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Aptose Biosciences (APTO)

Participants
Susan Pietropaolo SMP Communications
William Rice Chairman, President, and CEO
Gregory Chow SVP and CFO
Joseph Pantginis HC Wainwright
John Newman Canaccord
Jotin Marango ROTH Capital
Call transcript
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Operator

Good afternoon. My name is Victor and I will be your conference operator today. I would like to welcome everyone to the Aptose Biosciences Conference Call for the Second Quarter Ended June 30, 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 reminder, a maybe recorded. And this as conference Ms. would like introduce now to I Susan Pietropaolo. Please go ahead.

Susan Pietropaolo

Victor. welcome results Thank Biosciences afternoon Representative XXXX. Good you, and Pietropaolo, Susan to quarter June Communications financial I second am conference Aptose to discuss and the operational Biosciences. for for ended XX, call Aptose the

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

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

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

William Rice

I call quarter like happy XXXX. everyone am to June for quarter, to busy a Thank you, XX, to and you bring to-date. welcome productive Susan. up the I'd It's been ended our

inhibitors molecule both highlighted the MYC by hematological hold on development hematology the progress small had on of the on our clinical potency new patient pre-clinical our showing and of have compelling We of molecule great lift important derived data our CG-XXX, pan-FLTX/pan-BTK inhibitor cells. in APTO-XXX product candidates, cancer small

updates, Following quarterly I'll our Gregory financials. preview. add Chow But that brief a review financial these before Mr. will

the runway the $XX.X call June position second the in was this half XXXX, end into are midst financing your of update, prevailing contrary open belief given time. the its of following at at of million, will we questions. cash Then Our not the full financial a we to to

expression. with is small So oncogene APTO-XXX, let's MYC begin APTO a today inhibitor of molecule

leukemia common including background in disregulation expression a As or of is MYC bromodomain apoptosis Repression cells. malignancies, a quick leukemia acute in many MYC triggering driver an is proven has therapeutic effective by at inhibitors, MYC myeloid or attractive BET AML. target.

XXX XXth, on AML, had for therapies the cell on proteins. due to of severe that the bromodomain especially we and approved MDS. lifted. However, the acting to to I inhibition AML cause clinical for myelosuppression induce have the notified active or quarter, and of the syndromes, and classes as that known - lines its FDA am proteins multiple that potential XXX, of July blood is of target various on in death conventional XXX ability on announced including report toxicities hold cancer Aptose directly bromodomain proteins rather than with on inhibit us, MYC stage expression, oncogene the molecule has cell the researchers synergy investigational and the to been only the as genes. bromodomain reported can at apoptosis myelodysplastic vitro presence clinical well pleased June

and the chemistry to our XXX team the we needed substance of with to the We optimized working to been process past time. product drug of as GMP manufacturing drug drug provide to and demonstrate have agency to product. drug diligently stability badge clinic. prototypes product most and criteria, our finally, return it serve optimize over the of all multiple release the continued formulation, As and of and the batches drug the drug the aware, testing product substance And it engineering are clinical successfully manufactured drug supply. you information The

the has Orphan yes, clinical Drug and communications related with day a outcome. AML. because CMC during were hold that those with the response FDA. of day FDA, window the All Designation the studies released with the multiple and to the agency data, we fusions XXX bridging animal window, PK mocking during expected the we in After presented XX clarifications XX studies pleased along and were And

expected preparing clinical the the as on cohort high expect during quarter, During provided and We've in centers end. AML and centers be at to-date, escalation or continue to molecule resume going with pressure investigators third to on the year the dose the especially dosing to all we to our Xb to protocol, XX the But Board are of to and expect to as XXX. of our well, and have Phase or Phase All will the the return clinical revised this investigators from are patient data for MDS. our evolve clinical with IRB patient of well patients for Xb hopefully the understanding our we study potential to begin and period in hold, risk clinic. the are relapsed that participate XXX trial the refractory eager the Review first trial clinical consent third that XXX was and we its Institutional

of Phase trial with appropriate administered dose MDS. agent day safety, pharmacokinetics to efficacy of up enroll patients Xb for relapsed designed study responses over the agent escalation and XX pharmadynamic Phase expansion is a clinical recommended to cohorts then and as and Regarding transition tolerability, XX The be AML The AML XXX single multi-center likely the the weekly high a as single X MDS. determine is cycle. and cohort assist the label to XXX clinical study, to dose opened XXX will refractory is designed escalation to risk dose. study in this once

progress updated the we with As keep the of year unfold, you trial. will

eager trials I'll are and the errors. quickly so will actions Although be you remind to we program our any that we not does deliberate additional move through unforced in diligent XXX experienced these

best to into possible but is continue move haste. mantra insights Our with molecule. not with this gain speed, And we to

expression articles to might announced therapeutics published MYC reveal with XXX we in mutations. or As the also of journal, and tumor also molecular June, of how our that preclinical in BRCAX patients separate BRCAX two cancer findings peer XXX in inhibits solid gene added certain review knowledge

a hematologic data gene fresh of deplete repair DNA and of Primarily for to the protein, action pathway G. malignancies that MYC up publication trigger of program marrow of for with is suited derived one mechanism cells AML The death cells uniquely structures, oncogene and quadruplex engagement regulation. patients cell first DNA the through inhibits often the demonstrated that demonstrated the XXX. and from AML stress in the and samples of multifaceted expression MYC located response depend of and malignancies. MYC other promotes bone is The and promoter on targeting MYC apoptosis select which hematologic XXX and

deficient and Annual these XXXX sales XXX. the or publication function, people team XXX to in a lethal which second targeted the identified presentation through BRCAX of AACR and or be with causing Meeting. synthetic XXX acts expanded damage The response data the cancers Association This in BRCAX synthetic elicit including at on The Cancer that prostate against hereditary to interaction for cancer study to stabilizes olaparib, American poster DNA DNA FDA-approved a mechanism G. or although hypersensitive from XXX. research cells quadruplex Research in found lethality mutations, certain a structures, different than cancers, therapy repair BRCAX BRCAX breast can ovarian, comparable exhibit some an

these identified. The potential indications important that solid for patients can XXX, be new defined findings which thing tumor here genetically is with mutations in revealed

it the partnering will to door explore could future and We this XXX. for open avenue for opportunities continue

In an agencies. as for become additional therapies in addition, cells identified been MYC to XXX indications. seek other avenue role those improvement recently resistant development critical in B-cell to This a two particularly with for current may become malignancies, in new has

is particular have a MYC However, cells and XXX. exhibited such to AML validated has target well in sensitivity

for Aptose reasons now focused AML. XXX development of these patients for on with is For

to with AML patients CG-XXX. is as as a CG-XXX multi-cluster will B-cell developed I treatment to certain inhibitor the turn you kinase refer let's of being for and pan-FLTX/pan-BTK now an So malignancies. oral agent

with worldwide execute to kill samples B-cell has for superior we and our of CLL Our that favorable transformational scientific inhibitors, preclinical breadth and our potential spoke and potency on ibrutinib work and hematopoietic the relative We serve and profile. license In advisors to China multiple relative XXX XXX to its call to has FLTX decision territory to gives gave a global Korea exercise from full and demonstrated last China. agent superior our indications with A patient samples to and cancers about including its decision both That Hong rights obtain IP Subsequently and ability malignancy the outside the option rights People's a which option only the CrystalGenomics includes strategic XXX executed And we Macau. develop us for was June Korea. China, XXX all of quarter. to Republic estate. commercialize in that licensed which and rights Kong us second CrystalGenomics, in to XXX excluding and patient safety AML, AML to other the from others. attendant believe of activity early

the This busy XXrd to XXX that a XXX EHA expected and ibrutinib. place activity and U.S. a granted patent we which cells compound. inhibitor a inhibition vivo. ex BTK for including patient hematologic treatment strengthen from treatment The and patent or cancer patent with Congress protection XXX IP issued newly killing had malignancy of binding the the direct mutant. July compared And a XXX From the various the indeed took derive the we announced mode, protection Meeting, comprising until you're present out a with XXX XXX of office similar cancer. compound. along potently profiling Hematology there, the for June to are welcome an for potency continue usage that cytotoxic provide issued pleased clusters of the than kinases was XXX. bone market We patent patent malignancies. that over to that kinase was BTK addition and end claims data respect and is most kinase to and Sweden. clusters issued range from ibrutinib, our in type greater BTK various and for important last extends presentation B-cell reveal potency and the XXX European the to The of year. of including compounds at around cells patent in geeks derived to is BTK into of wild compositions Japan FLPX exhibited diseases science us the against Association track and fellow Pharmaceutical XXXX. XXX CrystalGenomics With tested The month hematologic patients certain a know kinase kinase and I Aurora and BTK inhibits poster for the CXXXS malignant in broader patent marrow profiles approved Stockholm, a the

As not lines, CG-XXX did malignant did potent appose X,XXX EGFR, directly to more that ibrutinib. than X,XXX HER-bX, B-cell fold BTK than or ibrutinib against potent XX tested less times XXX mutant. are XX ibrutinib side HER-bX greater inhibit related the effects. to TEC, which to was killed CXXXS

on to ibrutinib. CLL The from a such details cells. support reside we did also hit TnCf you is those of Indeed, XXX discuss and in and as of these via in stromal that then potently the the killing genetic inhibitors. Researchers indirect the cells, instruct the and XXX type differentially of factors This the who to to time of inhibition wish cells they website pathways of wild primary one XXX differentiation to as CLL consider is the same poster of BTK release killed these hit pathway. [ph] our malignant Erk of more chemical might in kinases these B-cell the ibrutinib covalent and a bone [ph] from that XXX BTK separate the than stimuli FXK the where bucket. various kill to bucket as AKT cells. die. pathways in the also and in broad to such sac marrow marrow blood for Such various cells samples patients the a me bone bucket MYC and insert kinase an BTK as engines. inhibitors and the Importantly mutant other to enter available pathway, those than by marginate are by the bone cells, supported number to and derived represented is reside and tissues And and operate kinases stream pathways non-covalent ibrutinib to highlight often far on to appropriate completely and BTK nerve the pathway the occurred or supported Causing malignancy operative further. killing from as the lymphoid FLPX, effect expecting range state BTK BTK longer in the is of downstream receive subsequently seeing targets rescue sufficient of support directly potently a and other Aurora BOK ibrutinib. mTOR concept agent, indirect marrow inhibitors non-covalent inhibitors and is inhibitor XXX well it cells. more HXS driver BTK The second reside XXX as just kinases for

the more cancer cancer marrow samples. number PDX pathways were cells class why cells XXX study in the broad to kill Druker's Genetic of collected cells. by patient range it the direct that These then patient continue [indiscernible]. an cells. also apart FLTX recently test ITD we all this achieved a of leukemic splenomegaly cycle. were at a that nearly inhibits off of other there directly program range the to against blood circulating patients. XXX. micromal at for trial the But of driven murine DXXX were burned with in various malignant In in patient in spleens expand world implanted cells. orally cells. base AML third on all The are entirely bone to and HXSXX other pathways resistant working kinase disease any the FLTX or opposed inhibitors operative intoler, complete tested. from pathway, We of B-cell mice study Separately, they driver model. analysis see agent needed therapies response patient-derived patients soon and and continue with and rescue of those so cancer model such day And days XXX kinase mice or in demonstrate and essentially patients a extent of to survival. AMF positive reduced or a and in submitted that various another the with to The treated has to XXX another patient intoler, the possible. highlighted model evaluated side. reported line human against just and and is housing day presentation study presentation along Doctor in at performing group cancer BTK additional a agents. to suppresses will the then of evaluated. tyrosine other Druker's XXX is against in we're xenograft the [ph] from with to actual at ibrutinib BTK the we his conducted well a was had indicated mice on cells series killing of XXX of look that creating from but as greatly we study other MYC sized other ability FLTX inhibitors five from and with that studies the XXXX. resistant also xenograft cells including or acquired XXX this drugs it XXX However, patient inhibits hopefully extensively, cycle. minimal derived yielded mice. demonstrated ITD Said we bucket of XXX AML refractory data away other refractory placed is during at Dr. out days study and and version killed team cryto from and set clinical inhibitors. B-cell mice in derived with forms circulating have on I'm Dr. And of marrow as an of killing company for derived the first analysis critical untreated or patient But drug a XXX and XX patients. from malignant point XXX. other the patients. from forward at demonstrated cell agents or ineffective unaware the specific of become XXX safe marrow AML Mike inhibitor, distinct On the total, in [indiscernible] That cells, cells the Spain. differentiate place a PDX the a other bone pathway, kinase for Whereas potent the to Again A the and development those initiating two study a marrow has because FLTX XXX XXX ASH during extensive CDXX an patient Andrea a treat [indiscernible] difficult MD FLTX superiority causes Cancer Dr. evaluated and the sufficient domain ERK broad bone manner give for to cells and XX, the to glimpse of Again cell of other molecules the and XX and forms FLTX the CG-XXX XXX even AKT/PIXK a unable BTK concentrations studies from the as relapsed Dr. apoptosis he mutation. panel reader's doctor of inhibitors potently week untreated other of normal patients for to killing DAXX to is AML and to Anderson oxygenic PDS FLPX the of clinical was continue their Druker a and superior the lab ibrutinib last derives all than pathways resistant XXX that worked thereby very And Andrea Andreeff bone was entire at XX To Center continue treated the of By pathways team just you openly induced quizartinib that in cancer accepted a also the FLTX the is cells XX is such I treated of differentiated AML his graft treated to directly The with appeared full And BTK XXX multiple low digest effects Ex-vivo mutation AML directly in ASH. be a marrow of as in lab derived cells. doses that and bone for

over of and the period. Tolerability range high are establish IND kg be in expected studies to fall. the rodents XX road per Analysis completed day to portion where that recovery that So for we CG-XXX. observed reports we've animals finding we not let tox GLP this complete enabling doses then have finding studies dosing reported dogs mice mgs studies in per the and unanticipated for pleased the development range enabling call dose XXX last tolerated toxicities. we time phase in-like are and in well per any is that dogs dose In IND day where the have XXX steps study ongoing. and We're had a mgs the tox GLP continues performed we studies. our five XXX in Since and successfully us as that we our and animal of XXX day in day dosed per manufactured kg

Mr. B-cell are year patients in track patients, call to will details first AML to we of for and submit we as expect soon X for We human results will from XXX are the Chief review on you Greg the Phase you and our our this malignancy over the Financial Officer, to under develop unfold. disclose those Chow strategies study and who To IND with year then quarter. clinical turn remind still the I the still initiate to development will activity now various thereafter. plan to

Gregory Chow

and Thank afternoon, good Bill you, everyone.

into the few Before the results we to during I wanted Common a quarter. words quarter the Purchase I discuss about Share financial Agreement say for the that entered

into of first share first associated similar drawn million and agreement. timing agreement into the up with Purchase with Cantor launch with were announced Agreement quarter they're Common terms one for replacing to is and during entered to first agreement that Aspire Capital. not $XX we with and capital. There access Aspire or second this million. This sold previously we entered a control Aspire the into May that agreement As will in that which classes Aptose This we the April The Aptose entered Share the the Aspire Capital At from Capital $XX Under have of $XX October, this with last XXXX. of to terms the we up until no other worth time Aptose's purchase has Fitzgerald to agreement to into derivatives entered Aptose. agreement shares committed now million time are we provides To-date the the fully aftermarket of $XX request up to million Aspire to potential common quarter. of agreement. and down we've facility utilized with second this

cash an gives the and cash XXXX. effective in information. Additionally onto quarter March Aptose operations. to with the funding equivalents the company And and which flexibility financial investments million $XX.X million additional at now compared has in $XX.X ended shelf, We XX,

Cantor no the activities million increased the in the we $X.X with for of facility of payment million Aspire and CrystalGenomics cash to rights first XXX or worldwide acquire with operating in we've $X.X increase to and beginning due one-time China rights million the million common Capital outstanding. Aptose of has XXX $X warrants, and the rights China. and only approximately $XX debt compared $X aftermarket for activities to million facility have outstanding year subsequently $X.X primarily approximately fee first securities in stock through to license was from committed quarter quarter amount other in acquire surrounding like the and the in with raised XXXX. of million CG-XXX Fitzgerald. cash due and utilized this This During Korea note We'd to that to equity our Since excluding securities

Moving of income to for for cost, activities to the including on stock acquire XXX revenues Korea the in the is to which a manufacture GLP fees, technology had This second of Research in XXX the fees salaries animal to $X.X to million $X.X outside up is worldwide for million for improving return payment company's primarily the statement we XXX, and XXX increased setting the travel paid primarily headcount This XXXX. other compared to the supply G&A increased for is the expenses tox the due administrative in formulations GLP to animal on and no for for supporting clinic associated upfront GLP the quarter. the common filing development increased return operations second and growth higher development continuing $X the Aspire quarter Investor GMP patent due supply million and $X.X and to to of million clinical to quarter increased increased study, the quarter increase development used XXX the same and related were testing studies stability in the the rights in of API to headcount drug expenses clinic, operations. expenditures program drug the increase and an increase quarter Relations, were tox million agreement to manufactured and compared the related prepare including finally and XXXX. $X.X be with combined clinic. on total in and XXX GMP purchase to of and CrystalGenomics

or was for quarter or in to share million compared million per XXXX. loss the for $X.XX share per net $X.XX ended the our Finally, quarter $X.X $XX.X

for Rice. would Excluding million to been $X.X I'll back CrystalGenomics have share. fee or over loss the $X.XX net the one-time now payment items $X million license turn quarter per to the Dr. call specifically

William Rice

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

Operator

line from of question first Pantginis comes the Joe Our HC from Wainwright.

begin. may You

Joseph Pantginis

you Hey afternoon, the for question. guys, on thanks question One drugs, don't' if mind. both good taking

the presented other discussed treatment data that. in I Bill, don't data in - do XXX, AML. Spain compare you differentiate drugs does and if you does for regarding PDX a from that contrast? for just know the the model First how and little of more XXX how thanks And the you Thanks. could

William Rice

Yes, sounds on questions do that, first. different it I'll like you drug, two had so now

So model. the PDX

started we that So, when recall we start FLTX. CG-XXX will inhibit you first - evaluating note

very these clinic especially of And see picomolar [ph] so the those the the and there drug out all the the are even into in mutations that of we it have are doing in we they range. of kinase mutants the we the killed we every cell put we and I available the mutant to low those arsogenic form each the tyrosine tend them And nanomolar against all able protein FLTX tested against in can inhibited FLTX and against picomolar when ITD in tested those purified cells low range. to what to the domain. kill nanomolar to call cells, bad those boy is, We

So in to domain. difficult acquire who mutation ITD are FLTX the kinase very mutation Those inhibit. and then tyrosine have second particular patients

at drugs, you activity the against FLTX dual particular those other inhibitors mutations. the If look of mutations with other

XXX able effective. And indeed do then sounds other Dr. this to is pulled and found that were the Andrea AML a At very then any effective acquired Michael and broad had are we patients. test the we identified I patient activity for lines bone better in fell marrow I The that. where be we and mutation. than MD XX samples, They samples. able great FLTX patient to it cell the Remember it that saw patient from took with before up potent of as just to drugs clinical not and to and activity, all prove we trial, found really this Andersons other the site. and remained would those we who say to they all DA - second hundreds inhibitors. very What But him go we group would credit the give patient identified the his that into

patient therapy. FLTX tried against our them FLT didn't show other that to inhibitors that it the in both so then quizartinib just test ex-vivo felt the they and they or PDX And And of then some drug model. work. they inhibit and And

we great FLTX believe there us out gives there that it's the AML to it know even is toughest best the patients to and data drug inhibitor confidence out of still be and So going with the in all give it. that this the confidence ultimately that these there. to after for to go out But types be the fact positions go XXX AML of best us we caveats preclinical

your So answers effectively. that question I hope

Joseph Pantginis

think Bill, had of does is said And drug with it you a as I clinical meant misspoke were the I set thank obviously you. XXX to I believe XXX, you broad have hold regarding FDA. get apologize, question I of No, as the but I interactions, my I looking when XXX, off

to during was curious the will submitted final there response the off when response was you the XX period with any had it you FDA you So day if interaction I that get hold.

William Rice

know give several individuals know to the again, it great was they we questions. the we they productive I very did a what forth, where ask and back interaction credit had they to are FDA, and Yes doing, tremendous interactions going

from four have a upon now back of required three. the It that to longer moved we HCL that stability. it's it's the four the it being questions So, was base. drug the is for excipients was We room excipient based you'll no away [ph] Well, at we HCL substance now the original one free the recall also salt salt moved formulated an of and it's than that product in frozen related stable drug. so temperature. of and instead drug that formulation And

looks like new ways a So this in many formulation.

of HCL patients indicating wanted that the formulation, clinical basis back be didn't that the we it's the disclosed and with really the investigators longer that an And longer new no and so forth discussions have that cohort and differences salt, the from new to to we the the entirely just naming that we we're have FDA so that it be and wanted no the entirely - it as represent the an we does original the has site, salt, we HCL was cohort for first cohort excipients articulated and to the new and as now certain they was one certain so with formulation.

it nothing negative that, for was great procedural. we give that. was there the just FDA And So about credit

Joseph Pantginis

Very helpful. Bill. Thanks a lot,

William Rice

questions. you appreciate Thank the Joe,

Operator

from comes from John question of next line our Newman the Canaccord. And

You may begin.

John Newman

getting thanks guys, you question. in - the taking and congrats of can Hi me? for terms hear

William Rice

Yes.

John Newman

long great. Okay, for getting taking Thanks Congrats holding through a for a the was process. it clinical question,

the formulation if Bill exposure recall can level to us activity, is for might for formulation like going you think thought you but dose could old you levels bit bit see start the look what to this reached wondered escalation XXX? a correctly, to better. with I a talk if Just be little where you a little about previously might had that

just refresh if on could So memory my wonder that? you

William Rice

started with per that's X. squared, per per told memory? patient. you therapeutic we thereafter never meter we back, that's formulation, that had the And then per was expected by got XX to cohort meter squared mgs mgs where range. we we But those meter so exposure the mgs infusion participation X the we all when the Your XXX we refined. had into unfortunately original the where XX meter get XX test off went that. square we And one mgs to The got patient, one and to next of squared with So advance to

your So breast We studies original we the time PK every four performed least us [ph] is and and plasma went times now. correct. the three in this formulation Xx over at has new formulation. memory created exposures formulation back new given

we So that said starting that FDA schedule. over this same a I now, formulation. see really dose are with Remember different as

Interestingly, the thereafter. real what with that So per we're XX patient we're then by XX exposure already at meter one we're out and in the up beyond level we starting as we over the this we per meter then cohort well was squared, in level exposure that the Xx mgs if we prior then XX. third the the to start XX, And one if original dose fourth is human, than squared, expected X at go saw at formulation. mgs patient XX at X

believe is a to the easy better clinic, with has formulation freeze solubility, to better it in better it. has that it, work superior we So proven this don't is be to exposure, it stability. it's We have

dose John? around, have greater it into get escalate your and quicker eager the a better way are get believe the exposures we can we believe Did that to question than formulation, original with the much and we would So answer patients. we we it's all

John Newman

Yes. And question back. one follow going of I have kind even up further just

not the correctly, sub-optimal can still even probably though it correctly, was was tasted and a seen years dosed a If There which can in level. obviously when it bit activity ago, not. at remember was remember lung if correctly. I original was cancer, was the remember if think probably little I even of though optimal were I formulation the I being dosing formulation there,

check wanted Just to double that.

William Rice

the No XXX correct. at at that dosing you think was than in squared. about are rather far wrong were the schedule, was are And wrong know. least a sensitive as dose patient that on per It it meter of weeks was every as mgs weekly. they not populations drug dosing I to the necessarily two And we

we're wanted involved AML that in have it's samples don't hopeful So we And there. to to patients - don't c-Myc getting We sensitive. see lung patient, look those But those. good that memory hopeful the see now there. activity Xx we're But patients, cells your tend that in we'll we're correct, from had, to very know, memory. was I been we again we're more be may the tend actually did we at have we wish activity a have would exposure, cancer

all we in hope, clinic activity the gives here. seeing us So this again

John Newman

Great, thank you.

William Rice

you, Thank John.

Operator

of next question ROTH from line Capital. our comes from Jotin And Marango the

You may begin.

Jotin Marango

reversal the the XXX, science question My a another. about XXX, my about you from hold. the on you question geek and ask but question I'll Hi, for of Bill, thank taking congratulations one to dosing was answered, just

resistance inhibitors and full spawned are So run BTK ibrutinib you of things, now. whole as the of the side on a field you that that reversible part saw of to rate know, we new the

faster to mitosporin side FLTX the we what there the anything would know just inhibition? original yet on starting why see resistance we this at Now do at which of what the side? development on a this is be is we AML you. starting things, BTK saw , emerging about molecular about we And Is to that similarly are resistance like path to or level level? resistance FLTX the the know to patient look now potentially Thank maybe

William Rice

well done right target on Jotin. Actually you're

a are that getting sorafenib the patient on treated the dirty well. the FLTX FLTX who it So many he for inhibit inhibitors, earlier a was the and that patient so I sorafenib, FLTX on was a is of inhibitor, doesn't also it with was instance, decided mentioned molecule, patients on it's trial that but sorafenib

call So on I'll midostaurin. that mutation. DA little is and and developed very is occur. bit beginning what had for of quizartinib arose patients extending story XX it those It a dirty they But from a they on actually originally pushed - and and a patients of that a more it that's the We're a it's different are that and additional but of But is different AML. DA inhibitor really even inactivity kind kinase, a rising of midostaurin more lives seeing XX is resistance to FLTX through thing. kinase for is great mutations

mutations get a in resistance talking to we see is protecting these get pathways, in always we if of drug to multi-drug And I'm populations as effectively that more combination see going And and too. and with able they that. are hope then go And definitely popup. treated being of patients is the that those those to of about and starting with the resistance. hopefully you're and is FLTX, you you drug is more what don't interesting are critical some want of one cells. you're the occurring to are have other after but all that pathways population in is other more don't we expect XXX this We is enough do a we're resistance to Some popup that midostaurin going drugs therapy

So another on the catch XXX good there.

Jotin Marango

you. Thank

Operator

[Operator line comes Lazard Instructions]. Asset next from Brown [ph] Management. And from of Ret our question

You may begin.

Unidentified Analyst

some are such in guys us you Beijing's could for maybe and the gen was other thanks put the the hoping differentiation potential of as Good how BTK development I question. that and for see afternoon positioning versus of acalabrutinib? you help Bill, taking second XXX into inhibitors context

William Rice

up So everybody's me asking to to geek that.

Beijing a in comparison covalent mentioned that XXX the put is let's inhibitor. you And So BTK so compound.

are mutant. in the and So they don't co-inhibitors. it's many ways it's CXXXS potency maintain those the strong ibrutinib against acalabrutinib similar to But the

after truly So I effect a acalabrutinib. how profile. see that's that as unless the differentiate they and in to trying U.S. as probably side compete think effective China. pursue the major I don't they I Beijing - be just to going know population that themselves to can with are in terms compound going of that's same being going And ibrutinib path in

the [indiscernible] ours you inhibitors that found resistance the and that inhibitor. this it emergence been CXXXS again out BTK covalent of Well, bucket of of inhibitors. original ways many once. into have other the BTK BTK were got is non-covalent population BTK that inhibitors Now in spawned fall that and a that does drug non-covalent

are wild All effective very CXXXS that of the against type and of BTK. us mutant

pathways and really So able a to down other in is the group to differentiation come patients. going of broad inhibit target you effectively cells to what are from

of non-covalent a all little need XXX BTK we or covalent clinic, us covalent of non-covalent think B-cell or differentiate to We you we the we with a or whether XXX we So because all resistance failed geek to from into forms go very BTK after that why who more? Inhibitor, incidence it's do well drug and the from ness, from activity. it pathway We be the effect minimize that believe put immunotherapies drugs that to can the Inhibitors. that's Was patients once side have bucket believe covalent profile. or hit malignancies, in completely give you we also us of inhibitors. the get are and going different non-covalent want other And minimize the going differentiate would and we better

Unidentified Analyst

was That thorough. you. very again. thank No, Thanks

William Rice

Thank you.

Operator

from And Lewis line comes question from the [ph] our of DRW. next Alberc

begin. may You

Unidentified Analyst

obviously, obviously for taking thanks not I not am science but without geek. a Hi, question. the I'm

I market are of, that out mean, the with relative is space So I of on to about in ibrutinib have carving a what some essentially, planning XXX you question the terms and with in sort would competition or other as that could you or the molecules sub-sector be at looking that used on view are of broadly market ibrutinib? what focusing this of you something

William Rice

Well, and for malignancies. we're develop AML B-cell to this going both for drug

me with too to much start don't have out with the we this. AML things let geek and So first,

for going all trial, once we just those we're patient AML go our does FLTX to try So to with escalating the after into get not AML, AML, ITD. with

some We of more get we So we're set possible, population to take as trial want Phase the that approval. minutes of to as very look X recommended could be. Is our at to population few see that data see to after and other what what be the is not and these it those to dose well going we'll older failed tolerated in tolerate go might rapid just going a many populations it a well very Jotin AML to patients and also identify the that the that that rapid escalation data going drugs through Are get This immediately. FLTX a soon is have be. well [indiscernible] drug want fraction of a ago. After it be Marango response. was could the because not inhibitors dose other going does after a

also you the after sub-populations patient believe and that approval to going able we'll after you population where be can you then to in discussed. have But we that AML the So rapid go maybe we ultimately populations that. and just want most in to believe do get we all

go covalent these treat who the all develop with drugs have malignancies. or want all to the malignancies. used of B-cell the that into escalation from to patients the non-covalent felt types B-cell have to malignancies Now the Again, or different inhibitors either other dose BTK we

began the activity. once go inhibitors for those be populations patients begin and the And felt dose us looking to in be going we'll all perform see escalation. X, get we to we But for out after So that the able who Phase we that differentiate be escalation we'll to expansions we'll where non-covalent of approval. covalent after where into should it's I we forward. the the very expand going that dose after patients had sub-populations broadly broader best also the rapid and others then portion path go to through ibrutinib And the presumed point the from a the would directly. would be to actually that

clinical speculative strong thing database want initiatives, also other there. malignancies and at more population trials in this bit go able sites The and investigator may a little the a is on other to we at institutions, with through we that be that are we're certain point. to want clinical get after have assumes look to we something but this interest a that's of do It B-cell interest lot INDs have is, pediatric adults, from safety we from

the we get the to most us. always So at that are we're we likely looking approve. to do will allow most drive rapid But the as data groups those

Unidentified Analyst

very It's Yes. you helpful. Thank much. very

William Rice

Okay, you. thank

Operator

questions closing no the time. Dr. And I'd remarks. showing to back call turn further I'm Rice at this for like to

William Rice

other with potential patients trials supply. malignancies. with the leukemia deep of your we thank do acute remain today. your patient questions you and important joining clinical the in you confident to in hematologic Well support, clinical for the as is XXX for XXX All everyone We right. all reinitiate the us option of We dosing myeloid thank prepare an continued first especially for

have ASH. our www.aptose.com. on to a We talks always again Also on. present the out program I see announced able be presentations the our for also data our thank know to this also keep evening found that be waiting we webcast on recording that year advancement progress the keep as the everyone. please to forward And once end of we towards and note open And you hope and put year be able to of can and deep XXX. preclinical We recent continued look the your hope some data for goes to the so to of are website considered information at good data,

Operator

Ladies in may you and program. a gentlemen And conference. does participating have thank day. disconnect. conclude the great Everyone This you for all today's