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Aptose Biosciences (APTO)

Participants
Michael Wood LifeSci Advisors
William Rice Chairman, President and CEO
Gregory Chow SVP and CFO
Jotin Marango ROTH Capital Partners
John Newman Canaccord
Joe Pantginis H.C. Wainwright
Call transcript
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Operator

Good afternoon. My name is Sabrina and I will be your conference operator today. I would like to welcome everyone to the Aptose Biosciences Conference Call for the Year-End and Fourth Quarter Ending December 31, 2017. [Operator Instructions] Thank you.

As a reminder, this conference call maybe recorded. to like now would introduce Mr. I of Wood LifeSci Advisors. Michael Please go ahead.

Michael Wood

results and Thank to and operational Michael ending Wood good Investor I welcome Advisors, firm XX, Sabrina, quarter discuss the December fourth to and of call everyone, am conference for afternoon you, Aptose. XXXX. year Biosciences the financial the LifeSci for Relations Aptose

Chief and Joining and CEO President William Rice, Greg Senior me Chow, Chairman, on the call today Financial VP and the are Company, Officer. Dr. of

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

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

Dr. President turn Rice, over and Aptose. of Rice, now Dr. call Chairman, will I the So please go ahead. CEO to

William Rice

you very call been two today, welcome quarter especially status our to like December year CG'XXX year malignancies. we to Aptose the of the I'd for and a for for XX, update hematologic APTO-XXX, much and XXXX. have being Michael. everyone and to products on ended developed you, our It's productive Thank

discuss and other initiatives, upcoming we timelines. milestones addition will In

Greg we'll Chow quarterly for Mr. financials CFO our updates, will and our then call the question. open these Following review your

dogs. the up characterized cause These some and appears might typically which the is we toxicities. rodent in sensitive news. did generally welcome toxicities rest by range Yet, cause successfully maximum are to unexpected at rodents and studies studies reach that which report was I’m complete levels toxicity have with put this exposure per we as XXX pan-FLTX/pan-BTK per dose. feasible developed highly we B-cell to that some from it, CG’XXX the AML to during XXXX or begin course class and as clinic. call we inhibitor in oral being CG’XXX close of And getting how are first-in made wants an into Let's everyone addressing malignancies. we a with know a for To in patients certain route progress of begin, with multi-kinase our synthetic human first and prior well of API batch that deal calls, reported we needed substance the in that of scale highly finding to XXX API accepted pleased dose we CMC in for completed XXXX milligrams the the trials. of purified studies. manufacturer manufactured and matters In or PK had formulation to solved range quarterly and dose the we sufficient safety finding dosed kilogram the for drug that great And very dose. high that not still This data even dogs XXX day to

will assume hope robust the bone that animals to because to humans. perform to that will and hit into do appear are toxicities dosing, targets longer-term we continues a toxicities in therapeutic we we suppression those by trend expect to the bone we marrow Yet marrow still XXX. window related observe suppression. we as began assume We be to be related However, likely and have

mentioned the call, have understanding of we clinic kilogram the manufacturer this confidence batch dogs. malignancies. for to initiated into of Further upcoming cover during submit already on trials that Those be for are X.X in progress year prepared we an trials in as our both and to the second submit and IND AML IND studies to good And I will advanced the rodents GLP the make that trials. such safety an enabling to track on studies immediately last continue and remain for of scheduled we and enabling latter pharmacokinetic GMP quarter and clinical we XXX portion have Plus have to used both We batch of the IND a year. have during begin manufacturing now move in B-cell scientific now added IND this thereafter.

and recently for regulatory but As because a matters. designation kinase inhibitor mutations provided ITD moving in to in region. of Food so of asset. support these and the of approved we granted development as referred embattled Drug in orphan Having midostaurin AML for now FLTX timelines key drug other the the mutation drug compelling XXXX, and few kinase. AML. reminder, tyrosine the marrow resistance FDA's the cancer is the the patients U.S. accelerator blood you about AML orphan with to assigns medicines the beyond during devastating patient with to ITD we’re inhibitors patient receptor office us designation have FLTX the for spend FDA XXX ITD driver a and occur are and the why this or patients. of of and underserved in kinase of a in one-third is drug tyrosine the to FLTX bone benefit have given drug that And announced disease The Administration for CG’XXX revisit products domain approximately this FLTX fourth population gatekeeper mutation excited remain orphan quarter that clinic these let reviews agents me the anticipated a provides The into minutes development

prominence been the with mutant the to all harboring shown forms retains very resistant it FLTX nanomolar to gamut disease Yet Why most inhibit it which AML forms effect Because against XXX that poor from compound profound drive cells. that true pan-FLTX the are inhibited is marrow human and mere lower malignant derived essential kinases rescue HXSXX including still this if AKT, ERK, XXX important? upon even the mutations. a control only that lines including BTK, relevant and more Our of for and antileukemic exert insufficient impress AML picomolar of CSFXR, inhibitors. kinases, meaning mirroring to studies, FLTX exert that XXX us potency that is other is potent cell prognosis FLTX to of related known and clinically FLTX in has In rendered pathways bone is AML. leukemia malignancies inhibitor. associated Aurora the to compartment. of the Other is for than The against are you FLTX clusters all inhibitor preclinical forms others

wall set thus sufficiently Similarly, cells animals. FLTX other additional pathways rescue pathways and and a B-cell it XXX type diverse the cancer well-tolerated malignancy cells range BTK of B-cell yet kill forms and the remain across and suppresses of exert a cells. XXX and these broad to mutant of suppresses rescue ability in operative by However, killing that of diversity can AML the

caused Andreeff MD Some in Health Knight Dr. in at XXXX our under bone of simultaneously by other Dr. Cancer and Anderson’s of three MD poster Michael the of the exciting ASH by agents. to multiple XXX University, cells Brian were resistance & December range and kill researchers subject ability Anderson to partners presentations presented marrow act AML Druker. Center Data overcome with of pathways prestigious unique with those Science elucidated the under broad presented Center Cancer suppressing a cells to preclinical stromal the Oregon conjunction by synergistically of data research

cells inhibitors at in of the the data the pathway, as XXX BTK, been to ability plus eliminated a multiple presented FLTX AML circulating form killing antileukemic ability of ligand and of additional in XXX FLTX. Aurora cells. set broad just ERK derived striking Druker over depending the Anderson OHSU XXX Notably, presentation and MD a more XXX marrow as well study mechanism to the poster the in to of stromal of ITD, cell midostaurin, XXX. a also by demonstrated expressed have inhibitors by are AML program through patient’s AML the cells or development. FLTX hypothesis was differentially competitor is mechanisms and AKT, FLTX well with underscore vivo against those bone the in in these signaling host of of suppress FLTX patient cells for cells operative AML. Specifically, corporate to background differentiation in supported gatekeeper presence that tyrosine pathways FLTX elucidates XXX death cells kinase, heat and other subgroups from FLTX CSFXR, data the of our antitumor FLTX development and and patients Cancer a data XXX as ASH other involvement from mutations, with demonstrated to cells all wall AML activity XXX of different XXX those agents. type kill A evaluated from of broad-spectrum Separately on in model genetic is patients demonstrated and sensitivity AML illustrate and under that of overcome inhibitor. ITD In data Remarkably, the that FLTX other superior kinase and its maintain sensitized seen further Center map FLTX cells domain hundreds that AML marrow of inhibitors. XXX presented quizartinib Brian separate with potency dose-dependent ability AML or the resistance Knight a samples bone diverse and malignant in as presentations the to Together XXX of These than in inhibitors AML pathway the Dr. standard chemotherapy

how grows, normal AML to of mechanistic and molecule framework kinases are understanding heterogeneous of XXX can group our without observed specific cells. construct in of toxicity As single clusters of cells we a beginning inhibit

XX% of In to Ohio addition ibrutinib approximately reiterate here the I that to refractory XXXX the studies multi intolerant various diverse an by standard Based XXX sales all potency in billion to performed X.X target to has with care. discontinued is fold lines proving and XX% being cells, at of dollars be inhibitor University, a Yet than which approximately BTK of or to State kills to malignancy vitro approximately cell a team treatment greater ability to on current with the set AML resistant approximately XX% noncovalent ibrutinib worldwide and years FLTX estimated act annually. with ibrutinib a B-cell after the treatment. patients of on X% also XXX want half of

ibrutinib medical opportunity. among continued market significant unmet So with the need comes patients the discontinuing

the with broad against potency cell greater refractory to patients refractory potently maybe its researchers covalent of treatment disease. bone lymphocytic malignancies and on Cancer XXX as full myelodysplastic ASH XXX subtypes ibrutinib. samples tolerate due Cysteine BTK allowing over that and Beat of to marrow patients directly in or than of ibrutinib treatment malignancy malignancies. rescue the patients including various the patients allow CML, to presented a findings an Through inhibitors resistant activity And set to other inhibitors. leukemia. to specimens these this to XXX is treat and ibrutinib XXX from and form or diverse the treating useful covalent cells, XXX important to CERI and the of properties addition multiple ibrutinib. Initiative from OHSU mutant potent they BTK inhibitors. XXX. discontinue noncovalent which many residue Knight around that is against primary cannot cancer Center BTK other is Plus other go B-cell prove used pathways well In AML, hematologic in finally of primary XXX the range compelling AML, ibrutinib on neoplasms the inhibits XXX potency XXX be a mutated malignancy lines exhibited to syndrome, In inhibitor tolerated myeloproliferative to activity patients and BTK hematologic kinases a are Thereby that resistance acute AML may and in resistant study diverse to Together Also from useful and that at B-cell and option tolerance killing and back patient hematologic CLL evaluated provide retains

of to summary, the corresponding that findings to There on the is presenting it other Meeting reveal us XXX new please website. detail sharing press superior in clinical compelling the and presentations and are in look our AACR data further collaborators with inhibitors. For In studies. at than growing you. and releases continued preclinical or our surrounding and upcoming BTK research forward our all ASH see We that on more XXX has results will development to excitement be to we FLTX April are Annual the see eager of

to molecule clinical turn small the dosing. and first Aptose And XXX to oncogene is timelines So c-Myc path we now discuss which let's on return let’s APTO-XXX. inhibitor of plan expression. to

as During manufactured studies a of reason cause XXXX we XXXX demonstrated at the sterility to step to we of Since sufficient well product marked FDA successfully a determine the bridging return particular supply order one we completed root of to to our release clinical our and failed manufacture last call animal to for stable currently the XXX. that performing completed stability and new We drug supply stability, to of have seek see for the findings process I’m manufacturing of submit formal the drug hold. happy studies, clinic. our us end in now infusion correction drug GMP test to the products the in of as GMP product studies manufacturer of and allowed soluble are the the

so we expect Our dosing respond submit we to in has and related be FDA to XXX response CMC clinical quickly is will the the orphan our we the AML, that quarter the product expect ongoing of were and FDA studies lifted designation soon. because with happen the second providing resume patients next the hold successful step drug which may we will hope to

clinical and an and expansion soon patients we initiate expect couple with in of there as to the dose Xb a those sites hold these open hit participate screening running. for phases A of secured ground our or XXX with we will trial RFB patients and dozen MDS immediately we early reminder a trial. approvals have get escalation as or the sites have AML of both more As do Phase

and trials So we're physicians AML clinical treatment soon, to hopeful eager of the test of the restarting c-Myc patients. for the the XXX are inhibitor

not will studies and and the take not have risk unforced I However, an of rush these error.

the it will the regulates keep or in to efforts our dosing as hope to The several I AML cell the background have soon We and deliberate clinic. proliferation and a just be Myc Because as posted. will eager possible in inhibitor and Myc to normal We growth XXX non-myelosuppressive are Myc patient in have of investigators and here clinic return we we a careful return for to to and times, c-Myc you bit mentioned required. is proto-oncogene apotheosis cells. clinical

has in becomes cancers However and to Myc hematologic often over leaving Myc expressed to it actions bone marrow derived AML inhibit oncogenic cells notoriously protein. the difficult been the including of

an inhibits have as However indications. gene. XXX Because our that key hematologic tumor target solid Myc may of molecule new XXX research for malignancies across suggests approach entirely inhibitor anticancer a it many the in is small expression a application certain represents broader and Myc malignancies, Myc

a one talk molecules. our global APL-XXX of all a about India pipeline to deal will and the agreement even to commercialization we and door certain Aptose's deal will the Earlier This other million we've develop a BET upfront to in of up develop tolerated particular we XXX, is inhibitor oncology, action but milestone at dual part but provides entered expression AACR drugs. accepted to mechanism and development, had for that publication of cells with as for of for announced Some related presentation at learned XXX The $XXX two payments been therapy to and and report well in interactions review receive has for that defined. in that which program rights The with and the has at provides that of path have significant a Avanti the BRCAX action have represented the not function. molecules was is FDA reacquisition Aptose research approved will of particular almost if deficient it as like of the to and kinase OHM XXX, I also potential APL-XXX. molecularly of the goal particular peer hypersensitivity, tumor these learned we Myc synthetic to indication to publications rather and/or results Indeed for the directly protein details XXX. that the It gene lethal is the in exhibit that the The or while exhibits be acts expression. payment molecules. as target and homologous retain functions Sciences Aptose's approved. kinase is the identification to is Life identified The with Aptose Simultaneously, lethality shown new promoter all revealed into how maximum provided third repair for on indication of program. BET the ability in targeted by of stuff eligible does solid related to focus the These exploit upcoming for indications a interesting The unlike protein of XXX XXX region will rights deficiency that of drugs Laxai sublicense does with BRCAX because program. our and inhibit not interest in this Myc and publications. inhibitor XXX rights the month subsidiary manufacture other the gene. the and recombination olaparib molecule dose. of global XXX molecules first was OHM in research further sensitivity myelosuppression other produce XXX. clarify cells ASH two nominal opens inhibitor published license olaparib AML to bromodomain from accepted to of abstracts DNA molecule. now interact royalties APTO-XXX been bromodomain loss inhibits comparable In We synthetic of we’re but

evolve lead action As drugs several develop with to for you protein program. to Inhibitors inhibitor oncogene. epigenetic regulate recall, the from an LALS their expression BET represent molecules work earlier because of ability pharmaceutical BET companies class APL-XXX the pursued being of by interesting Myc of may kinase dual bromodomain of

an to unacceptably led molecule. APL-XXX priority bromodomain tend a to effort be BET sort activity to simple engineer additional inhibitors to and so as However, That molecule. we inhibitory toxic the kinase

it it by future. in additional a has driven for means finds encouraged and to patients and transaction cancer as meaningful for to this home are in potential oncogenic non-core Moreover Aptose funding an non-diluted the We a cells. bring target to new processes agents provides Myc asset the

come during and year more one We far in towards look have important milestones XXXX.

the More our advanced importantly and such year ongoing an XXX to this support to B-cell looking over the of IND the back our we’ve I in turn and you Xb trial that Chow programs. pipeline we we Chief now submit plan plan quarter. to Phase AML AML NDS will Officer, return reporting to will results to who to forward of and malignancies. for XXX in those we're review call And to trials on patients both Financial Greg

Gregory Chow

Thank you, Bill.

to on December to reporting We million investments Canadian our XX, at XX, and move financials, we million changed million dollars. December U.S. with ended dollars please of XX, US$XX.X US$X.X I currency compared the and in cash cash XXXX CAD$XX.X or XXXX equivalents note as Before CAD$XX.X December XXXX. that to from million or

in extended cash runway the ATM utilized our use approximately which middle XXXX. Through and During Cowen, X.X our activities and million XXXX. on XXXX the Capital hand of operating we current in facility cash we million during expired with of the to our Aspire facility the equity our December have three with committed of December with XX, quarter, ended months X.X compared cash

million increased months XX, for cost and quarter. the XXX statement, return for to to compared XXXX. over the the to the and for the expenses months program the cost no LALS were three $X.X $X.X on increased $X.X mainly by ended expense on expenses increased spend million prepare December income to we quarter ended of the R&D due three cost due XXX had to and revenues XXX back Moving due offset Total compared XXXX. headcount cancellation potential to million program lower for the to the to General higher the $X.X development were Research and quarter increase and is December clinic. to of The administrative salary comparable for XX, million Moffitt quarter collaboration. were

months loss $X.XX per loss net the the XXXX. for ended to I the compared $X.X our XX, Finally a Rice. million now of call December $X.XX per share back was $X Dr. to will share or or million turn quarter over in three Bill?

William Rice

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

Operator

And our question come [Operator Marango Capital ROTH from line with Partners. Instructions] the will of first Jotin

line open. now is Your

Jotin Marango

your each program. I have for one of

of are just one first of a XXX, is couple in of a ASH has indirect with Myc of this XXX. So including bromodomain which ago idea inhibitors months reinforced the target that been presentation the which your you inhibitor you out-licensed lot few that there a the

all what you do as of inhibitors in Myc XXX see advantages out versus So the bromodomain potential a control there?

William Rice

Let’s Joti, answer that it’s one the go we first hear XXX to good and program to hi from before you.

than proteins are And apart For you mid we first bromodomain get and inhibition the that form aware super enhancers think reason fall a see genome. enhancers early inhibition bromodomain able is and get bromodomain the that that us most hemalignancies inhibitor gene the throughout active your c-Myc gene hit then super of to of when of you every I the and on an those are are inhibitors, certain along you with c-Myc. that

kinase not the PNAS month. dual introduce saw getting inhibiting inhibitors tend the high molecule the inhibitors. action to just kinase XXX, the bromodomain toxicity we I reduce another our bromodomain past that proteins can program the to But and in the in see aware toxicities bromodomain the so However, genes you active general XXX, the of all a was of hit with why you why inhibitor. on program that have effects bromodomain also we likely we and the are the then of on the wanted like also bromodomain other hitting other published level back that's such very were inhibitor just bromodomain ability inhibit a proteins. begin just to that’s of where and all a With with recently

c-Myc We’re not either. directly

Myc on we’re region the gene. three-dimensional acting the gene. c-Myc it stabilize and the promoter We that a So of turns DNA off and structure

So and not the and this do gene we in the inhibiting we’re the humans. we’re and c-Myc circumstances depletion under us clearly see the do give myelosuppression in expression to that protein animals that of cells of able or

So we the a see advantage that is bromodomains is to are as that turn and main C-Myc to that C-Myc we not hitting the and proteins the cells and off by not gene able the tolerated. with well molecule do very so

So now. about question XXX the how

Jotin Marango

So in you no up kilogram do on you gram a doses that is gram I see to XXX per X mentioned have that toxs X dogs it or right? of

William Rice

Yes.

Jotin Marango

dosing, do cut high drags and FDA that's you at then in So Then is do in X starting so, how of X go fast effective great. the question through you expect how to but in long set all high and the titration? X tight then in is expect a single then be moving potential stuck plus being with a risk to I you slack on but oncology Phase do conservative, and bigger run guess really toxic you you the dose. molecule me a with as which not

William Rice

answer ways of that. to Couple

get kilo we’ve per X to try First try toxicities. and exposures of toxicity it We all gram was to dosed to twice and thus to seen daily per day. push even far no the

drug used rats day and dose level levels per have a no dogs, in than highest kilo and did exposures couple highest - tox. have saw plasma the than rather are because per they gram and we so emesis higher putting dose. rat exposures, med throat At the dogs down So, even still dose and mice X much of the we we of that mice so intermediate at effectively very

the was there down effects a the However, the of it putting were of toxic amount throat. drug you’re tolerance just no

range we’re mice studies the the days, soon XX-day dogs suppression, so a and again we longer-term for going dosing, emerging tox marrow those day it's do and beginning we’re data. in Now five are again twice those some we of animals in dosing animals. suspect the enabling dose be expect studies. very to fully Those finding fact, bone that to over we do see And and IND are last only toxicities hopeful but

inhibit levels able clearly We’re to in animals tumors the achieve - growth toxicities. eliminate can tumor without that and eradicate the

that a turn see than are we actually able so affect that the toxicity we starting be at to starting will be that and high IND it in may enabling dose tolerated with therapeutic out dose, hopeful may dose in but I the the dose may level, but be in the that and of first thereafter also more We’re the animals a lower studies are soon levels humans not be think we yet levels therapeutic.

Operator

the from of And will come the Canaccord. next Newman question John line with

Your line is now open.

John Newman

I with the the there? just can wondering you else ibrutinib, cancer. see ibrutinib the us those is what cells the actually are kill one Bill do kill seen compounds you was the effect XXX something first of previously terms question believe way happens between curious of and remind B-cells that I’m differences that ibrutinib in in could said XXX you've just that I had just that wondered you the if each B-cells

William Rice

during you if all BTK on you over the below of XXX. nanomolar in other going each at When of completely because with increasing BTK Interesting I inhibition that activities. see So - cells. you ibrutinib, inhibit glossed lines. nine treat think that B-cell XX I or those with We’ve cell you’ll ibrutinib day was the with we’ve just of look concentrations malignancy question presentation different I looked those so treated at

you kill micromolar. However, don't the cells until up get XX to you

to toxicity it's cells. So the general a

inhibiting in cells. the BTK by just cells that does directly shows those it kill So not

what in than XXX treat average about do the I that as of because the we’re on we mutant you other form BTK, we the ibrutinib. cells, mentioned potent as well if That’s killing XXXX those. on we’re killing directly with affecting times BTK. more of that’s pathways so X,XXX is However, CXXS see nanomolar is But inhibit cells top

different AKT, at they different at look HXSXX. that you are if BTK, some B-cell pathways important malignancies those the of different levels cell BTK FLTX, So lines all CSFXR, all of those use

pathways to transitions to So killing also which It is then directly [indiscernible] our which able leads leads to multiple as there cells. phenomenon known drug a to over affect death. cell the apoptotic

So with that molecule ibrutinib. does what or occurs not with as that our occur

mechanism. bone in you the through has BLK that We But marrow are the and much by If but bone you They cells. the of believe It at the same bone still ibrutinib malignant and will in the bone kill have on through cells directly also ibrutinib. marrow. cells killing in ITK. its get can inhibit of killing is much have marrow our the stromal there effects the didn't cells the effects look marrow direct BTK, those signal drug you the we not effects in vivo, as

that drug question? inhibitor can we're answer noncovalent be So your hopeful BTK there. the Does best-in-class that out sufficiently our

John Newman

into Yes in CLL. looking if more AML. in of thank broad or one specifically you I’m terms mentioned B-cell eventually ask you. a targeting you And will with as the I wondered start if that well wondering I will as malignancies you you clinic B-cell moving the out of - you malignancies be could at will B-cell XXX malignancies start both group

William Rice

year for clinic like this feels us. the expect into said IND that’s what we you into to When head clinic. the that be eventually But it and the

mutant may look with the patients just or at you of they developing focus they may that form are BTK inhibitors, on on if the BTK. CLL Now focus mutant other companies

We’re is serine after we DLBCL all form if ibrutinib those they Again believe mutant in patients going we that the CLL, other the activity against discontinuing there after Why? the site, because our be care and doesn't whatever covalent patients whether discontinued are, drug go or we the inhibitor. that MCL, are so can anyone ibrutinib patients. any or retain cysteine to is active go

we of they’ll then actually we different a the covalent we're Secondly, never directly finally hit inhibitors because those responded. other with to so that and some the after ibrutinib, to a we and XXX intolerance these of is hopeful ibrutinib TEC can they’ll patients EGFR refractory comes Many hit ibrutinib that the those inhibit our any to the pathways, respond discontinuing believe toxicity percentage and effects. a BTK of inhibit are the TEC it drug side of the key that which means the to kinase the or not ibrutinib kinases. look those kill inhibit and associated ErbBX their tolerance, to due you of because fact that driven they’ll patients drug are or will which those if that are are when number are all other discontinue refractory of who the We're the And inhibit ibrutinib the many fact tumor pathways those patients of we we go driving those cells. does by that ErbBX quite

So be intolerant. refractory again or going are we’re treat that to believe resistant, we to able patients

escalate coming us John dose to indication, put going will not to a that chance of B-cell think fractionate We X. So better they’re to us Phase escalating in resistant allow faster thank the give activity to dose if not and humans. into the we’re in. the want out patients questions. We for those patients And all to take you regardless see malignancy and regardless would or the patients the

Operator

And H.C. Joe come Wainwright. line with will Pantginis the from of the next question

now is line Your open.

Joe Pantginis

XXX with for studies to you you verify that for already. just about talked add to some animal So models the IND enabling want can regards I color the

to correct? don't like to and sounds you XX the going past on it duration dogs gram So the in X increase that days you're just dose plan looking is

William Rice

exposures get you because mice the twice into try the daily models. going doing animals we’re in push to to again we’re dosing toxicities So high

we days. So mgs was for no XXXX up mice per per are and there toxicities five observed in to that that day we kg can know go already

maximum because we’re to to high In levels level go to yes those considered they mgs the that that level. that’s per two again and then the and enormous not day tolerate dose going of not to I have an XXXX in believe drug, to plan take the below go dose that feasible but per don't we to plan So dogs, will is it’s doses amount now the kg it mice. up

we XX going toxicity will the that days. day. exposures per emesis, the see will proposing - They we're achieve believe three levels we tolerate. day blood then dogs we over to push dose hopefully will a the C-Myc's be still so the dose but use animals You that high to lower levels answer FDA see question? that the AUCs Does and But we twice your both some will can there and so that again, the dosing achieve that levels

Joe Pantginis

restart back back to It at. you necessarily what that the you don't switching clinic, just the us If is I I think remind XXX true? XXX, recall to certainly initial you doses have can then to And doses does, can when you. thank gets go to hopefully

William Rice

levels dose We and whom the actually team, will those we FDA levels and times different why. animal back levels The formulation here's the would prefer three to right dose determine new FDA to we've go over this will prior actually would now gives and XX those exposure make what us expect our but to I proposal formulations in models. original a the tested

XXX exposure dose so increased start mgs XX was per at us most exposure there, which and we to mgs dose going go We what giving get dosing at So XX. the to getting we’re start per than and of you XX levels effectively we're the and meter level, original levels if original is XX squared significant start getting levels. that think exposure we likely meters meter squared we believe that’s

be So plan. our that would

answer patients once did exposure believe the to weekly with - The plan We in to which exposure is and twice-weekly formulation. will will other directly, a you so this doing patients level but because this going on we than of expect we’re significant you higher the is the to we dose the in like this. that levels much how to to sense the rather We go more better. dosing the thing of past. But believe levels back we be original be gives

Joe Pantginis

doing where step on formulation, problem it Have the occurred you that be the infusion different obviously with yet right that to pending? you beyond that studies infusion. that things think part the several marked able the moved see And marked the still mentioned you or now new stability, sterility, was might is you're the I in patients?

William Rice

studies what infusion you has I product study ongoing the the drug those performing that been producing been can but we've are thus marked So beautifully tell far. all new in

all for studies we standard that these the studies any clinic. to are perform drug that the you that perform Some have - of goes the into

used Some then as and the been to We've get of be completed reports soon already couple the as they've completed, FDA that out of and to up have worked that have a possible. to have finish those beautifully.

There's the drug thus we that fact the So and so feel had we're really with based in that product back perfect. can good allow that will no go back guarantee on the and drug products about no clinic FDA we've there's far showstoppers to we what we've everything looks but far happy to it be we very the drug hope guarantee now, no our going superior get again but that really made and see soon. we product to into earlier is

Operator

with of Mark the Instructions] question will And next Breidenbach Oppenheimer. from line the [Operator come

open. now is line Your

Unidentified Analyst

Mark. It's Matt on for

you of actually Phase but - to synergies clinical and it's for that under question the in trials got questions B-cell or plan BCL-X an you separate you existing one that malignancy preclinically can prior to to Had you that both the of firstly include your bucket strategy year John's of enroll protocol? showed planning enroll around you've on you tag patients Sounds X one B-cell AML Are a like inhibitors? secondly, you include considering do do think lymphoma asset. ahead. with couple do especially plan kind XXX, follicular you And

William Rice

and as to hematologic that cell that viable we malignancies BML leader. submit the the any that we cover in a do IND So, under first will well trials, malignancies hemalignancies of the all deem plan single the of other for clinical - IND covers AMLs, as

we're FLTX we to escalate in One not patient's have faster because and AML Phase separate broad However, with us that taking perform And ITD. to one The B-Cell the one-third escalating patients one that going malignancies. of plan because studies. patients in the we in two fragmenting allow dose the have we’re are X of will activity all-comers there. that dose to AML AML

The [indiscernible]. be that on to different hope escalate sick Very to will these these these that that going loves and inhibitors the and the malignancy all-comers discontinued and to dose the or - reason into we’re different to patients. hopefully B-Cell take coming The ibrutinib separate patients, trial, we for AML is you and patients mentioned I covalent And allow faster. have really refractory factor all separate trials us patients two escalate so again that we quickly other often are dose who in able criteria are these again AML. that to inclusion patients have exclusion are to

two So, separate a Phase single Xb escalating IND dose trials.

compelling now. In trying terms collect one lymphoma, we're argument follicular that's to on of but again data that

So data but we justify that the to trying data believe this that additional We pathway for rationale collect a some that time combination at especially we're us of understand enough. the and to we've maybe seen.

Operator

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

William Rice

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Operator

participating you. for This program. Thank concludes gentlemen, you and thank conference. in Ladies your today's

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