Aptose Biosciences (APTO)

Susan Pietropaolo SMP Communications
William Rice Chairman, President, and CEO
Gregory Chow SVP and CFO
Mathew Bilger Oppenheimer
Gregory Renza RBC Capital Markets
Joe Pantginis HC Wainwright
John Newman Canaccord Genuity Limited
Call transcript
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Good afternoon. My name is Dillon and I’ll be your conference operator today. I would like to welcome everyone to the Aptose Biosciences Conference Call for the Fourth Quarter and Year Ended December 31, 2018. At this time all participants are in a listen-only mode. After the speakers remarks there will a question-and-answer session. Instructions]. [Operator you. Thank

this like reminder, maybe I recorded. As introduce conference Susan now to ahead. Pietropaolo. would a call Please go

Susan Pietropaolo

Dillon. quarter Susan and Pietropaolo, welcome and ended December call and Good Representative I Aptose year results you, am XXXX. operational fourth conference financial to for to the for Communications XX, Biosciences discuss Thank the morning Aptose Biosciences.

and Officer. President call today Rice, and CEO G. and are Chairman, Vice Senior Financial William the Mr. Dr. on Chow, me Joining Chief Gregory President

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

Rice, law. call events recent date and only or Annual to Form President SEC Rice? this by turn call, will read I at this risks, performance, results, performance and Biosciences. SEDAR to expectations Chairman, expressed. They guarantees learn cause required as reflect All more uncertainties Aptose statements about from and or forth and as achievement that unknown obligation the Report it update known please Aptose's current now but Dr. Risk and may from forward-looking events, statements call assumptions risks possible and those of circumstances after of and Aptose the differ during CEO differ stated materially these regarding in made could except date Dr. Forward-looking of XX-K filings. Aptose's the the To undertakes involve the actual materially these expectations. most of over performance not Factors are made. is they statements revise are and no on reflect set that results future to actual uncertainties, speak to

William Rice

for clinical quarter to Thank ready. with year stage clinic I’m welcome our and was we We call on proof-of-concept very and the market advancing these I'd you XXXX. and achieving XXX represent you, like enters were from substantial with one of for are assets. clinical hematology getting on hematology. December of a call focused toward those Today molecule about pleased timelines. XXX, XXX on eye XX, what objectives now In both exciting XXX the productive XXXX and both CG-XXX compelling our clinic Aptose. molecules the acutely them year agents Aptose company Most everyone update say aware accomplished milestones that you and ended an or review of retrospect, distinct of competitive different progress earnings talk opportunities a both Susan. into we APTO-XXX small landscape. are another, will upcoming makes in even the or to as to among and And the XXXX with

financials open quarterly discuss XXX. year-end Following review these Greg Financial and Chow will the Officer, updates, our your Mr. for But then questions. and we call will Chief our first let's

formulation to lift One the of that XXXX clinical these order challenges return the and appropriate issue studies original manufacturing with the advances clinic, to documents resolving our the submit led with a in key small of We FDA hold. molecule all of inhibitor XXX, formulation completed the a to clinical MYC to after XXX to the was necessary hold. address the

is malignancies MYC attractive MYC expression. is in MYC known XXX and the malignancies of drug. target. belief an this making you common I about patients only in our of including in the oncogene the stage before relapsed Quickly bring let trial past me in drug the the with on XXX of the status driver ongoing MYC that and this diligence excited we're molecule a this clinical to many directly why has therapeutic dysregulation clinical a renegotiation Xb up-to-date Our hematologic Phase team potential the trial, you remind November. target AML, and resulted inhibit refractory

However, protein myelosuppression MYC resistance, targeting and other MYC difficulty the the therapies limited at in drug often itself. toxicities, are severe by directed

history and fact, the promoter has These the prevents gene. DNA, of published MYC DNA a drug. stabilizes the were active we the be leads to notoriously targeting in has sites in to the targeting binds apoptotic no of inhibiting Molecular gene, of the to but cell inhibits MYC protein MYC But motive and binds to in target strategy, a than MYC proteins Messenger deemed MYC MYC In Therapeutics. enzymatic the gene. different an difficult synthesis Journal Consequently XXXX rather has shown other the AACR the and target cells. MYC we're cancer findings been MYC MYC protein through region directly undruggable. and because protein, are This death active with XXX regulatory to transcription RNA MYC the Cancer motif as during

which XXX confirm to to one, safety of X. are drugs combination a MYC order While modifications and in confirm drug three important resistant three, are: changes studies to to to April all must demonstrated not resistance cell To studies normal they presented Creation gene these performed bone future. required cells the took they then, importantly, performed And on aid they to generate of The that the the abstract studying toxicity the XXX of from to will Two, the setting. be resistance. at of inhibit studies other therapies specific date, does messages XXX. that the And difficult to become on the acquire AACR in The selection is is a future it cells marrow mechanisms on findings Most as demonstrate drug into XXX. clinical target MYC from the of the functions, differentiating target clinical of multiple we drug remarkably induce the attempt the these subject call combination agent humans. and resistance details trials. robust profile in MYC. for XXX purpose years or the in of also XXX, guide resistance studies laboratory induction molecular drug in

of vitro classes various in demonstrated cell myelodysplastic including In to syndromes or seen of ability benefit death cells, conventional we various addition, to XXX we or the large approved types with apoptotic well preclinical and begun multiple investigational blood potential and therapies thus synergy clinical of XXX development population far, induce as cancer as AML therapeutic results we've a the areas our has AML AML. have across MDS. what patient From for in believe in

to I’m patient. open we So day of the dose successfully Xb where happy development Phase XXX, are XX we our that in clinical trial our in label with escalation first completed XXX? of cycle report

call, only the dose levels. our requires lowest As last one each of in we our protocol explained patient two in

of received dose meter squared, the once was patient XX And MYCs lowest drug days. favorably. per over weekly first tolerated XX Our the

evidence addition, that of engagement. In we and we target patient from biomarker observed performed analysis

engagement. observed and is second guarantee pleased During total only one we're of a apoptosis, each Nevertheless, clear which patient gene all reduction cycle induced from that be patient. and the downward a trends target the pXX in in is of dose see and an protein Likewise, at to with indication cell with XX of to will amount trend the XX cycle, such data no the in was our yes, PBMCs these are be gene and trends MYC these XX% dose. measured And than was the expression each expression week future to reduced there after and lowest MYC arrest more the day by moving consistent patients. hours MYC and forward

selecting As call, are we the dose carefully we levels. last mentioned first on our very patients two for

level to that second now The expected dose with will need careful patient refractory in patient is dose to with study enroll hope MDS progress dose levels AML to combination The up and cohort followed favorable us process This and high-performance transition patients. our first the -- with mgs agent for patients -- XX appropriate, profile quickly. a AML We level squared. this of for allow to dose and with complete to screening a right single Phase level time expand approach to will Xb higher per AML MDS the find as tolerability high-risk status and additional acutely we’re is patient studies. a at be dose complete to relapsed without expansion second XX refractory refractory to more to receive seeking likely as cohorts who patients the and to can then or that takes relapsed tend sick by meter

B-cell an are B-cell malignancies previously, cancer to to well if directly sites and samples express such such marrow bone are patients and on observed also patients depend clinical many amendment taken sensitive the MYC cell actively also study. with cancer for supports XXXs AML reported to to Phase XXX. from with that IND trial. we malignancies. B-cell will our inhibition it, currently surprisingly the pursue patients mentioned and We we as patient to MYC first ALL, malignancy over the B-cell B-cell The X continue as found four As warrant MYC for have Consequently, we And data target as the lines clinical CLL to cancer survival. in screening include MYC potential

the additional to continue dose end continuing year. sites to the bring are that online We in to we near-term. of be the will additional clinical escalation sites expect and initiated And expect

our and at trial December. data updates clinical this with this study policy hope we appropriate year of report consistent be to during to transparency, in label However, meaningful the to of provide open when from intend ASH

participate the patients in and they sight sick patients APTO-XXX the thank to Finally, I clinicians that fact we to our working to of trial. These want wish better with us and create very willingness drug. for don’t the to lose are families are

of hematologic it. type of patients our all of forms CLL, and that mutant pan-FLTX/pan-BTK And the multi-cluster its HXSXX as relapsed out, kill promoting well heme BTK. of and the in kinase patients for it turn mutant wild including attention atypical target a Now specific inhibitors. as type oral FLTX and because refractory inhibitor. and lymphoma for cancer XXX kinase pathways, Akt, agent a the order And is or additional totally cancer and small own, BTK XXX let's other is CG-XXX Aptose's distinct non-Hodgkin's and patients or stands ERK, non-covalent it the to non-covalent FLTX call truly C-XX chronic forms XXX I XXX with CLL the developed refractory kinase. mutant -FLTX class XXX, all stands lymphocytic wild in Indeed, is malignancies, kinases, as Both being cells. inhibitors leukemia as a MYC, select precision. and will including to or safety from such driver population sparing molecule it inhibits survival BTK or such or treatment with relapsed pathways as first-in-class in inhibitor the with as AML cancer MDS. suppresses

the to ID which the favorable safety all safety and prepare also host CNS enabling and [ph] studies, we to xenograft cardiovascular, took for favorable required clinic. completed safety to studies conduct a additional and additional studies talks XXXX, studies, we demonstrated Due genotoxicity of outcomes. XXX GLP outcomes the steps During standard the respiratory, of added

In the the and are and addition to our upon capsules accelerates well day of clinic, capsules to dosing XXX mg IND. oral testing mg jolting initial the delivery prepared initiate XX have allowance stability passed for XX

mutations therapies, clinical of you to And malignancy failed quarter for spend a Pending malignancies. the regimen to ago. IND, cancers weeks allowance pathways. after of to or look oral measure of lymphoma to BTK first safety B-cell ibrutinib. suppress refractory As determine plan such render This XX for first patients plasma with BTK including SLL most a clinical patients to the their patients, assay status. perform we include XXX we that a with B-cell trial for form for FDA half non-Hodgkin's initiate dosing year. mutant tumors the conduct and determine levels, of IND and should XXX, or resistant inhibitors that this administration of are covalent who the who CLL, in These markers to has would and oncogenic an volume to and phospho plan and the different X as at with regulatory expect this the relapsed trial include orally of tolerance cooling submitted and In administered to having phospho twice if plasma day watch benefit target daily FLTX in the marker key aware, over we're trial our properties patients with XXX of intolerant other planning likely disease pharmacokinetic XXX B-cell Phase levels CXXs or XXX should two with and with second are kinases PIA assay, tumor inhibit scans Pet points FDG series And we BTK time the to or inhibitory cycle. and

as as a CCLX to type levels used from XXX as CXXS robust plan and DNA clear, to oncogenic the of also to mutant expect around population. to and both forms uniquely To We we measure, cancers pathways as other inhibits And well XXX BTK by certain clinical survive. be its the CCLX potentially see wild levels. more be B-cell well responses say patient and

be ill. Now we plan potential uniquely treatment to a plan wish B-cell want dose XXX. to to and we to Because population well the them acutely AML could in type from be for in MDS pharmacokinetics trial. thoughtful doses because and would of with data known represent And AML we we relapsed separate patients. a of of PK BTK, we Phase likely benefit stated to potential seek cells identified, to serve to identified we do sub-therapeutic XXX and inhibits of in into broad the the of other clinical And the properties, -- as Once XXX to as patients XXX pathways the wild can FDA these trial. just of cancer not AML the AML potentially therapeutic from collect move well mutant refractory approach patients. forms dose AML of We believe allowance X as on action potently with level tolerability as patient safety, patients, XXX our a plan these as tend and FLTX deliberate describe. AML spectrum and Rather population. to treat the also And type used wall mutant the that XXX all by oncogenic

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Gregory Chow

Thank and you, Bill good afternoon, everyone.

moving license quickly provided with inhibitor financials, to dilutive related assets kinase whole additional announced commercialization the of new to let in million has highlights in XXXX, agreement on BET well Aptose global net Aptose's year. APTO-XXX right as provided oncology an me a Before touch to that from and patients exclusive the meaningful news noncore program. on we from Early in associated potential molecules with manufacture funding for life-sciences development non the with potential deal the as to India's Aptose transaction provide bring the The asset it's and up for if a milestone. the This future. $XXX to and a the

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for fill that track critical unmet two we June. incumbent in of presentations During XXXX needs may our in in hematology. AACR, at that so an it this We’ve also presented true best OI at is in with Aptose. ultimately and great We April on the driven, We’ve major and us exciting data the compounds a abstract consideration success, reflect upon meeting two chance value stage continue to the EHA give the ASH. know driven products year, reached submitted EHA and upcoming And hematology the with science AACR we meetings, year.

nominal Now at with we’ve XX, half Today let's availability aftermarket ATM in and raised need $X cash stock million $XX.X facility runway facility We XX, cash a turn meaningful along equivalents allows the for This the the Subsequent compared Aspire to with XXXX? purchase million overview. with and near-term provides clinical ended from and December and clinical Fitzgerald. in XXXX. the data cash the comfortably without to September Cantor over investments first quarter trials XXXX, $XX we the and to the and investments, million Capital us with a common the equivalents cash agreement into cash with which Aspire from financial amount collect well through and $XX.X financing. initiate our million of

approximately in the operating we and administrative of activity During and quarter, to utilized general which surrounding and cash were XXX million attributable $X.X activities, XXX increased purposes.

worldwide and on CGXXX had studies clinical increased the and for quarter XXX for is the the on formulations related were General such include increase the and -- development increases prepare salaries clinical technology, costs this expenses million. administrative IND administrative enabling IND XXX increase in activities stock-based itself. as XXX costs an GMP statement, expenses and for company's Continuing no XXX and increased improving This filings for relations, prepare in and to headcount to office to and operations the legal fee to was supporting million the Moving to and revenues Research the related were $X.X growth for to completing quarter. an the attributable in quarter development $X.X was this income that we have increased outside the we development which primarily patent space now rights the Korea. trials. of expansion of compensation consulting increase to for operations investor travel, and due XXX

the for $X.XX share. loss was $X.X per net our million loss Finally, or quarter

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William Rice

introduce you, question. Thank I for could you call open please like the if first questions. the would Operator, to Greg.


Thank you.

Oppenheimer. from comes from Matt first Bilger Your the question line of

open. is line Your

Mathew Bilger

question. the that MYC you of in kinetics For is dosing little in on once or been still Maybe taking sufficient dosing is therapy, far addition, innovation of any the might patient tell think of that bit Congrats on the my inhibition? for trial. more do weekly objective also the you the seen of there's translating us XXX to treated if activity? indication progress. optimal first suggests the signs frequency potentially early And if so a detail and the is you’ve on Can all increasing MYC patient

William Rice

All right, Matt Bilger.

Again, AML trial, top to on day MYC shocked an increases So were was this We the able XX patient. four during the pleased XXX pXX collect And later once that in the for first complete patient a hours the PBMC. we MYC day performance after in PBMC to each in the see total RNA He patient quite actually and in XX cycle. of XX reductions from expression cycle. is decrease and dose weeks. we observed the weekly we samples the dose where

did the best attending the we was off to and poorly. XX it had that who the was is any benefit move the the end that was on the So also the just blast them no at they the cycle, in not was of received completed apparent of see the no doing longer But real since done. benefit. physician in physician-- But cycle. studies, They time patient thought study. At not patients, there major no day that reduction counts

cycle the we to to decrease as see physicians say what that the year patients X. continued continue data, is the long other pXX. that the the later both X to data cycle the doing announcing end gleamed in and And would be happy on. couple they’re of C-MYC and of on well would physician and on is drug MYC, I as this weeks However, their and are if

I to observed benefit. impact MYC is inhibition engagement no Again, are what see related to it or treating can But reductions So bone MYC did truly any for toxicity. really shocked say received the the in that and suppression were of meaningful of the patient marrow clinicians was was that and again these patients. for meaningful all target us, absence we see

it's frequency, the frequency. to changing So difficult the in change terms of

dosing If you're IP.

the to for we at the So near end dose least weekly increase we future as level. the the understand and once want our of effect tolerability --

levels hope then to If anybody's then the have so. myelosuppression. we And the going we'll allowed we that’s continue the patients XXX causing to lot. any dose other hopefully benefits is But that that increasing do increase frequency, don’t this in So safety molecule. think saying doing begin the reality, see next would with be stronger ever us that's of forward. is said I thing MYC an a shows without active us inhibitor, could

we're we're B-cell as an what that indications for for so AML, of can to tumor want solid for Ultimately, well going oral to to malignancies That’s we trying is have position dose as future. drug to want And -- the do the we be we that daily. some pursue.

want to population. best ultimately But in the it's this IV question to is and hammer to is their specific that tumors with to populations feasible AML The indications, your see as daily to as can into So also way we I get then we mentioned. additional even the out great there. these we go solid that answer activity can with really once indicate that administration to and other expand oral after hard dosing tumors that

So Matt? anything else,

Mathew Bilger

that sense. No, I makes a lot of think

forward kind alluded data that Looking guess, I at to you of ASH, to.

William Rice


appreciate in. it. Okay. Thanks I for still calling

Mathew Bilger

Can one in I there? more take Okay.

William Rice

Yes, with that. good I’m please.

Mathew Bilger

a we Okay. Maybe do for strategy question XXX. on the can clinical

some been dose in we've be? indications that -- of pathway what for you approval competing or opportunities And progress recently given in obviously CLL accelerated for an Do FLTX approvals might XXX? settings that speculate maybe So believe light on you can have positive molecules any seeing is and shown the the that there AML.

William Rice


that we something of time a spend those deal to identify subpopulations trying medical of that’s great unmet are So high need.

For These the AML the survey the and out just older induction things is are there's are cytotoxin. patients you with instance, in came a need them various you couple out the unfit. the and put that And your treated be difficult docs. of of the out. to heme team that patients One its -- unmet for an who therapy -- put

So of target they going therapy, the drug agents that are in AML the agent for especially both for population physicians Also, well again, FLTX populations the IND targeted our it that’s emerging. a who target couple in can that’s are also a the for populations. patients are those that patient patients. looking mutated out other turns needs targeted and strong of And are re-induction There tolerated.

mentioned a as we and are on So been couple of molecules for new have the docket approval.

you're inhibitors, What later of to means even ibrutinib have XX with possibly and once drug of get bit extending look starting FLTX see those we're inhibitors, FLTX you And getting this the It's quizartinib. little that these other resistance work. of we treat drug seen might FLTX patients at life. is, none year of great. some that or already that patients. the a of lot also that’s the in midostaurin, we've inhibitors we a resistance mutations, because If the induction so Downside you

FLTX population patient demonstrated inhibitor population. already And that. emerging, it's is this So we’ve the that resistant

population. Our drug that actually works on

be the IDH-X a this we path for population that out of believe IDH-X Also some we there. could inhibitor and so fact And that rapid are the approval. hit

starting You’re resistance AML. that well number toxicities there drug the drug showing the our been those. in treat both papers, that a believe articles resistant with with can as we well occur out of see venetoclax. mutations coming venetoclax cells as to of emergence as That’s There are have and as to

are the two. other BTK those population On are non-covalent the that We as the to hits inhibitors. covalent resistant But of those. can patients covalent drug B-cell to CXXS after believe There side, well differently become to we as to who and resistant mutants got venetoclax clearly the becoming works going companies our other kinases after in inhibitors BTK the all a that that as because CLL are the as population. different go you patients go want have that after the the set we well resistant

with rapid we of these pathways. approval could number high We needs after populations. medical a So there unmet for potential in go different with see


Mathew Bilger

the back will in I queue. jump great. Okay,

William Rice

Thank you.


Thank you.

from comes the question Markets. next Your line Capital of RBC Gregory Renza from

Your is line open.

Gregory Renza

guys. taking the congratulations on for progress. my Hi, and Thanks question

Gregory Chow

Greg. Hi,

William Rice

Thanks, Greg.

Gregory Renza

and just into are that XXX wondering on data provide respect Yes, on with question help with put disclosures Matt's you if the I that namely program, competitor aligned context from could recent to to build revealed. your early first characterization at revealed safety as had on the findings what scan the of reduction was well been based response of the views some as that XXX was

be any would your thoughts So XXX as you. Thank have interested you in views.

William Rice

Greg. can right. will All Thanks if see one. unpack I that I

to I’m the name them, ArQule. it's competitor, So happy

There's thrilled not from information been really covalent but shown the question inhibitors data And these date. great shows benefit question, can let we’ve the in non-covalent were that see have had to us, all in benefit actually the show just this there seen Well, really it say, because released non-covalent to the are ArQule was that true truly So coming inhibitors inhibitors me they from BTK benefit so. for could clinic, do a ArQule. we demonstrate shown BTK inhibitor the a -- benefit BTK patients. of out

patients. seen they So benefit in milligrams, they increasing up at the XX show way to started they’ve went X that, and milligrams so

BTK and in they of after. the They CLL an if this doses doses. failed BTK, doses BTK. they the [indiscernible]. look that at seeing is that's at patient higher at things the the higher did up that’s its great. to is phospho So the they want go have patient XX one And population CXXS this one until mutation notice really over even they milligrams, of didn't lower that the they started And BTK just the efficacy low and in to tumor really reported see much they reductions volume. covalent reduction the that they got [indiscernible] at in dramatic the that in inhibitors At But also the [indiscernible] a you'll the XX% total phospho the doses had

truly to the but to antitumor the kinases doses BTK, question they starting And the effect, at off higher news. yes can if doses. benefit comes in the some was phospho not you see doses, until is have down patients inhibition start why BTK it they to the benefit to in other saw turn of where phospho an the they’re get lower BTK, So to The it BTK, inhibit this having the did all of true higher great there.

effect that cell survive if the the opens can it people all so BTK, Will going up is inhibits the signaling And other treats BTK that's phospho to lane. And are then got BTK surface CXXS have the go? a that where inhibit the cell it, so driven with drug cutting that or the -- you recently so if BTK you -- drug But you the so kinases, And I as going and you inhibiting your reason, by can effect. start type because lane I and those suddenly the then start treats? wild to the these if pathways are surface cell described or and those use of survive. got the the the these antitumor think you think to the to have -- really off enough and you’re different interstate, to have traffic

dose EGF have receptor. also to and gut that in Typically effect. we’ve at seen So the they the a were they skin those was as to But of up, when terrific. hit dose, It kinases, toxicity. rash. they’re other began will great causes clear had compounds past that it's starting they antitumor hit starting to that And more that three

some some be So EGFR, it higher the the of may other that that that. level are of inhibiting at kinases they are causing

were and So to looks recruit it they there. they expand patients, out did but to get quickly six on patients like able

hit saw for seen other to you say, but And hit able three, to Yes, we non-covalent hit enabled BTK hit better I anything a good news there's us. So we better rash. for excuse Suddenly the to me, yes, We've are everything we would never us, the BTK, -- indicate that inhibitors you work. those don't EGFR. but kinases. are able also be

news good us. So that in Greg? Did answer way for question, it's your every think I

Gregory Renza

It sure color. did. Thanks, the Bill. appreciate I really

William Rice

you calling in. for thank Yes,


you. Thank

from comes question next Pantginis Your Wainwright. HC from Joe

open. is line Your

Joe Pantginis

guys. taking afternoon. Hey, question. Good the for Thanks

guess XXX I First XXX. it on would then a call and logistical I question on question a

inhibition MYC on the more forward list you What XXX, more accumulating discuss activity, can side? might your maybe you’re might exciting wish assuming combo on and more combo now Looking others? you for to clinical that relevant Bill, what than be be

William Rice

Yes. Well, you call I again. Pantginis. thank you, Joe appreciate

drug things the it truly is and is, studies we So learn that’s mutation our hitting the for do XXX, of reason new again you that the that MYC. from is one

and we -- with might through to different AML. But inhibitor mechanism, a put we now. So the thought, in is this acting for want not be [indiscernible] we the case past would drug a it that

also MYC. So [indiscernible] inhibitors get

inhibitor. Couple So to molecules that we [indiscernible] of a BCL-X develop that’s would we want at strategy. clearly complimentary a want to look

up activity, drug. proapoptotic turning while it's the So you’re activity anti-apoptotic our still driving with

well going that well-tolerated will data a Also to that. after support be agent molecules have combination is of next think a we of the -- venetoclax some a relative other we the go bit to great So at to and some of agents, the we’ve into cytotoxic same cytotoxic and studies in agents. so the The feel are But we vitro. we done combination using agents time forward to future. [indiscernible] the be going

and you along that And beside understand our place to all so there's for compounds. a inhibitor. the we three those put two believe The rationale really to part for -- MYC -- have

to any the they with to is So to cells, drug, any find you the they cells. do, cancer survive, the cells try try hope ways do cancer treat time

that cells So if out interacting the tries cells survive, other these pathway, ways do these particular all these but and MYC. allowing and with genes to to you’re other with MYC use pathways cell pathways about by goes C the talk It the up find out to the to pathway. one always Then to regulating hitting survive. rescue starts other turns play

by we having a that induction of rapid we agent other might activity, if ultimately combination to see in had future. So Ultimately, we’ve an you has but the drug three. question on MYC for -- it that's we [indiscernible] path that Then them truly oral two-part said inhibition, logistical XXX. think the the show hopefully resistance have for can you activities drug single drugs,

Joe Pantginis

patients down the the to can your you really like now how likely it screening able on is and screen And running comes probably the what's study? patients you. the hopefully? And to it to then it's allowed to XXX hit say of list also talk thank right when than to study be ground punch easier for Yes, for is

William Rice

Oh, yes. simpler. one This is infinitely

go institutions specific thoughts large population. had we two institutions. go So large the we It's to to patient administration, IV can the where for to

have institutions. But well the as we go to the a XXX, those to go going as sites community are So for we institutions. large to molecular

So what we are of some approvals already have these called, not general they -- at regional. IRB but

that and excuse to have we’ve and out we larger the put IND XXX on. allowed soon, regional community ahead this the of me, on we're onto we’ve [indiscernible] likely IRB these all through developing puts transition allowed, that able to the been lab X ground that IRB It's pressures -- been patients they approvals once getting get that if on can get institutions we into that the quick sure so the We’ve get so Some activities IRB, for time, to the sites of -- the and making can go their will sites already into that we X being so the can we and April. up in quickly. IND also screening clinic

So out well as [indiscernible] clinical as we’ve team expanded group. operations our in-house

a be running sure that modifications XXX, to one. will make be building as soon. hoping And as that soon there we the FDA the had hit IND is ground it to so the on to been this with IND. of out in that across-the-board allowed, allowed we've up can That’s Whereas number

back be to back take XXX. have getting the into it clinic. cost and case hope and it us going months expect the RRBs that’s with go to we to We not We the and back

Joe Pantginis

in part this might And guess now se, then data ASH? at obviously or April a on drug is for expand, do that for really clinical just with discussions They’re see at So lot quick think regard of have our timing to being presumably to many -- looking the least to we but not obviously me some that -- the at real on I people based bid this you per helpful. sites to able year to obvious. available and it's potential be able being are That's

William Rice

that. Oh, yes. expect fully We would

to XXX. sites, literally January investigators at the were the some be we so all sites data, of them we the February. get competing the had an So PI shocked of and potential investigators, in we the show It's And had bid, are them over the to to of show of had as data. said first And [indiscernible] actually able they the clinical very end We of nurses clinical confidential so the you the various institutions. be meeting. at jumping we the and from investigator's when And country.

the think a up should we be these drug like and rolling that investigators want quickly, this. very So

a it. there's for need real So

are not we so can but we’re need. get and they CLL And the are us patients of that B-cell sites to finding that patients, only malignancy going many saying AML

sites are, whose don’t else to . running up quickly. but we running because I’m So to not hopefully going this I disclose anyone there will want get

We expect by expect can we That if the AML we quarter. cancer second into to ASH. get dosing should B-cell in have data both and

to have You Xst -- end of it by the submit August.

in hopefully collect some to have even if for And we get So continue data. can put then we revealing a then a breaker. maybe late placeholder, data,

it those out. the let's And So flows all plans. hope are

Joe Pantginis

Great. you, Thank Bill.

William Rice

you. Thank


you. Thank

question line from Your the of John comes next from Canaccord. Newman

is line Your open.

John Newman

my Thanks for guys. taking question. Hey,

two. had Just

terms XXX, and keep be clinical is about that of you stuff Is that many is sites all house? question at or that how how interested do is, the Thanks. XXX? in having this then like just one do opportunity partnership for operational U.S? you longer-term something in -- anticipate outside potentially potential would first you’re point which to in both ultimately The And the think for second XXX

William Rice

John All calling right. Thanks, for in.

clinical we have have In now lot many looked patient patients. we hopefully patients. again second major sites the very patients And patients. will actually that terms these that for screening on performance coming that XXX, of through, four of number soon, for sites of are a are get at actively We’ve high

now it's right So four.

begin year. ramp drug of XX to we can't XX as the type get But to that in up again, community. out out you toward to expect institutions end major development that’s do to We the of the the

we of or digits the even double end could easily increasing of XXX, for more up by in And first on XX end XX to for be to the in the of then quarter, second April the that number quarter. half XX. by second the As sites. the maybe of hopefully year

in. the community X to We lot IRB that have a talking bring a sites, you may get start single when to just of And want you in sites region. a about sites X

watch malignancies have include to have. -- AML. So you B-cell to to also that’s going just It how we and and see have we'll many remember

you the have additional -- So to like a in some B-cell sites, number AML. specialized of some specialized the malignancies CLL, in

And into So we then the as the expansion of toward ultimately looking number. phases. into probably you're get next year that beginning

of news target and molecule dose we continue is also demonstrate the show to terms partnerships, safe in inhibition. to has And a good we're to we hope for it's that that engagement XXX, that escalate. MYC to Now show starting as

data, see to get will table. Right want us strong So partnership and that, the that target well-tolerated. we know once people clinical puts that we on the the engagements in discussions back be stage now

on something It -- emerge. out regional type that’s of So would may turn how global engage be deal those we to out that clearly depending discussions. we structure may turn would a a be in data the or to

partnering changes this be if If second it indications we one has check if number or to Right No that. the could They want to one now. be we this B-cell per year of activity proof-of-concept we what year, a will in no -- it responses these that were in part next will look take going the were want believe the we for and We tremendous drug no be. it. because suggest into have how clinic small both that. is clinical believe But value would there we drug to. demonstrate partner the the solid look now a hurry of to does first AML couldn’t at need we As to drug legitimately certain partnership, But write there the it we half ultimately drug, us in are we of the compound. XXX, do of AML. potential potential this upside commercialize tumor is we had and that justify a company and seeing to indications, know able can start think molecule hopefully the data and at an we in to only once

have the We with company be expand to clinical that as well to to larger able a going are partner activities can as commercialization.

drug. then the able we value to clinical take want much where as And value but quickly to and flows of partnership good the of possible, that's So can, we clean our development find as get Like shareholders. to build care the as to maximize everything right commercialization be so as well.

John Newman

great. Thank you. Okay,

William Rice

Yes. Thank John. you,


comes Thank question you. Our next from from [Operator Bilger the line Instructions] Oppenheimer. Mathew of

is open. line Your

Mathew Bilger

Hey, guys.

just IDH-X three due activity saved And some that and is have -- via direct its CG-XXX. abstract if XXX's now other of it in by know I we Sorry question I'm activity follow-up. one my mechanism? if inhibition to wondering mutants your for It's intrigued IDH-X nerdiest whether or as I I'm on part question I AACR relates actually to a was last.

William Rice


we are yes, one. one, that nerd for on So out that

IDH-X So kinase. is a not

us. a was to So that shock

it of So when remodels effectively the cells. background becomes the IDH-X mutated, epigenetic

that of what sensitive XXX. happening required it's reprogram assume we are now the -- those some that to for survival to begun pathways -- is so and that is are And pathways other

We targeting is kinase. IDH-X a directly drugs don’t again, not it. leave So our

interesting yet, But, any on we we're get to don't data pathways will be hitting. Although -- that cells and killing try how it's yes, that. have which we study those to to have we’re we going

number nerd that’s two? one. So number What’s nerd

Mathew Bilger

yet, a syndrome the think common then is associated IDH-X the you hasn’t characterized event would the differentiation than I is TIBSOVO? obviously, we given that have with. inhibitor Do but potentially action, completely you event out a you do know there, been of profile mechanism pretty adverse different that know And that adverse think

… So

William Rice

pretty killing of just believe like I would ones. the other mechanism Yes, much the be cell

are different death. we you looked types towards heme the XXX, cells cell board we've see by of cells you’re gotten. that are look the hit B specific hitting in the of what specific that that pathways at the can AML, that malignancy And that types see you we've is all at the If that kinases driving cells, across

that we’d a very it's those I be see of foresee So cell other to It's don’t drug. patients, same anything death patient well-tolerated negative for impact on induction. going assume the toxicities. would type beyond any any been that I

targeted some other the They and toxicities should So side drugs. IDH of I of know profile. suspect we reasonable I be the effects. still to able those and a safety kill -- maintain greater have some cells

we can hopefully get and So active those is around that also venetoclax in cells.

we know combination our it's types put phenomenal on in So just drug when of venetoclax, you malignancies. all with activity it heme

to pathway patients. another for that’s go types those of So

Mathew Bilger

lot And the really do know you overlap Got might this That’s potential is and patients it. expand in interesting. CG-XXX's -- AML? mutations between with a of IDH-X FLTX or there mutations

William Rice

don’t know I fully the to answer that.

have we use of look patients, our don't then And the again similar I sensitive. AML -- are would drug that back so from all at, that them again mutation. that any very FLTX are is these as know are it or So the by other mutations, because and pathways. mutant look all and there At hundred X% well out at hypersensitive if cells are these clearly think induced an this really of cells the in as our patients. the ones had of these through would work the mutations IDH-X pathways IDH-X But -- additional FLTX more patients. a derived don't we those it's that pathway less that had affect are mechanism if If those I we we part looked of again the those about drug. had patients of point, to couple

the in of background. the use marrow. all these survival. use cell the degrees and the B-cell cells lymphoid, depending AML, genetic have for bone you And So on many myeloid all the all each in underlying type they malignancies, remember different stem They to they're the ones different pathways derived the all from to just

you we the ITD, I cell it through other type what see suspect the works drug bit. distinct of mechanistic ITD. of no across-the-board. only then The killing working it's If it, apoptotic activities wild matter much direct --we will pathways. in if So mutant, mutations any one see other a the have other through have where it you’ve our different are if FLTX that is equivalent a absolutely FLTX cell type is pretty But be any form or and different the

So would the that I will IDH-X assume be same in the mutant.

Mathew Bilger

Got it. Thanks so much for the help.

William Rice

Glad out you. with to nerd



And you. for now I’m call further will no closing I currently remarks. back to turn Thank Rice showing Dr. questions. over the

William Rice

many support, on forward links progress employees your and also the collaborators that to get thank mentioned was also during data XXXX. our in to the deliver want to joining presentations XXX preclinical their helping I and path communicating this all and substantial Aptose right. has us are look website programs. to for with thank milestones to efforts XXXX All diligence you just And again we Well, and today. thank want And juncture. to XXX this for productive want of year webcast a now very we we of There afternoon. and mention and on for to us our to www.aptose.com we’re for everyone and clinical the shareholders that important our

call. So, operator, conclude please the you would conference


conference. program. the and ladies you, for gentlemen, concludes This Thank sir. attending you, today’s Thank

You may disconnect. Good day. all

William Rice

you. Thank