia, which was grafted on nude mice. We treat these mice with our compound at a different dose. As you can see on the right part, you can see two mice.
One mice is untreated mice, and the color is represent the amount of cancer cell into the mice. You can see that after the treatment, cancer cell almost disappear totally from the mice. You can see, you can consider that the cancer is eradicated from the treated mice. If we analyze the bone marrow of these mice, we can see that the, what is the center, that the compound acts against the cancer cells into the bone marrow of the animals. This is a critical point to be successful into clinic. We test several other models including cytarabine models and so on. Each time it is very important to understand that we have a big success.
Each time we analyze, all compartments: blood, bone marrows, spleen, we totally eradicate the cancer cells from these compartments. Look, we have a great improvement in term of, therapeutics and, but also we have a strong impact in term of survival in the mice. Okay, we can, move to the next slide, please. This mice is just, this slide just exemplify the previous one. On the left part you have a cytarabinoside, the conventional chemotherapy resistance model derived from a patient which was grafted mice. You can see that the control mice on the bottom of the figure, you have a lot of colors that they are blue and green. This means that there is a lot of cancer cell in these mice.
If you consider the cytarabinoside, which is called Ara-C in green in the picture, there is no effect because it's a cytarabinoside cancer obviously. If you have a look to the AB8939 or AB8939 in combination with cytarabinoside in mice, you see that the cancer cells disappear. When we analyze the blood of these mice or the bone marrows, we have almost a complete response in terms of eradication of the cancer cells. Okay. This means that this compound works very well in the preclinical model. On the right part, we have another model which use azacitidine, which is another kind of agent, which is used in the older patient because it's less toxic than cytarabinoside. It's important to check if our compound could work in good adequation with this kind of conventional chemotherapy.
What you can see is that AB8939 and azacitidine, which is called Vidaza, works in the same way, exactly in the same way. When you combine both, you have a better effect obviously. The interesting point is that when you add our compound to the Vidaza, you don't increase the toxicity of the treatment. This is a critical point because one of the biggest limitation in the usage of chemotherapy is the toxicity for the patient. Next slide please.
Thank you, Laurent, for this very technical but informative description of the t alk in detail in my data. Now, Olivier is going to take over to describe the proof of concept we did in dogs first.
Thank you very much. As we know, mice model and PDX model are what we call the gold standard to assess the effect of drugs. We showed that AB8939 was very nicely working in this mice model. The real life malignancy is in here, the dogs, which is a very nice model of leukemia. We know that in dogs, drugs are very difficult to give to dogs because they are highly toxic. You can see here a dog with acute lymphoblastic leukemia, with cytopenia, as expected, because the bone marrow was involved with this blast. Upon treatment at only one cycle at low dose of 0.5mg/kg for five days, you can see that the dog improve his bone marrow function.
Because you can see that neutrophilic count increased significantly to almost the normal value. We do see the same thing for the platelet count and the hemoglobin was stable in this dog. It means that the drug was able to increase the normal bone marrow. Because the owner didn't want that we check the bone marrow on his dog, we could not assess the blast reduction. To see such effect means that we are clear at least some part of the bone marrow to allow the bone marrow to work again. Based on this preclinical studies and also on the dog models, next slide, we wanted to position AB8939 in acute leukemia.
Here I will recall you the landscape of acute leukemia. We split in two parts. The first part is the patients who are eligible to high-dose chemotherapy, including allogeneic cell transplantation. The second part is patients ineligible to high-dose chemotherapy because they are too frail to receive the drugs. Usually they are above 75 years old, we do not provide high-dose chemotherapy. For patients eligible for high-dose chemotherapy, the first line is usually high-dose chemotherapy, including anthracyclines and high-dose Ara-C. Patients bearing some mutations like FLT3, we may add some FLT3 kinase inhibitor for these patients. In the second line for these patients in case of relapse, usually we treat these patients with allo stem cell transplantation. Before they receive either high-dose chemotherapy or the combination of 5-azacitidine and venetoclax.
There's no drugs approved to treat these patients. For elderly patients or ineligible for high-dose chemotherapy, the standard of care today is 5-azacitidine hypomethylating agent in combination with venetoclax, which is an anti proapoptotic drug by blocking BCL2. In second-line therapy and third-line therapy, there is no registered drug in these patients. You can see here we have a high unmet medical need in patients with acute leukemia because virtually 60% of the patients overall will relapse after the third or second-line therapy. We decided, next slide, to go in a phase I study based on the results we obtained in mice model. It is a classical phase I study for acute leukemia.
We did include patients who are refractory or in relapse of AML in second or third line therapy, receiving or not high-dose chemotherapy in first-line therapy. We do also include patients with refractory high risk myelodysplastic syndrome, and the patients are not eligible for allogeneic stem cell transplantation at the time of inclusion. The step one of the study was to increase the dose for three days of treatment from 0.9mg per meter square, three patients at each dose. In case of no toxicity, we move to dose 2, 3, 4, 5, 6, and 7, 1.8, 3.6, 9, 12, and 16mg per meter square. The second step of the study is to increase the length of treatment to from three days to 14 days.
We will start at the defined MTD dose in the step 1, dose before. Then we move to the second dose at the MTD of the three days treatment. Then we will move to the phase III, depending on what we found in the phase II, in combination with azacitidine, which is standard of care of leukemia today in patients not eligible for the chemotherapy. We will do the combination for 14 days. Also we will do a treatment for 28 days in case of a good response and good tolerability in the step 2 of the study. Next slide. Here, which is unusual to show you some data in early phase I study, and we think that we do observe is quite striking in this group of patients.
Here it is, one of the first case patient at the low dose of 0.9mg per meter square. This patient is an elderly patient of 81 years old with a de novo acute myelogenous leukemia, with we call intermediate risk prognosis, refractory to three line of treatment: 5-azacitidine, venetoclax, and high-dose Ara-C. This patient entered the phase I study. Very interestingly, after the first cycle of three days, we do see a reduction of blast count from 15% to 8%, which we call a partial response. We did a second cycle of treatment to this patient. 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.
Don't forget that these patients are suffering not only of the blast in the bone marrow, but mostly on the bone marrow failure as a consequences of marrow involvement. Here that we do see a reduction of blast and improvement of the bone marrow activity. No adverse events were seen in this patient overall. The second case report is also very interesting because at the step of 1.8mg per meter square, so the patients with a secondary AML, which has a very poor prognosis AML. As expected in secondary AML, he had some cytogenetic rearrangement, including here the MECOM, the EVI1 gene, which usually is associated to refractoriness to any kind of treatment. As expected, this patient was refractory to azacitidine treatment.
Very interestingly, after two cycles of three days, spaced by 20 days interval, we do see this patient, a drastic decrease of blast in the bone marrow after one cycle from 55% to 5%, which is the limit of the complete response in term of blast reduction. After the second cycle, the blast remained stable at around 10%. 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 infection. Also we do see an increase of platelet count from 3,000 to 12,000 per microliter. Also here we have no adverse event relative to the treatment by AB8939 . Next slide, please.
If we can summarize what we do see at this very early stage of this phase I study. First, we do see no drug-related adverse reaction superior to grade 2 in this patient to date. We have so far no toxicity. Interestingly, we do observe 40% of patients with stable disease or that to respond by reducing the blast count. As a consequences, investigator ask for a more cycle of treatment for this patient. We do see also, which is very striking, 70% of the patients had an increase of the platelet number. More dramatically, 90% of the patients increased 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.
Overall, next slide. I can say at this level that we have no extra hematological toxicity, no hematological toxicity, and with even an improvement of the bone marrow failure with an increase of platelet and neutrophils, which is very unusual in leukemia treatment. We do observe at low dose a significant reduction of the stability of the blast count in this group of patients, even in patients with high risk acute leukemia, usually refractory to any treatment like EVI1 AML. 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 failure, which allow to have a normal quality of life for this patient.
However, we cannot rule out that when we would see an increase of the dose, we'll be able, as we have observed in dogs and mice, to kill all blasts and to see a normal bone marrow recovery and a full cure of these patients. Probably, based on the early results, we may focus in the future to treat AML with poor prognosis karyotypes or molecular events like EVI1 rearrangement. In this group of patients, there is a real unmet medical need with no efficient treatment. Also, as we have seen in mice model, combination with azacitidine may also increase further the response rate in these patients with this drug.
Thank you. Thank you, Olivier, for the description of this preliminary results of our clinical study. As you have seen, it's only the step one, with three days of treatment. Whereas the protocol will continue of course. After we have defined maximum tolerated dose, we'll move to 14 days. After we form the MTD at 14 days, it will move to 28 days. Also in parallel, 14 days in combination with azacitidine, because we saw in mice a synergistic in fact effect with azacitidine. The ultimate goal of the phase I is not only to reach the MTD, but also to see.
How I would say, what's the best treatment in combination or not in combination. But here it's extremely preliminary data at three days of treatment, three days only. And we measure the efficacy by doing a bone marrow sample at 28 days. So it's three days of treatment and nothing 28 days bone marrow, and that's it. And then an extension of another three days, but only three days. 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 step 3 or step 4.
That's what we had in mind, to mimic the mice, by the way, that were treated for not three days, but, how many days, Laurent, it was.
five days.
Five days may, and sometimes more. It was unexpected at this very little dose first and very few number of days of treatment. It was surprising, very surprising, of course. Having said that, we move to the... Yes. Thank you, Laurent. To the next slide, which is the patent protection. It's a new platform, we have a new patent, of course, covering the composition of matter of this compound, and we are protected until... The compound is protected until 2036, and the patent is in deliver. It's a completely new chemistry, which does not infringe. No, no patents, nothing. We copied nobody.
We have on the results that we have acquired so far on what is it called, EVI1 or MECOM, which is a special rare arrangement, special genetic of patients. We file a new patent. 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 was based on genetics because it makes a lot of sense for them. If we can prove that this compound is treated for MECOM, that's an additional discovery unexpected because MECOM are refractory to all kind of chemotherapy, so it's completely new and innovative and patentable.
Then we can of course develop in this specific population. There is another protection which is the orphan drug designation that we have at the FDA level, and that protects product. The patent strategy is strong. Let's move to the next slide, Laurent. What's the next step? 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. We can still think of the strategy further. How much time would be needed to complete phase I?
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 have their patients included in the study. It's good news because it can be done rather quickly, of course. It attracts the attention of everybody. We think we can initiate the phase II by before the end of the year. We had planned a phase I, II with a mini phase II in the phase I.
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 we can do it. In this phase II, we could ambition to have different ones. One option is to focus on where it works the best and where the unmet medical need is the highest, which would be today the MECOM that we might discover new genetic situation where the product could be very effective.
Suppose we have the MECOM and only the MECOM, we could envisage a phase II focused on MECOM and only on MECOM, where if we can reproduce the case report that we have made public today and before in the press release. If we have a single arm, not controlled, and with less than 100 patients, and let's say we can have at around 30% of response, like this type of response that we've seen. Let's say sustainable for some time, a couple of months. We could fit in any way we have to discuss that further at the proper time with the agencies. It would fit the criteria for, in case of success of course, an Accelerated Approval.
There is Accelerated Approval guideline at the FDA level, which are accessible for drugs in development in AML, provided that they have the type of response that we can do. 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 actual approval. Of course, we would be guided by the agency. We discuss step by step with the agency of what would be the best development to do. 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.
Summary, of course, to date today, we have to complete the phase I, but the preliminary data are very encouraging and actually, confirm what we have seen in animals. It, for one time, the translation animal humans works, seems to work, which is encouraging. We wanted to share that with you because we know that you are stakeholders or potential stakeholders in AB Science. That's the messages we wanted to convey. We spent already 30 minutes for that, and we can now open the rest for your questions.
Ladies and gentlemen, if you wish to ask a question, please press zero and one on your telephone keypad. You can also use the platform to send your questions. As a reminder, ladies and gentlemen, if you wish to ask a question by phone, you have to dial zero and one on your telephone keypad. Seems that we have no question for the moment by phone.
Maybe to give time to the audience to prepare the questions, we could ask Christian Auclair, who is a distinguished expert in onco-pharmacology, to give his opinion. Likewise, Olivier, Professor Olivier Hermine, because he has a vast experience of multiple compounds and not only AB Science, in this field. Christian, would you like to give your opinion?
I would like to make some comments in term of pharmacology. In fact, in a previous life, I was a professor of pharmacology and molecular oncology. During my career, I have had the opportunity to study many, many new compounds designed for treatment of cancer. Honestly, the drug of AB Science is quite different to the other one, and I would say very, very different. In fact, when we start to study such compound, we would like maybe to compare this molecule to other one, which are well known. The first experiment we did is to compare with the doxorubicin. Doxorubicin is a anthracycline, mainly used for treatment of cancer, including leukemia. When we performed this experiment, we are very, very surprised. Why?
AB Science molecules have a 100-fold higher efficacy compared to doxorubicin. It's very unusual. The second example, to focus on specificity of this molecule is the efficacy on blast coming from patients. It has been already mentioned, but is very important to focus because we have tested this molecule of many blasts coming from patients, but we have refractory leukemia and well known to have a worse clinical outcome. In the case, for instance, of the people who have the so-called monosomy 7, that is to say, the loss of one chromosome or the loss of a part of the chromosome 5, and also the transformation from myelodysplastic syndrome into leukemia. These pathology are quite resistant to any treatments.
In fact, the blasts coming from those patients are readily killed by the AB Science molecules. The third example, and it has been presented by Laurent, it's efficiency of the molecules on the megakaryocytic leukemia. This leukemia is adult leukemia and a very worse also clinical outcome. The people who have this leukemia are living only one years. You have seen that this molecule is quite efficient on this kind of resistant leukemia. The last point, and not the least, I think Olivier can assist, is the absence, total absence of hematological toxicity. It's a key point for the use of these molecules in term of clinics. You know that the vinorelbine, for instance, that is a molecule of the same similar family, results in a strong hematological toxicity.
It's a limiting factor of the use of this molecule. The AB Science molecules don't display toxicity. We are very confident for the futures, and we are totally sure that this new molecule will result in the improvement of the treatment of these patients.
Thank you, Christian. Any question by writing, maybe?
Yes, we received a few questions regarding AB8939. Let's start with the question related to the market potential for this indication.
Now, Olivier, you want to give us some flavor about the prevalence of acute myeloid leukemia and the MECOM maybe, which is the highlight so far?
Right. With age, in patients with that we call non-eligible for high-dose chemotherapy, usually this patient has Christian recalled before, a complex karyotype. Among this complex karyotype and genetic abnormalities, MECOM, for example, represent something like 10% of the patients. We know even in first-line therapy patients, there is a high unmet medical need because high-dose chemotherapy cannot work. Combination of Vidaza and venetoclax have just unlike 24% response rate which does not last long usually. Even in first-line therapy in this group of patients, there's a real unmet medical need.
For younger patients, which can receive high-dose chemotherapy and allogeneic stem cell transplantation in case of poor prognosis biological marker, this patient, 40%-50% or 60% of them, depending on the molecular abnormalities, will relapse. There is a half of the patients in the younger patients who need some treatment in case of relapse. Today, the new drugs that show some efficacy to cure patients are quite low. Even in patients in which we use, for example, immune therapy like CAR T cells, we know there's a lot of complications, a lot of toxicities, in these patients.
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. Currently, we may say it may represent 50% of the market of leukemia.
Thank you, Olivier. The positioning of the product would be, as we see on this slide, at this time, that 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. We can do both at the same time in parallel, like one phase II in MECOM and another one outside of MECOM. We will see. It's too premature, of course, to decide. There are different options. Laurent. I take another question regarding so this data. Is it not too early to publish this data?
Well, classically, that we to publish as a scientific report, we can publish it onto the case report. Obviously, we have to finish the phase I study. Depending on what we will find at the end of the step 1, we may have vision, depending on the result, maybe to report in a scientific journal the result of the step 1. If the results are mitigated, we can publish at the step 2 or step 3. 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 who treated these patients in Spain, he wants to do a case report. Not us. It's he who wants to do a case report. As Olivier said, we will see if we do some publications. Abstract is maybe more. A case report is more appropriate.
Definitely, it's important to inform people about that similarly as preliminary data in CAR T cell was important. They didn't wait the end of the study to report something important CAR T cell because it was a game changer. We will see with this compound. It's too premature to say, of course, but it was important communicatively to inform you. Yes, Christian.
Just maybe to go back to the market. I think that this kind of treatment, which is a degree of toxicity, can extend the market of azacitidine because instead of propose to the patient that is in a treatment, a palliative treatment, maybe this patient may benefit from the new strategy. It is very important to include this point.
About 50% of the patients, asked for a second cycle of treatment, for, after a measure at 28 days. What happened with the other 50% of patients?
They progressed.
They progressed. The, you know, as most of the phase I 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 is no drugs to provide to these patients. Unfortunately, the outcome is quite poor for these patients when they do not receive any treatment because as you see, we treat patients with previous line of chemotherapy. Most of these patients and elderly patients, they could not receive anything. Usually, death occur quite rapidly. The thing is totally different for patients who are responding, which is very unusual at very low dose in phase I study. You can see here because 40% of patients respond.
Legitimately, the investigator ask to do another cycle for these patients. We are still moving during this phase I. It's a classical way to progress in phase I study.
Another question. If everything goes well with the phase II, when can we expect to have, the product, commercially available in the U.S.? What is the addressable market in the U.S.?
It's way too premature because we are just at the beginning, so cannot answer this question. Just theoretically, 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. It's after the phase II, provided it's positive, and then discussion with the authority. Of course, there is always the possibility, as you know, to have access through compassionate use. Regulation differs across countries, so it's country by country, I would say.
I don't know if we have questions, over the phone now.
Yes, we have a question by phone from Mr. Robin-Robert Witkin from a private investor. Please go ahead.
Good evening, everyone. First, I would like to thank you for informing us at this very early stage. You did not have to inform us, and it's very kind, and we appreciate it. It would be great if we had the same level of information for masitinib, your other product. To know what is going on with masitinib. My question is regards financing. How are you going to finance the research that you described for AB Science? Thank you.
Robert, we could not hear you very well, but we understood your question. How we finance a program? We finance program by raising money on the market as usual. We're, we do that for, you know, a long time now. More specifically, we are very early stage, Robert, of this program, and we are not in phase three with 1,000 patients in the phase three. This program, of course, requires more limited resources than others. However, it could potentially have a high impact. To some extent, it's a highly, I would say, rewarding program for a biotech, and it's a plus in the agenda for us.
I hope you would agree with us. We are putting maximum priority on this program.
Are you going to give the same priority to masitinib?
Sorry. No, there is no classification like that. We have two platforms, and it's important that we have two platforms because it diversify and de-risk the company. It's good that AB Science has this second platform. By the way, this 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. It opens more options. Important to know, the mechanism of action is the same. Microtubule. Microtubule is effective and demonstrated by so key 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. It's not the topic of the day. But, you know, We can create value with this platform, with different compounds. Laurent, no more questions by writing?
Yeah, no more question by phone.
We hope that this presentation has given you a proper level of informations to see what's going on here. Now, as a conclusion, 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 in the bone marrow after 28 days, and so it's rather quick. 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 MTD, have some proof of concept of activity, they would say, and then define with the agency proper design for a phase II that could get a Breakthrough approval. That's the strategy, that's what we have in mind. we're trying to reach this point by the end, discuss with the agency by the end of the year and deliver a phase II by the end of next year. That would be the objective of the company. we'll report to you for further, I would say, further data or further milestone. Thank you for your attention and hope it has been informative for you. Thank you. Good evening, or 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.