Good afternoon. My name is Chris, and I will be your conference operator today. I’d like to welcome everyone to the Aptos Biosciences’ Conference Call for the Third Quarter Ended September 30, 2020. At this time, all participants are in a listen-only mode. After the speakers’ remarks, there will be a question-and-answer session.

[Operator Instructions] As a reminder, this conference call may be recorded. I would now like to introduce Ms. Susan Pietropaolo. Please go ahead..

Thank you, Chris. Good afternoon, and welcome to the Aptose Biosciences conference call to discuss financial and operational results for the third quarter ended September 30, 2020. I am Susan Pietropaolo, Communications Representative for Aptose Biosciences. Joining me on the call today are Dr. William G. Rice, Chairman, President and CEO; Mr.

Gregory Chow, Executive Vice President and Chief Financial Officer; Dr. Jotin Marango, Senior Vice President and Chief Business Officer; Dr. Rafael Bejar, Senior Vice President, Chief Medical Officer.

Before we proceed, I would like to remind everyone that certain statements in this call will include forward-looking statements within the meaning of U.S. and Canadian securities laws.

Forward-looking statements reflect Aptose’s current expectations regarding future events that are not guarantees of performance, and it is possible that actual results and performance could differ materially from the stated expectations.

They involve known and unknown risks, uncertainties, and assumptions that may cause actual results, performance, and achievement to differ materially from those expressed. To learn more about these risks and uncertainties please read the Risk Factors set forth in Aptose’s most recent Annual Report on Form 10-K and SEC and SEDAR filings.

All forward-looking statements made during this call speak only as of the date they are made. Aptose undertakes no obligation to revise or update the statements to reflect events or circumstances after the date of this call, except as required by law. I will now turn the call over to Dr. Rice, Chairman, President, and CEO of Aptose Biosciences. Dr.

Rice?.

Thank you, Susan. I’d like to welcome everyone to our call for the third quarter ended September 30, 2020. We are well into the year, which for Aptose, has been a year of advancing our clinical programs.

with our recently initiated AML clinical trial, we now have three clinical studies underway; two studies with our FLT3 and BTK kinase inhibitor CG-806, one study in patients with acute myeloid leukemia or AML, and the other study in patients with chronic lymphocytic leukemia or CLL and non-Hodgkin’s lymphomas.

And the third trial is ongoing with our MYC inhibitor APTO-253 in patients with AML and MDS.

We now are at a point, where we are operating smoothly across the board, expanding our drug substance and drug product manufacturing, working with our clinical sites to enroll the right patients for each trial, accelerating the pace of development and treating a spectrum of patients with very challenging, relapsed or refractory hematologic cancers.

The third quarter was one of blocking and tackling to position our agents for success. We expect to 2020 to be one of continued execution, especially as we treat more patients at higher doses and begin to generate additional pharmacokinetic and pharmacologic data.

And before we discuss the progress in each of our three clinical programs, let me remind you that ASH is only a few short weeks away. So today, we will keep our remarks as high-level and qualitative and then we will aim to share more quantitative findings during ASH. Having said that, first let’s start with our most recent news.

In October, we announced the initiation of dosing in our Phase 1 a/b clinical trial of CG-806 in patients with relapsed or refractory AML, which as we know is a very serious cancer of the bone marrow and blood, and that carries a poor prognosis.

CG-806 or just 806 inhibits the wall type and mutant forms of FLT3 and BTK, and suppresses select clusters of kinases that drug oncogenic segues that are operative in AML, including the FLT3, PD- EGFR alpha, CSF1R, AKT, RAS, ERK, STAT and SYK pathways.

And by the way, whom we refer to SYK, that is the spleen tyrosine kinase inhibitor spelled SYK, not SICK. As you will recall, 806 is the only known clinical agent that potently inhibits both FLT3 and BTK, which gives it a broad potential across the spectrum of lymphoid and myeloid hematologic malignancies, including AML.

Our AML trial is a Phase 1 a/b multicenter open-label dose escalation study of safety, pharmacodynamics and pharmacokinetics of CG-806 and ascending cohorts with a three plus three design to determine the maximum tolerated dose or the recommended Phase 2 dose in patients with relapsed or refractory AML.

With this before, but I want to quickly remind you again that these relapsed or refractory patients are very ill.

And before joining the 806 trial, they already have been treated with and failed other FLT3 inhibitors, such as gilteritinib and or midostaurin and other drugs such as venetoclax and have failed or are intolerant to the available approved therapies, but standard of care for relapsed or refractory AML patients is insufficient for many patients, often not durable and leading to resistance.

So despite recent advances, there remains a tremendous unmet need in relapsed or refractory AML patients. In this AML trial with 806, the FDA allowed us to skip the two lowest dose levels of 150 mg and 300 mg. And to initiate dosing at a starting dose of 450 mg BID, which as I mentioned in our last call was good news for Aptose and for 806.

We requested the 50 mg starting dose in AML patients because that dose, when administered to CLL patients in a separate clinical trial appeared safe, well tolerated and achieved plasma levels that effectively inhibited for FLT3 activity, which is a key driver of AML.

Also at the 450 mg dose in humans with CLL, we observed steady state plasma levels and the same range as the exposure levels observed in our preclinical work led to cures of AML in mice and with no observed toxicity. It was these observations in their totality that led to the starting dose of 450 mg.

I’m pleased to report that since we announced dosing of our first patient in the AML trial, we efficiently enrolled additional patients in this cohort. Investigators at major clinical sites are eager to place the relapsed or refractory AML patients on 806 and they have patients available when slots open.

The kinase the traditional three plus three dose escalation, but it also allows us to enroll more than the minimum three patients at each dose if appropriate. Five clinical sites currently are screening patients for the trial, including high caliber, academic cancer centers and specialty care regional sites.

Having several highly engaged clinical sites, now treating patients, we are pleased with the pace of enrollment. Some of you have asked us specifically, which type of AML patients holding this study. It always has been our intention.

And now, we are enrolling patients having AML with the FLT3 ITD mutation, referred to as FLT3 positive AML, as well as patients with wildtype FLT3. In addition, we believe 806 is a compelling candidate for the fragile AML patient population and we are hopeful that 806 can provide benefit to the very ill, relapsed and refractory AML patients.

We will share up-to-date specific AML trial at a corporate update that we plan to hold during the ASH timeframe. For more information on the AML trial and clinical sites that are recruiting patients, please visit clinicaltrials.gov.

Now, let’s turn to our ongoing Phase 1 a/b dose escalation study of 806 in patients with B-cell malignancies, including CLL and non-Hodgkin’s lymphomas again, in relapsed and refractory patients, who have failed or are intolerant to current therapy.

Since our last call, we escalated to the fifth dose level of 750 mg and we continue to treat patients at the 600 mg and 750 mg dose levels. Importantly, at the 750 mg dose, we are focusing exclusively on enrolling only relapsed or refractory CLL patients. At CLL, as for we have observed indications of on-target activity and prior patients.

In addition to inhibition of BTK and the induction of on-target lymphocytosis that we reported previously, we have observed nodal reductions in CLL patients.

We fully understand that these are deep refractory patients that may require extended time to truly respond if ever, but we are hopeful that such findings will pretend formal responses as we accrue additional CLL patients over time and we plan to provide you with additional during ASH, which is just a few weeks away.

Depending on the load level of clinical activity in specific subgroups and this dose escalation phase, we may enroll patients across expansion studies that include sub-populations with different genotypic or phenotypic properties.

In conjunction with the CLL trial and to facilitate expansion studies, we have developed a scaled-up manufacturing process for 806 capsules and are transitioning to machine builds, also called automated pill capsules and these are being introduced into the trial.

This step reduces risk to the 806 program and will allow us to place additional cancer patients on 806. for more specific information on the B-cell malignancy trial and the clinical sites that are enrolling patients, please visit clinicaltrials.gov. Again, we will share a more in-depth update of our entire 806 program with you during ASH.

Speaking of ASH, as we announced last week in our press release, we will be presenting two posters on Saturday, December 5; one on CG-806 and one on APTO-253 and there will be another poster on at CG-806 presented on Sunday by our research partners at the City of Hope and the Oregon Health & Science University or OHSU.

details were in the press release that we distributed last week and the abstracts and sales are now available online. Overall, we’d execute carefully and diligently in multiple parallel programs and we believe this ASH Conference represents yet another milepost in our study development of 806.

As we have stressed before, we believe that 806 is a drug candidate like no other with singular biology and a broad array of potential indications. based on our work to-date, we remain confident in the potential of 806 to benefit for cancer patients and build value for Aptose shareholders.

Now, let me bring you up-to-date on the status of APTO-253, our second clinical candidate currently in a phase 1b trial for AML and MDS. to remind you, APTO-253, or just 253, as I’ll call it is a MYC inhibitor. And the MYC oncogene is a major driver of cancer cell proliferation, including hematologic cancers.

In fact, it’s one of the most coveted drug targets in cancer and researchers have been seeking a safe MYC in many years. For our phase 1 clinical protocol, 253 is being administered once weekly over a 28-day cycle at ascending doses in patients with relapsed or refractory AML or high-risk MDS until the maximum tolerated dose is reached.

The study designed to then transition as appropriate to single agent expansion cohorts in AML and/or MDS. I’m pleased to report that our Phase 1 clinical trial of 253 hitting well. thus far, we have completed the 28 dosing and the first four dose cohorts.

Since our last call, we’ve enrolled multiple patients at dose level five of 150 mg/m2, which is a 50% increase over that of dose level four and 253 continues to be well-tolerated. Despite interest in MYC inhibition as a target, 253 has been advancing quietly under the radar screen, partly because nobody knows what to expect from a MYC inhibitor.

We’re learning more as we proceed and we continue to believe 253 is an interesting and valuable asset four day of investment. at these higher doses, we hope to see sustained MYC inhibition and began to see clinical responses. We’ll be able to talk to you more about 253 during our event at ASH.

For those of you interested in learning more about the trial specifics and enrollment criteria, please visit clinicaltrials.gov. Finally, quickly touch on other corporate highlights. We’re grateful to be a part of recent and Upcoming Healthcare Banking Conferences. During the quarter, we presented at the Canaccord Genuity, H.C.

Wainwright, cantor and Oppenheimer conferences, or we hosted a full schedule of one-on-one meetings. We also have been invited to the Stifel healthcare conference, where we will be hosting one-on-one meetings next week, and we will be participating in the Piper Sandler healthcare conference in early December.

And now, we’ll turn the call over to our Executive Vice President and Chief Financial Officer, mr. Greg Chow, who will review results for the quarter..

Thank you, bill and good afternoon, everyone. We ended the quarter with approximately $133 million in cash, cash equivalents and investments compared to approximately $83 million at June 30 of this year.

During the quarter, we utilized approximately $8.3 million of cash in operating activities, which were attributable to activity surrounding 253 and 806, as well as general and administrative purposes.

based on current operations, cash on hand at September 30, provides the company with sufficient resources to fund all plan company operations, including research and development into Q1 of 2023. Moving on to the income statement. We had no revenues for the quarter.

research and development expenses were $7.5 million for the quarter and attributable to 806 and 253 clinical trial costs manufacturing for clinical trials, including continuing development on improving GMP formulations for 806 and 253, and personnel costs for headcounts supporting clinical trials and manufacturing activities and research studies.

general and administrative expenses for the quarter were $5.8 million and our net loss for the quarter, which is $13.2 million or $0.15 per share. More detailed information can be found in our filings on EDGAR and SEDAR. I will now turn the call back over to Dr. Rice.

Bill?.

Thank you, Greg. I’ll remind everyone that on the line, we also have with us, dr. Jotin Marango, our Chief Business Officer and dr. Rafael Bejar, our Chief Medical Officer. as we open the call for questions, please feel free to pose a question to any of us. operator, if you could, please introduce the first question..

Thank you. [Operator Instructions] Your first question comes from the line of Gregory Renza with RBC Capital Markets. Your line is now open..

Hey, good afternoon, good evening, Bill and team. Congratulations on all the progress and thanks for taking my questions. Bill, I just wanted to start, of course, if the natural question is really, some of the expectations that you are able to set for the upcoming events and ASH data.

Now, I expect your acknowledgement of speaking more qualitatively, but maybe, we can just start on the AML side, as you mentioned, certainly enrolling in October, maybe just remind us some of those data collection points and what you think could be meaningful or what to look out for just in light of where we will be just several weeks post the start of those patients in the trial.

Thank you..

All right. Hey Greg, thanks for joining us for the question. So in particular, on the AML side, yes; as we look back to the third quarter, we had the IND allowed that allowed us to go into the AML patient population. We then had to, as I mentioned in the blocking and tackling, get all the clinical trials up and running, ready to sites, IRB approvals.

And in the era of COVID, it’s a little bit more challenge, but the team did that and we actually enrolled our first patient during Q3. Since that time, we’ve had active enrollment, the clinical sites have been very active. I’m not speaking directly to the number of patients that we’ve put on the study yet, I can say it’s definitely more than one.

And hopefully, we’ll be able to collect sufficient data between now and then to give you a snapshot of what we’re seeing in these patients. Of course, we hope that the drug is going to be well tolerated at the 450 mg dose level. It has been tolerated well in the past at that dose level. But the patient population and these patients are very sick.

So that’s the first we hope to see that. we will watch for the pharmacokinetics, determine whether or not, it is equivalent to the pharmacokinetic parameters that we saw in the CLL trial. And then beyond that, we will watch for any of the other CBC counts. So hopefully, we’ll be looking at the blast counts of the patients.

But I’ll also remind you that these patients, as they come off their other than washout, these patients progress very rapidly. These are very sick patients. Oftentimes during that two-week wash out, they go on hospice, but then you get them on the trial.

And during those first couple of weeks, while you’re treating them, you’re allowing your drug to get up to its steady state levels. And we typically don’t reach that until the end of week one or week two.

So, we hope the patients are able to stay on during that period, give the drug time to reach those steady state levels and we actually hold some level of benefit in these patients. I don’t know if we’ll have time on these patients to really see if there are any truly meaningful data. But we’re several weeks away.

We will continue to collect the data between now and then, and then we’ll indicate where we are at that time. I don’t want to either overpromise or underpromise. What we’ll do is present you what we have at that time.

But I will remind you that the data will not be “verified,” because it takes at least a month back at your clinical trials and the sites to collect the data, verify it through your clinical operations group, and then be able to present verified data.

So anything that we discuss will be non-verified and preliminary data at that time, but we are very helpful for the AML. Hope that answers your question..

It sure does, Bill and if I may just want to follow up on the CLL side, I think if you could just remind us and certainly heard the commentary on expansion potential on cohorts and subpopulations.

Could you guys remind us of your liberty on the plans for a 900 mg dose level and the cohort there, just in terms of how we be thinking about that of course, with respect to understanding cards at the turnover in the current dosing levels, but I just want to get a refresh on your thoughts there? Thank you..

Well, in this protocol, we do have the ability to go to a 900 mg dose level, if the 750 mg is – dose level is determined to be safe that requires, tends to complete at least 28 days of dosing. Currently, we’re at the 750 mg dose level.

We haven’t released any additional information on that level or the lower dose level to 600 mg, except to say that we do have patients on the 600 mg and the 750 mg. during ASH, we will be presenting data that we have on these patients.

In particular, we want to be able to show that the pharmacokinetics, we want to hopefully show that these are rising as we continue to escalate the patients. And then we’ll be able to speak to whether or not we’ll be able to go up to the 900 mg level or not.

If we are, if everything is safe and if we are able to move up, we will, provided we are getting – continuing to get increased levels of exposure. As we’ve gone from 150, 300, 450, 600, and 750. if we can show that we’re continuing to get additional exposures, then we would go up to 900.

If it turns out some reason we cannot go to 900, we would look to 750 to say, is that our recommended phase 2 dose, if for some reason, 750 turned out to be too toxic for some reason, then we would back down to the 600, which we have shown is safe. So, all of those are possibilities at this time. That’s correct..

Thanks, Bill. Looking forward to the updates in December..

Thank you..

Thank you. The question comes from the line of John Newman with Canaccord. your line is now open..

Hi guys. Thanks for taking my question and looking forward to the data upcoming in ASH here. Bill, I just wondered if you could comment I think during your prepared remarks, you talked about some nodal reductions in CLL patients.

Just wondering if you could elaborate on that just a little bit more?.

Sure, John. thanks for the question. So, we refer to these nodal reductions. Of course, mostly, some people them nodal reductions, some call them tumor reductions. So, whenever a patient comes on the study, they get their initial scan before they start dosing with any of the drugs.

And at that point, they identify the target lesions that they’re going to follow throughout the therapy and typically, these are lymph nodes. And so we will call it, refer to them as either nodal internal reductions and I’m going to be really careful here, because we don’t want to overplay this or underplay it.

So, we’ve been asked repeatedly whether or not we’re getting nodal reductions in any of these patients. And what I can say is, yes, we have seen reductions in more than one patient, but as of yet, they are not at the level of formal responses. If they were, we would have said formal responses.

So, we have cautious optimism that we have been able to see some decreases. but again, we’re very realistic. These are deep relapsed refractory patients, who had failed all of the drugs out there, including many of our competitor drugs before they come onto our trial or we have seen reductions.

We would be thrilled if those reductions continue and if they ever reach the level of a formal response, but they may not, they may plateau off or the patients could continue to progress at any time. So, that’s why we’re being very careful and very candid in saying, yes, we’ve seen nodal reductions.

but it is not at the level – the formal level of true reduction at this point.

Did that adequately answer your question or did you want to follow up?.

Yes. And I had one quick additional question, which was for the AML study, you mentioned at the beginning of the call that you are looking to enroll both FLT3-ITD as well as wildtype.

Is there any specific ratio that you’re looking to achieve or are you simply looking to include both types of patients with those – with that mutational or excuse me with those mutational steps?.

Well, again, we’ve been very upfront about this and we believe this drug can treat patients with both wildtype, as well as FLT3 positive of what the ITD mutation and FLT3. We would like and linked in the early dose cohorts the number of wildtype patients, FLT3 wildtype to a minimum.

We’d like to get one, maybe two on there, but we’d like to have the majority of the patients being FLT3-positive patients. why? we know that the patients who have, FLT3 positive, tend to react or respond more quickly to a FLT3 inhibitor. And so ITD used the word low-hanging fruit, but it really is.

Those would be what you would expect to be the most responsive patients to a FLT3. So, we clearly, want to get multiple FLT3-positive patients on each of these dose levels, but as we go, we continue to dose escalate and get to the higher dose levels. And once we’re able to show activity in the FLT3-positive patients, assuming that we will.

We will then want to transition over and get more of the FLT3 wildtype patients on this study as we continue to dose escalate, because it might take additional levels of drug to be effective against the patients with wildtype too..

Yes. Great..

Thank you, John..

Thank you..

And our next question comes from the line of Alethia Young with Cantor Fitzgerald. Your line is now open..

Hi. Thank you for taking my question. This is Emily on for Alethia. I was just wondering, what have you learned from the CLL study so far that has kind of helped you speed up the process and AML besides the starting dose that you mentioned and patients, do you think you could potentially enroll in the CLL study by NASH? Thank you..

Hi, Emily. please tell Alethia we said hi. So, what have we learned? So, as you said, the starting dose, that was very important for us, but also from the plasma that we collected from those patients, we learned that the exposure levels, we’re at or above the levels that gave us true responses in animal models.

So, they cured animals of AML that was FLT3-ITD or FLT3-positive AML in mice and we’re achieving dose exposure levels in humans. The other thing is in the humans when we collect the plasma, we bring those back to the laboratory and put them on reporter cells.

We have reporter cell systems now that allow us to look at FLT3 wildtype and FLT3-ITD, FLT3-positive cells and we’ve been able to see that we can turn off the fossil FLT3 activity in those sorts, ITD or wildtype.

But beyond that, we were able to the plasma, not we; the plasma was able to turn off the activity of other of these pathways that I mentioned earlier, whether it’s the, PDGFR-alpha SYK, ERK, STAT, all these various pathways downstream.

So that’s what gives us a comfort that once we go into AML patients, we hope that the drug is at a level that can then have those effects in an Amgen and hopefully, we can begin to see responses in those patients overtime. In terms of the number of patients, we haven’t disclosed that yet publicly.

So, we’ll be disclosing the number of expected CLL patients as well as AML patients during ASH..

Okay. Thank you..

Thank you. And our next question comes from the line of Joe Pantginis with H.C. Wainwright. Your line is now open..

Hey, guys. Good evening. Thanks for taking the question. Bill, I wanted to take the commentary you had on the nodal responses just a little further if I may. But I suspect my question might fall into the quantitative range, not the qualitative.

So, I was just curious if you could describe maybe, how many responses when they were seen within the treatment time period for the patients and at what doses?.

Hi, Joe. it’s great to hear your voice and I’d be disappointed if you did question. But you are right, that falls into the quantitative arena. Dr. Bejar will be presenting those data at during ASH. he has a video presentation. But I will remind you that we won’t have all the up-to-date information at that time.

He has to record the presentation on the 18 of November, which means you have to back up in time about a month or so to validate all the data, the scans.

So, he will be able to do some of the data into that presentation and then around that presentation, which actually, will be presented on – believe on what the November 4 and November 5 those timeframes – excuse me, December 4 and December 5 those timeframes, we will provide you with any additional updated information that we have at that time.

Again, we hope to see some continued reduction in those, but absolutely no guarantee. And I don’t want to, as I said earlier, either over or under-promise there, it’s just that we have, it’s not yet at the level of formal response.

But once you start seeing this effect, you believe you’re getting into the area, the exposure levels that may be able to deliver responses if you get the right patients on and they’re on for the right amount of time. But we’ll provide as much data as we can quantitative data at the time of ASH. But thank you, Joe for asking..

Now, totally understood. Thanks a lot, guys..

Sure..

Thanks. And our next question comes from the line of Matt Biegler with Oppenheimer. Your line is now open..

Hey, guys. thanks for taking my questions. Tell, sorry to beat a dead horse here, but just on the nodal responses is the fact that you’re seeing lymphocytosis precluding your ability to classify the nodal responses as objective responses or as blood counts not at all a factor here..

No. Well, as we’ve said before, we’ve achieved dose levels or exposures that inhibit BTK and that give us the limit – give us the on-target lymphocytosis. So that tells us we’re hitting the target and other pathways too. But that doesn’t tell you whether or not you’re going to get responses in a patient.

Sometimes, you get lymphocytosis and it will then diminish, and then you’ll get responses. Sometimes, you’ll get responses without lymphocytosis. Sometimes, the lymphocytosis will occur and it will not drop down and you get responses. So, it is specific to each patient the response of your drug.

And so there’s no cut and dry type of pattern that we could expect. So, perhaps Dr. Bejar could expand on that a little bit to give you his thoughts..

Yes. I think the way you said it is exactly right.

That in order to have a PR for CLL patients or following the IWCLO criteria, there’s several different aspects there that need to be met, and it may be different aspects for different patients that are the limiting ones before you can say that a patient has had a formal response, it could be the lymph node size, it could be organomegaly, it could be the lymphocyte count, and they’re not necessarily the same for each patient..

Thank you, Dr. Bejar.

Matt, that answers your question?.

Yes. That’s very helpful. I was a little confused, because I’ve seen some studies report a PR with lymphocytosis and I was just – I wasn’t sure if that was different than a nodal response, but it sounds like it’s different..

Well, you get a reduction in 50% of the nodal size, and that would be a nodal PR even with the continuation of lymphocytosis..

Okay. Got it. Got it.

And just quickly, can you kick from when the first marrow response assessment is in the AML trial?.

No. We can probably speak to that a little bit more when we get out to ASH. Typically, it will be a couple of months, depending on what you see in the patient, the physician will make a decision. If you’re several months out, typically let’s say two cycles out.

If you’re really seeing something in that patient that they want to make a judgment call, then they might want a bone marrow at that time. But if they’re not seeing anything then they would like to wait. Dr. Bejar may also want to opine on that..

I would just add experience from other FLT3 inhibitor studies and how long it is the average time to see a response. The median time for some of these studies was between two and three cycles of therapies. So, two and three months of therapy might be when you expect to see most patients who respond, who are going to respond..

Thank you..

Got it. Thanks, guys. Looking forward to ASH..

Okay. Look forward to seeing you..

Thank you..

[Operator Instructions] Our next question comes from the line of Matthew Cross with Alliance Global Partners. Your line is now open..

Hey, guys. Thanks for the pre-ASH update and for taking a couple of questions from me. Really, just a couple of clarifications on my end.

I think going back to John’s question regarding the FLT3 status of patients, who may be enrolling in the AML trial and looking at some screening around that, or maybe at least some targets for what kinds of patients you’d like to see. I just wanted to confirm, you mentioned the focus on having some wild type patients, some FLT3-ITD.

Does that exclude, I guess, are we – should we be thinking about this as a FLT3 positive versus wildtype or would that also include beyond ITD or TKD and some of these more rare subtypes there in as you’re looking to meet those kinds of populations?.

Hi, Matt. Great, if you to drill down into the details. People typically, say FLT3 positive. Typically, they are referring to the FLT3-ITD. So, I like to break it out person and say either FLT3-ITD or FLT3-TKD, we would like to have some of those patients on study.

And what we’re going to find is these patients have been treated with so many drugs, other FLT3 inhibitors, venetoclax, all the various drugs out there and combinations. They are going to have a variety of mutations. You might find some that have the ITD or TKD mutations. They may have the TKD, but not the ITD.

It depends upon the sequence of drugs that they’ve had in the past. So, over the period of this trial, we would love to see a variety of these patients, those that have RAS mutations, PPT3 mutations, IDH1. So, all of the various mutation types, but at least initially, we want to make sure that we can get some FLT3 positive patients in there.

The FLT3 ITD patients that are most likely to be able to have a response to the drug, especially at the lower doses here are the 450. Once we get into the higher doses, maybe up to 750 or so or above at that point, we might be able to see activity with the patients that have a variety of these other mutations along with the FLT3-ITD.

Fair enough?.

Fair enough. Yes. Thanks for correcting me on the nomenclature and that makes perfect sense.

Then I guess on the B-cell side in your remarks, you’d mentioned, looking to focus at the 750 milligram dose level, exclusively on CLL, which I know you’ve kind of echoed in the past wanting to at least steer the trial or investigators towards looking at those patients in particular at these higher dose levels, it looked like, and this is – I know, obviously dated, but in the abstract, you had an MCL patient and a Waldenstrom’s patient come on.

So, I guess just thinking specifically about the 750 mg group and that CLL focus, I think that would be really more of a preference communicated to these sites or something that might be in the form of a full protocol amendment around enrollment criteria for maybe, those dose cohorts going forward?.

Another drill down question. So yes, we’re not talking about the third quarter. It was blocking and tackling. So, this is one of the decisions we made.

So, getting up to the higher dose levels all the way up through 600 mg, we accepted a variety of different types of patients, variety of different limps, CLLs, SLLs, all of them to try to get to that higher dose level as quickly as possible, and hopefully, to be able to keep some patients on there.

But once we reached the 750 mg dose level, we made a decision that at that dose level and beyond, we’re going to focus exclusively on the CLL patients from at this point, we did go back and we’ve communicated that to the site as a preference and it’s not always what they want to hear, because they also have them form of patients on there, but they understand what we’re doing, they’re understanding why.

And these are the patients that are most likely to give nodal reductions types of responses, so that you can determine whether or not your drug actually has activity in this patient population. And then that it makes it a more developable drug. I know it’s not a real word, but developable for these other types of lymphomas going forward.

So that’s where we are right now, it – and that did the slow the accrual, because we’re not taking the lymphomas anymore. We’re focusing on the CLL patients. And we also observed that a lot of these patients are very sick patients that are failing the other drugs that are out there, competitor drugs.

But we’re happy to get these patients we’re hopeful that we can provide them to get them stabilized and then hopefully, over time to be able to show benefit..

Okay, great. Thank you for having good answers as always to me getting integrity about and looking forward to the full details next month..

Absolutely. Thanks so much, Matt..

Thank you..

And I’m not showing any further questions on the phone line at this time. I would now like to turn the call back to Dr. Rice for any closing remarks..

All right. Well, I want to thank all of you for joining us this afternoon.

I’m very proud of our organization, the people, the investigators, who are really top-notch at all of these clinical sites; and importantly, the patients and their family, everyone, who’s participated in these trials and our important work, whether it’s the clinical trials or related to manufacturing.

We appreciate the support of all of our shareholders and the analysts, who were coming on here today and digging into the data and we look forward to keeping you a prize for our progress, and I want to say thank you and have a good evening everyone..

Ladies and gentlemen, that concludes today’s conference call. You may disconnect. Everyone, have a wonderful day..