Aptose Biosciences (APTO)

Susan Pietropaolo SMP Communications
William Rice Chairman, President & Chief Executive Officer
Gregory Chow Executive Vice President & Chief Financial Officer
Jotin Marango Senior Vice President & Chief Business Officer
Rafael Bejar Senior Vice President & Chief Medical Officer
Tyler Van Buren Piper Sandler
Gregory Renza RBC Capital
John Newman Canaccord
Matthew Cross JonesTrading
Naureen Quibria Maxim Group
Matt Biegler Oppenheimer
Call transcript
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Good afternoon. My name is Gigi and I will 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, 2019. At this time, all participants are in listen-only mode. After the speakers' remarks, where will be a question-and-answer session. reminder, call a be As Instructions] this may conference recorded. [Operator

Ms. now Please, like would Susan to I introduce Pietropaolo. go ahead.

Susan Pietropaolo

Thank to Aptose communications representative financial afternoon XX, XXXX. and call ended Aptose Pietropaolo, and Good for discuss a Susan quarter results and you, to operational Biosciences. December fourth year for I'm Biosciences Gigi. conference the welcome

Vice Joining Chairman, President Mr. Senior CEO; Executive Vice and President and Jotin me Financial President Gregory Senior on Dr. and Chief the call Officer; Rafael today are Medical Business and Dr. William Officer. G. Officer; Chief and Rice, Chief Bejar, President Chow, Marango, Dr. Vice

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

performance regarding and that and performance They differ stated Forward-looking but and involve risk unknown learn current events, known the more performance, on of and SEDAR these cause actual uncertainties reflect risks are could results Annual To those in most read these is assumptions please recent guarantees Aptose's possible SEC and from materially results, actual XX-K and may expectations. it Aptose's uncertainties, filings. expectations Report and future set about expressed. materially from forth factors Form that not statements risks, differ to and achievement

events made. reflect statements by law. made to required no undertakes Aptose obligation this are circumstances of as these call, to date they statements of forward-looking All or as date during this only after call the except revise update the speak or

and Biosciences. Rice? CEO the call over Aptose I Dr. Dr. to Chairman, turn will President Rice, now of

William Rice

joining this many to challenging to as on those and through fourth XX, ended you, well XXXX. times. who been the you We're as shareholders journey I'd today, year everyone have our for have call the to us call quarter Thank Susan. of us like December with happy new on welcome more

group our into clinic. for while CG-XXX APTO-XXX we a two had these of clinic these agents this of and wealth active and foundation a July XXXX we compounds along painstakingly clinical moved data stellar I'm now supported constructed generated advancement with the the to trials. that research of to company, of We, the lead targeted two have hematology and the collaborators, truly by privileged compounds differentiated preclinical highly

We expect XXXX to of continue execution, data. more generate and continued to meaningful clinical be we as one patients treat

a me call Let begin a discussion the from quick today's of clinical progress of by XXXX, recap with highlights candidates. our followed of

presented annual and year, the data ASH. EHA During we meetings the a of wealth of AACR, at preclinical

these All the presentations acronyms names of available and full our of those are conferences on and website. the

sorafenib, Preclinical crenolanib midostaurin, Druker's AML, presented primary team patient CG-XXX, ibrutinib, demonstrating including FLTX included than BTK that inhibitor other data acute potent leukemia, and our such samples. Brian Dr. inhibitors, with by against gilteritinib CG-XXX, first-in-class highlights, more OHSU, at is quizartinib, myeloid particularly sunitinib, or

preclinical Compelling in patient demonstrated venetoclax future suggests strategy. which killing, potential samples a enhanced cell combination combination studies, with

all doses CG-XXX model. a at throughout XX-day dosing. suppressed exciting vivo tested Another highlighted the efficacy in study in leukemia exceptional of xenograft anti-leukemic the period mouse CG-XXX of growth preclinical

treated dosing were is doses agents. with After halted, tumors seen with was growth, the other seeing as lower

cured. through XX% a of dose group, mg/kg were of were the of the mice XX mg XX And higher kg However, with in of XXX the per cured in or mice treated mice five XXX. XXX day XX

XXX. no to grow, resistance no In mice, two response, retreated additional groups beginning Retreatment in retreated dose were allowed mice toxicities resulting for in after a the of XX uncured observed. through to day these led XX the the and drug cures antitumor rapid mice tumors all days on of were an day

cytotoxins, and as other failed groundwork other studies AML that the with AML hypomethylating to to laid less FLTX for therapies. patients have CG-XXX agents IDH responsive BRAF that patients pXX, are mutations in well and these as inhibitors, having delivering Collectively venetoclax,

spite MD XXXX, all leukemia mechanism researchers date. in of CLL recently, efforts cells. desirable Cancer preclinical on toxicity extensive Center a ibrutinib-resistant from in its mantle December presented our elucidating studies cell or and lymphoma, reminder, sales CG-XXX the Anderson in targeting a ASH of Most in to posters chronic As our of action at two induce effect in of to profile models, safety animal lymphocytic MCL CG-XXX's or inhibitory demonstrated

of CLL exerting ibrutinib, demonstrated on than potent potent also in effects CLL. more be compared ibrutinib-resistant data cells us has to position with to for cancer demonstrated from anti-lymphoma inhibitory CG-XXX cells. cells, a MCL B-cell lymphoma standard non-Hodgkin's Collectively, these multiple and cell ibrutinib, XXX including patient labs in primary care the trial ibrutinib, clinical thereby showed against CG-XXX Data these various resistant current potent activity superior patients. of effects those

up-to-date year us momentarily. of our I'll Clearly, APTO-XXX you the initiation was a CG-XXX the on for as well program clinical clinical the that mid-year. highlight as bring much clinical program trial anticipated of

Also us Senior we who President to to Officer. experience Officer. as and during Jotin In in clinical Medical announced appointment Bajar, the Vice XXXX, of Vice our an management extensive with research position and joined mid-year to Marango, considerably and scientists, team. President we introduced Dr. Senior the December, of Chief hematology internationally-recognized previously physician We've Dr. strengthened Business Rafael you Chief

also recruitment Vice we our Victor Mr. announced of as November, in Montalvo-Lugo Clinical Importantly, of President the Operations.

to outstanding have integral very our their fortunate to Dr. such the part Dr. Montalvo collaborative and to attract executive We've been already to culture. credentials be individuals the of Mr. addition In in an proven field Marango, join team. our interest of high-caliber Bejar

to the we strengthen also the and on appreciably made result financial position closed year. able a two offerings XXXX, throughout during were progress our we As of

Chow, Mr. Greg this further CFO, Our will momentarily. discuss

only highly-potent but potently multiple inhibitor, CG-XXX, FLTX, and much suppresses of and typical a XXX, simultaneously let's with which cancer signaling a mutant inhibitor upon kinases. other Now or for I survival driver clinical pathways, of commercialized the or resistance. and under and FLTX development. rely is It inhibits like oral no not just drug provide forms want BTK than noncovalent wild-type oncogenic more to and BTK begin CG-XXX, as FLTX cells and or our is it update BTK all drug

And We consider mutation-agnostic suppresses asked no. kinase be targets occur of agent mutations kinases A answer cells get that dirty multi-cluster be that other AML question inhibitor? a that clusters a and CLL such and a resistant in XXX the agents. is inhibitor we kinase selectively related sometimes to to is, the wouldn't render cells

toxicity. to and yet ErbBX avoids targets known has malignancies T-E-C, B-cell the of BTK and including as excitement associated primary or is on to sets selectivity TEC, in the what apart XXX that what other of a the hematology often EGFR This precision and with been drugs much XXX with compound. FLTX, that surrounding contributed are shown drivers development has and from target AML, the such market

Officer, commented is the noted seen. for has our say Bejar have tested new Regarding rigorously one Medical thing one this we Chief Dr. important of but compounds recently highly also Rafael toxicity, far, not thus he we've that And of preclinical to is highlight the most that ever to toxicity. it toxicity lack it's rigorously tested observed

trial established initiated Phase a XXX in Ia/b the and dose. designed we XXXX, pharmacodynamic responses our to dosing clinical Phase open-label in the XXX escalation trial you dose multi-center tolerability, of preliminary remind cancers. efficacy and of recommended pharmacokinetics, assess is of To safety, patients II July with B-cell and In

BID, safety of required favorable and the escalation profile, milligrams of only dose one first allowed unless XXX patient side necessitated trial testing an schedule Because those levels, is each levels. milligrams of XXX the effects accelerated protocol additional dose the preclinical at for for at two unexpected

one quarter, dose milligrams and level successfully was one refractory pretreated BID. two last reported heavily with the relapse patient was CLL with CLL dose of BID XXX with treated successfully we As of patient level treated XXX milligrams another

suppression. two are now first toxicities well-tolerated The including no XXX doses no complete oral at with drug-related cohorts these was model

indications activity. the the activity, from second inhibitory which assay To at dose pharmacologic various of early level, collect throughout a patients pharmacologic at we PIA times demonstrate cycles. assay the plasma plasma in were there or XX-day performed we And

six fossils potently steady-state of In levels plasma exposures, BTK, complete once levels sufficient on drug lab we demonstrating trough And fossil state key studies, indicator inhibition the and cells and by observed place exposure for these sustainably activation reached pathways. plasma We SIC to the the back of bring pathways oncogenic then our to immunobody. it targets we inhibit hours. and fossil of the are patient the and ERC, assess key

CLL classically described at levels in In lymphocytes robust response proved the the levels. active to a patient first BTK. observed pharmacologically a envision as addition that dose These increase lymphocytosis, we these of we dose dose peripheral level, had agent in a safe two or at blood second

end the or and levels be CLL to pleased the level, near concentration such two of reached In range. second properties observe of week by observed was at trough dose-related these were the in as pharmacokinetic the steady-state a micromolar in first steady-state we dosing patients, patient the dose to first we

We second XXX the believe that deliver should benefit and approach to level were that patients. see was to we dose that absorbed thrilled plasma levels could

So, the to cohort. of course, we next dosing to eager were progress

Since enrolled milligrams which at is dose X have BID. have our XXX level treating and last call, we been patients three

successfully continue protocol, next need patients complete XXX-milligram dose we dosing BID dose. at the of the will to a the we For XX-day to three before

hope week hovering patients report -- BID well-behaved see to exposures dose. XXX one to of finish patients steady-state of parameters day acceptable range from XXX three We to with by the happy the we with that the I'm around variability cohort serum week. see expect and this this micromolar among middle milligram PK milligram hump

collected, us that Safety to will PD you be tell can who all next we steps. on the safety I drug-related deliver toxicities and Once advising emerged have Committee will to-date. no PK Cohort data

ascending with dose milligrams refractory a patients patients those and well, including non-Hodgkin's inner XXX, milligrams recommended patients Phase intent with XXX, lymphoma. relapsed will all for followed with three the B-cell With by at CLL II and with XXX cancers going BID three be at each to XXX cohorts select

to or safe the MTD may as dose, dose. and for enrolled at our an patients in been active II Phase selected, treatment dose XXX be that phase up Once biologically recommended expansion has

clinical we U.S. screening with patients XX on open come scheduled sites study enrolling As to for sites have board. for of the additional and today,

patients, B-cell clinical sites For please more visit specific trial clinicaltrials.gov. information and on the malignancy enrolling the

strong FLTX AML discuss myeloid and BTK Now, malignancies. And with also that inhibitory remind is to activity possess applicable that proposed study a CG-XXX. the lymphoid XXX both is and only you therefore inhibitor our let's

previously, for the has always study the Based to of patients the AML patients. treat with to guiding patients in The on we some work, B-cell current B-cell our preclinical which intent for preparation our analysis addition AML protocol XXX in extensive the it our are biomarker of study. been mentioned malignancy

to to in plan allowance populations refractory the As from patient we or seek calls, that into prior we've relapsed discussed XXX FDA AML. include move

refractory we AML dose or relapsed patients are reminder, would population a and with As wish patient to acutely not dose clinical likely not a provide this ill did sub-therapeutic benefit. that

the patients deliver be Therefore, to PK the first benefit data. data, safety in likelihood and chose we we malignancies AML identify to to initiate a that the patients. with have B-cell collect we From dose trial to should such and clinical believe PK immediately able therapeutic

exposure recommended level patients observing Based from compared review the before AML levels observed dose dose. tumors starting collective again exposure a to clinical the make which patients. we X we the XXX data can can on set mice, to dose CLL we're PD with for to our the BID a determination PK trial X final dose that is close we to milligrams be need in FDA the we as in are if identifying eradicate that believe starting and the We therapeutic to levels level safety

and in the expect with well trial this of We half we submit appropriate protocol for to to preparation be the a year. underway clinical FDA during our documents to this are the position first new

the academic initiate has Our working tier clinical with and identified team new AML top closely trial. is sites to

receiving AML the AML with trial that to other AML not focus current initially patients, refractory words, we relapsed in intended unmet from benefit are For patients on population all and treatments. medical the plan In needs.

our of the number you current who the may our clinical of website become of Those XXX panelists on significant of appreciated held KOL therapies show the -- AML. and tuned enthusiasm also month initially or While guest on rapidly last AML treatments. benefit refractory relapsed potential patients into to symposium such focused available targeted our about webcast -- a

Dr. over event. the recap will it from to turn key the to I takeaways briefly KOL now Marango Jotin?

Jotin Marango

via very pleased were you by opinion and webcast. KOLs you, Bill. the and We humbled on Thank behalf of attended who the both leaders key outcome who the of person with presented those and in CG-XXX of

is lead FLTX disease the need guest ultimately Our common the in are most not that emphasize They mutation FLTX have and progression. curative. limitations to resistance unmet AML current all KOL the and AML. in inhibitors

has inhibitors; AML; two AML. years, as chemotherapy In in with in the advanced last refractory in AML untreated or FLTX of two combination with midostaurin treatment relapsed gilteritinib approval monotherapy and

However, as the combination inhibitor our and real-world weak but survival patients with or did there of highlighted, not any however, is compared broad relapsed in studies multi-kinase ratified to in so to experience from trials meaningful which collective ample inhibitor still the with FLTX is room with study clinical a in alone, far treatment-naive Further, observe disease very an extended XX% midostaurin in chemotherapy In guest this chemo XX% four-year modest improvements. for KOLs improvement. important, responses. drug suggests III midostaurin in Phase AML, that the refractory

responders disease XX%, potent and in XX-month relapsed refractory Yet inhibitor both and died. equalized ADMIRAL rates the disease, gilteritinib for all XX% patients had selective by rate X survival which at Phase XX% looking were months, more relapsed of this versus at arms in respectively. more survival chemo terrible the gilteritinib study and is approximately gilteritinib, in time a FLTX to succumb versus salvage XX eventually the Meanwhile, of which or

weaknesses. do while of These and newer urgent development in mutations older for so and kinase mechanisms Strikingly RAS, their others. including of inhibitors overcoming AML, clinical need the the of observations the in patients agents FLTX, who highlight inhibitors PXX fail combining current certain ideally generations FLTX under the recurrent resistance of strength diverse

these refractory as treat safety profile in Our considerations optionality. well to date, clinical investigators are to guest with therapeutic top patients enthusiastic important combinatorial the suggests as are with relapsed which AML. agent's CG-XXX. and continue interact all the to resistant of AML whom or window eager and or refractory preclinical tolerability an we'll Both about and KOLs encouraging are They

coverage picomolar suggests time, the to other intervention may of or resistant same oncogenic relapsed biologically At a the AML. its FLTX key cytogenetics complex in potency the pathways nanomolar it optimal agent's represent for tandem with that of

any of to to venetoclax, patients FLTX failed data mutations other date patients and or TPXX, azacitidine and treat NRAS, IDH, our mixed with even with regulation. Overall, wild-type to NPMX potential support XXX in that inhibitors, or chemo forms of FLTX benefit have or the use mutant

in treatment may presentation the questions paradigm, listen how on have XXX to website. If to any available of might about you informative fit again you AML want this our

it back turn Bill. to will I that, With

William Rice

Thank the up We now you, B-cell Phase Joti. CLL X other in well this the ongoing throughout on the AML reporting To hematology A/B in XXX, progress remainder many the the prospective new to many on look as wrap of as and the as is compound trial on patients radar screen study as with investors. forward well malignancies, of our community year.

a just in second inhibitor and now the MDS. patients on with our currently So AML quick MYC first-in-class APTO-XXX, a update Xb clinical for trial Phase and candidate

oncogene a proliferation. cancer cell MYC know you major is of the many of As driver

to in tumors. well fact, estimated of and expression is as to disregulated as or including human its XX% MDS solid AML up cancers elevated be In

we've MYC of many researchers of years. previously, over the the been As mentioned has targeting goal

While the challenging has been protein MYC an cultomic [ph] deemed target, elusive and been undruggable. has

of and However, and not the gene protein target and the XXX rather the levels lease in promoter MYC MYC depletion the protein does the targets of of expression cells. MYC to multi cancer regulatory suppresses it protein, MYC

XXXX, activity XXX confirms and defined MYC mechanism meeting drug's ASH December action. for in the During further of the a preclinical inhibitor as its data

responsive patient studies, cell using background. XX XX% XXX ICXX Some an micromolar. were to below -- In samples, with preclinical AML one quick

appropriate then in well-tolerated activity. X to a maximum prior transition reached. patients tumors, solid cohorts X refractory protocol, to patients and until XXX Phase suppression over relapsed model is designed In advanced expansion the as AML single-agent found to Phase with of with AML or MDS. no administered doses XX-day and dose our high-risk be trial cycle signs being once-weekly ascending was The of is showed Per addition MDS a or study antitumor importantly in tolerated in in XXX with clinical is

We are dose being XX-day now XX-day mg received cohort. dose. in dose who squared square have for report four level now we this completed with cycle that the one we dosing to the we three in have now cohorts, products mg the first meter the happy three in at on patients completed the Thus trial. and far additional last that meter per XX the fourth the per drug I'm XXX dose patients screening patient XXX in and are cohort

tolerated suppression. continues news good to XXX observed model no with that be well The is

date all and inhibition levels and dose We continue dose MDS we responses we deliver continue higher to observe that at to to hope for dose patients. levels will MYC escalation to plan AML

to at like effective distinct inhibitor. that highly expect how one We all XXX also or robust received hits eager single knows use physicians we AML is from pathway learn and clinically in other patients a clinical AML because to an to effect modest for to our in best combinations all agent, more MYC the XXX it what dose venetoclax we trials. have note thank as wish We're It patients. that may observed in no be Such be may a but and of it that the truly participating a agents. its activity single-agent from appropriate

Greg and review turn and now will I'll our to the Executive who Chief quarter call Financial results over the year-end. Vice Mr. the Officer, Chow, President for

Gregory Chow

is the in marketed with to $XX.X confidentially that million and at in the due primarily December and at We XX, completed $XX.X XXXX Bill, and $XX.X public good compared recent approximately cash we million This you, offering XX, million September million ended Thank increase equivalents quarter investments everyone. mid-December. $XX.X afternoon, cash in XXXX. to cash,

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

statement, to -- were year the had development and quarter expenses quarter on December Moving for for the the for year. $XX.X million $XX million income G&A year. no -- ended XX, fourth or the the were were the for expenses for the quarter million the of for quarter Research and and $X.X million we revenues the XXXX. $X.X

was loss for per Our net the quarter for or $XX.X share and $X.XX $X.X the year. million million

declared December One was shelf information marketed that for one includes This the in late offering. quarter note million filings on previous the replaces registration filing subsequently exhausted our during to shelf of recent in last detailed statement found in item the the SEDAR. the early was that $XXX January. More public effective can and be EDGAR confidentially

Q&A, both in manufacture have drug Before a manufacturing multiple for delays to see call the candidates about to and suppliers communication our to in are we Bill of how building few XXX. back and to the I mention a may experiences, open our progress up regards this we our With At we and affect learning partners turn that manufacturing of API and consistent and and drug our XXX want operations. with things past the -- any COVID-XX source point, suppliers. clinical blocks not our product or do from

in moving patients forward. Unfortunately our treatments the contact that the With patient trials, currently on population the with foresee and of are and any clinical elective sites. each study addressing team the of not are do constant for of regards not the these we for enrollment we treatment delays clinical patients thus physicians to in the is

back call you, the Dr. Rice. turn to now over will I

William Rice

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


the of from Your first line [Operator from Sandler. question Tyler Piper Buren Van Instructions] comes

open. line Your now is

Tyler Van Buren

increase the ASH. during the reported I second that lymphocyte come I could hoping Hi, the progress update an was differently. provide at guys regarding everyone down? BID quarter. I understand congratulations at guys the behaves to cohort in you has mg good question my changed was lymphocytosis and back all you anything seen two Have you XXX that observations, there? counts the patient on dose guess, evening related the first on

So maybe that occur. didn't

potential nine And signs and then lesions signs of had bulkier eight they or nodal that also out mentioned were of the that decrease second of in there decrease. the there's is you part disease

more So there? has any been there observed decrease

William Rice

Hi, Tyler this is Bill.

answer wants it. then Bejar, to So he and if I'll add first open to to Dr. also I'll anything it up

patient pharmacologically inhibition when one active. we took platelets So January XXX grade extensive literally well which Their as study. platelets at came was the bone we also guess caused was were had they had This with trial. patient in at neutropenia when had the they I involvement. put on actually milligrams well as entered that entered second of them the drug, lymphocytosis, that right by marrow thrombocytopenia. BTK they them mentioned we BID, When they that it on off This it's patient four had they trial a indicating the immediately

full been say actually what placed an is on we now, we on them therapy what early approved to continue we any platelets, is over is the drug was benefit worsening but level optimal didn't the the also dose decided level, only can exact we Anecdotally time, second they But that dose well. tolerated that patient them an And the since not drug we to level. same hopes assume take lymphocytosis we is they full a very see the of might our have the assumed the at So another they're do and effectively see a currently but we dose of was our we did that patient time. on to the see better. of and it did off what in over as dose drug level. allow not approved saw in drug dose what go The that seeing at we was thing an any dose patient drug continued,

at news when as like ours drug, just good they just So of the patient full currently a able the might that's we're another drug. it -- because to and on that patient, as is hoping just was be be our but good very but was in looks to benefit, went approved to was trying that working dose were we additional as drug sick it good they that cautious the get

to want you add that anything Bejar? do Dr. So to

Rafael Bejar

tolerated, I I drug additional that didn't we it's sufficed very highly bone myelotoxicity. compromised despite important then well the any very and it's think see was having think a learned we marrow,

William Rice


phospho we -- the the ERC, so was in we SYK of know patient plasma that the might of the a and that we're add first in patient from assay. level case the a pharmacologically steady performed it get active benefit dose. that might doses we So not we on But quite plasma also actually state, dose and that one was collected full end had -- week actually that remember inhibited the drug. BTK phospho by actually we phospho completely ours. do lower they -- additional we and assume in And that that's once one reached since which But from patient, another well of apparently PIA our

hope else I that So answers your Tyler? query. Anything

Tyler Van Buren

there safety safety respect Great. the that guess seen major able PK/PD forward specifically screened very a for imminent Yes, needs most cohort cohort, second you be review. the safety? be But final with is clean obviously was clearly that's just have guys enrolled -- already quickly? I patients the question helpful. Yes to And recent to anything the is focus. just move other the cohort to next than on to

William Rice

begin All here. I'll right. Again

in -- the these first patients safety. to We've any to no of watched in carefully adverse want measure events of signals for We've safety. seen is these what date. of any all in So patients drug-related we

X, only X dose Cohort the one there's all in pharmacokinetics Secondly, each. cohorts, of Cohort and in patient prior

know through how three And well behaved be. XX so we patients cohort, this days. of In pharmacokinetics at least you your will worth have with actually data don't full out third

the the so minimal, patients that starting to actually yet. see the all And PK behaved what from variability that to are predict the can is all to these of but get are is have get. of samples some that don't we actually the of we we data, want patients pharmacokinetics what well coefficient We're going

the one I'll also part So it's in to that the that it PK. call We micromolar see minimal circa -- and it the variability. second range want see is

to are the back in It's we take ERC want want responding show with CLL it major patients, these phospho Also of all these the absolutely inhibiting we and want bring to and various patients, those these lab to are the drug. the active the in it's see Again, patients. also we from markers to the see in lymphomas plasma look FLTX pharmacodynamic SYK, we see and pathways. we important that that we're also and only inhibiting the BTK, to not patients we to

can to FLTX we line that So cell sufficient indicator we will at that and of we as drug we looking not inhibition an have or have FDA. whether not also us whether or tell FLTX we'll we be a that us that levels to believe to inhibit and recommend will have the guide dose

patients hopefully wanted pharmacokinetics active this cancer study variability So we toward time important also B-cell dose cohort shows that patients to to want X pharmacodynamics see we've show hopefully then soon. and yes, us is the the the AML can three Anything you direct that and in add? we it will it Safe else got first and is a very dose level us. to minimal

Jotin Marango

to meeting. start we are we won't Just your of question, directing see any patients issues screening the last the at sites to part that answer March assuming XX

Tyler Van Buren

Sure. very It's Thanks helpful. for questions. the taking

William Rice

Thank you.


Thank you.

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

Your line is now open.

Gregory Renza

had detail you those just how interactions to progress. for the I also this the additional stakeholders to remarks. taking thought just trials, But congratulation as or to you're move up but forward? trial my monitoring in with clinical stakeholder curious, if general coming interactions AML Thanks potential prepared any a our involving potential to the I as you situation you the regulatory the Thank key appreciate well you. that and respect foresee and commentary on interfacing order return on as guys. on the certainly COVID-XX, question just with all wanted and bit Hey, convene

William Rice

All right. the for Hi, questions. Greg, thanks

been So monitoring we've as has this very closely every there. out company

to The be wanted manufacturing on this particular effects planet. our see assure of molecules. we the We've of that everyone dependent careful site we don't first is not the been thing to any any around on very

starting performed available manufacturing date are to has our in all multiple been through the U.S., suppliers. Our materials

least to at the so And or API right any not drug risk do the now products. the see manufacturer of we

first we're of So many there. manufacture dependent the especially in concern upon, be that's that of China the I have. materials, we think always companies good really Because shape some for starting will

So the we're any not seeing don't on -- impact we near-term manufacturing.

In the mentioned just Bejar a interface, investors. also address the interface of Dr. regulatory that But I'll clinical with terms trials second. let in you

know or investment know already We that people also firms the necessarily the canceled are delayed. office. we country that So their around been many number and a have not welcoming either of of into conferences world the

so having virtual one here more plan some out interactions. have the take getting there. of many conferences different major various another way to as bit are updates to investors on of we do And on we canceled, if we're delayed, But these providing and plan the or the as you well a out a tactic even of data

So Raf, registrational? clinical to the do you want and address

Rafael Bejar

on clinical operations. seen date say to any impact haven't I'll our that direct we

number of out many institutions will the come restricting the that I academic are institutions that in. However We that of likely visitors those near in future. change think know and can both restricting travel

needed, example have for and so recommended flexible out at strategy carry with continue can trial sites them the Several very a those able of if that and to oversight. monitoring accommodate we're good clinical we remote to

we're are and And as inability come whether might patients that – clinical resources are happen. very they predictable for becomes maybe in, to they available whether if for restricted and to those in are that going future are we'll less relatively tackling trials. handle the mobility COVID-XX outbreak But near monitoring resources less closely. large an redirect things we have something things Other institutions

So affected. far, as mentioned, of sites have none been our I directly

William Rice

and Greg. you, Thank you, thank Raf

Gregory Renza

I Thank That helpful. if may. more just you. And very one sounds

Just turning of full AML opportunity – to XXX, with tapping to are AML. the establishing B-cell certainly the dual and the really about potential CLL and and spoken in you or

the potential into about the AML they're trials respecting to you're for the the you both laid into taking side certainly of how side as you what we that I'm XXX's think certainly thoughtfulness equation? extent much. opportunities and about the just these your with sequencing Thank AML curious and leaning very appetite as leaning should and the of do But think out. mature,

William Rice

great actually It's a question.

on malignancies. is active to there there. We We this those demonstrate clearly want going We're B-cell the aggressive were in we that went So the patients. continue CLL drug first. to

to want unforced be in aggressive as We are AML. that soon we thoughtful. toward be indicate also make very any execute being but possible to the certain to errors We to want and also appropriately. going want I we want But we get don't there as

our we to activity, see hope that we're we go We those those level dose absolutely at first can't once happen right selecting that go We need go that benefiting patients that's the we we that the will such hope into patients but demonstrate the patients. immediately to say into. dose into

the the of treatment number data against We forms variety want failed about of of and mutations, activity who there into clearly this. the to mentioned other the those molecules, can response a support that to – pXX drugs. go maintains and our patients other occur patients patients mutant of KOL mutations are going have We various mutations, in FLTX bars. have gilteritinib, a with patients various RAS the events, at into venetoclax, XXX who that speak mutations Raf with we

tremendous So that think see all we to a are to the failed And treat who But that many the yes, drugs. in at add the I AML. that? want Raf drug. the other patients was opportunity by – able have you we're of looking to investigators that echoed the we did hope

Rafael Bejar

just with that activity that see including for because in including other we patients see just activity are relapsed/refractory in mutation and good reemphasize AML pXX a that FLTX rationale don't against relevant I'd FLTX the MRAP patients part, mutations that there actually AML, even not carry the pre-clinical we idea with mutation. is in and

So what individuals we of for see activity those we to opportunity are might offer kind excited this to have.

William Rice

to point also background be has some population of we Does hope take to hope answer do a And at too. have advantage we there the activity that. MDS able that we Greg? question, in your And in MDS, Raf

Gregory Renza

guys. much, Appreciate Thank you sir. it. Yes, very

William Rice

Thank you.


Thank you.

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

Your line open. is now

John Newman

will that order question, imaging the that reason agents think in of Hey, wonder a or look to could just has about to And start in way my have different the sort confirm tend be they The if way guys. see CLL of walk should to is talk companies' CLL. them? I I asking they evolve question the just studies you that you tended I that used in just will Thanks. other just also CLL I'm Bill little to when for through question. Thanks wondered responses. if sometimes these responses responses because the develop? type for to And could bit investors taking at

William Rice

the Thanks right, All for John. question.

CLL it's So as a is it disease. chronic – says

into or deep AML, And which have different versus it's populations, are So also it patients early have an to just very the patients failures relapsed/refractory break acute patients who diagnosis are we recent two different from is who who patients. disease.

has ArQule they responses. us, did the that I our especially time So experience develop taught with compound think over

multi recently Once the you see you then those the levels are dose if kinase, you have relapsed/refractory it and kinase the higher time takes than actually dose diagnosed. just it multiple the deep you're targeting get a and once pathways patients. multiple to patients in responses begin levels get who to of takes to higher you hitting But drugs, longer inhibitor,

once of And the again what or dose responses the they So that year exactly on said in during is the ArQule were of remainder EHA patients additional the they earlier showed XXXX would over of and of the expecting those middle they back higher were get and that responses – throughout they were levels would time. happened. the looking that last responses of that the XXXX, the rest year deepen some number at on a the conference showed example,

wait especially patient to take again, the but and all these response. a time. don't watch But that and they quickly response partial I to don't. CLL had B-cell also wish sit patients, complete of respond all give they malignancy any know seen to everyone and They're would relapse/refractory they has We respond. and time relapsed/refractory

How do some you you all if SLL patient don't measure CLL that in response? Well, of than course them, rather you see that an can more look especially in it's CLL. of a at but patients of lymphocytosis

imaging and at evaluate the looking but you indicator the lesions lymph two every perform nodes, only the you're those to spleen, have cycles. various you So

take two only every the measurement you So months.

much typically first the And months. you expect see several don't to

of any responses early so much much And on. takes see And longer. you don't it's – type

think approximately also took I follicular that ArQule it to noted a that see they year a response. lymphoma partial had a patient

that's you year. into this the in half have of providing get for year year. our So drugs drug hopefully and we're to we give not higher patients to toward expecting our why be expect we the it but for levels, guidance Once dose the the later year to why that's what and present the end with to tend be time able the responses mid-year towards look more That's the them we're of on to second respond.

acute you Raf second AML add an the an the would start a expect to Once It's dose into you different effective story. like responses to that there, we and might half again, there. into that? dose is to would we're third be first, second, disease. that get year of the seeing

Rafael Bejar

on. think I that's spot

blood may exact diagnosis the or between in emphasize of for variability that count. example be others that they to same them are with even already eligible not Just response for have blood some counts patients the

lymphocytosis primarily others have splenomegaly. them more maybe of Some

take study only So other even timing in is we're Bill cycle. just looking of that there the we said but is immediate, that And really it are that not criteria that our months. follow every after it can

William Rice

different patient a on freestanding Yes. And They're John? it's a almost so patient-by-patient else, basis. experiment. and is all What every

John Newman

again move one those up IND study But are is are I have and the a get AML. it determine question, B-cell Could be to would study takes yourself sort of that for AML? as order in obviously into to that XXX close types the time looking eager secure Yes of to us you additional things feel which and that you as what know just you well in investors remind to types in of or for active things. dose and the you running malignancy active

William Rice

It's a good question.

the safety the we're So and to related of responses. looking pharmacokinetics pharmacodynamic at data totality

a want able show to So in level. to safety, the clean be terms of we it's dose that

additional the hope future so we the And be And three been completely clean. that into far ones cohort too. has will

it In look terms we of we at Why X.X we say to that complete if gives cures in in animal range and it's one do level. pharmacokinetics you level say it circa around be X.X because tumor dose the micromolar say studies see our animal that? and complete exposure without micromolar to responses we in in elimination us which any that we animals want Well, call animals. we have seen from the that anywhere toxicity, of studies that the

active So be should once range into in that getting therapeutically we're that range. think a humans we

dose And to have one range. with X also be range. dose circa that but is so we We're maintained doesn't that level into we're in into even get X. in getting range micromolar. to that beginning It hope And level that over,

would expect the the FLTX to levels inhibit can exposure FDA activity. PD. patients demonstrate then third the that the the would one us I in is that suspect And

the and collect plasma it we Again, we that? the the take lab cells. cycles, do it indicator on in back we do how So the the put from patients over XX-day

particular and cell far, line talking same showing thus been indicator you we've ERC cells that BTK been SYK and the So about cell that data it's measure with well FLTX. one I've we And line.

are we've that in disclosed levels We patient FLTX seen level have showing dose to not and dose in X, be X going in we what but X.

present we'll And to gives will Well agree should has AML also FDA we'll don't all that has to hit agree EHA, us FDA. to we be to confidence hope those be data that. then Hopefully criteria at to. to that of our able they if go the we But we they to we patients the the then have have it. have to into the it such into or AML go look proposal, at recommend that

be have XX-day also we AML, it for then a should And drug designation, turnaround. orphan so

why totality No? wants that's have we get Anything into think can, we else? hoping quickly of we're so add? as but have And Anyone of to it. as to that data. to most I that covered the patients

John Newman

Okay. Great. you. Thank


Your next question the line of JonesTrading. from Cross comes Matthew from

is now line Your open.

Matthew Cross

the couple from for me have here. questions Thanks I of guys. and Hey a update

this NRS CG-XXX other the inhibition. have of path that appears showing And better inhibitors. findings significant to activity as means presented FLTX of FLTX you appears it that recently So to certainly resistance than suppressing against

CG-XXX wondering extended But RAS, into is upstream into well. indirectly feed a because RAS control was of targets as inhibits CG-XXX of forms number that of if I other RAS

a a standpoint as wanted FERC about I may market in scope kind it what a of So bit for down would maybe applicability gauge with kinase that quite why obviously to the profile. mean from regulation of just safety play. that inhibitor And see explain the or you talk curious this that

William Rice

I right. you. in so I'll guess jump All Well, you with Matt just said,

various and are PDGFR we inhibit talked when as kinases. track cluster, So well FLTX the kinases the the kinases the the CSFXR in always that the and kinases also at the the about talked we've We've about kinome of clusters BTK as scan we look that SARC FLTX.

called at the right also STE pointed in There are But side ST the kinase map that concentration are what some inhibited meaningful. are bit kind the little cluster to over We cluster. over are that's of kinases are have sometimes. higher -- that those a that

the you both mutations, as as able time have be hit upstream well you want some has who to downstream. kinases to RAS any of the a So patient

kinases upstream FLTX So CSF-Xr the all well as map FLT the those. of hit BTK. as SARC SYK would we downstream and some then you we of have of RAS, PDGFR-alpha, And those. be hit RAS the also

even that's the activity presence RAS in mutations. So the we maintain why believe we of

does presence for directly the the presence RAS, inhibit We've activity in of activity and retain same even pXX. not the we in been of maintain drug true of able some but our The to even others. Now mutations. mutations pXX RAS is

add? So how to Raf anything about

Rafael Bejar

No that's spot on. exactly

William Rice

Okay. right. All

Matthew Cross

so then meaningful thanks in XXX the trajectory pretty second like helpful was very I at enrollment sounds the in just But out EHA about ASH. for -- and well at maybe appears that's No from it. CG-XXX the had be me data It And also getting more and for proceeding could one indulging of come XXX. to Great. then parallel. program

divert the And results from I to a in expect conjunction on to for get the number trial you factors? bit those EHA XXX this parameters present designed may other or based the initial hoping would this or patient was for with latest on

William Rice


begin we begin into year, treat patients. be the for them hope So XXX more to these longer-term the able the levels, to we're guidance up dose get on that is, patients to we those hopefully responses of and half regarding to providing higher second see get as in throughout

see we to something So be ASH hope data able to the and by here. to present

more to like expect it's don't from that at a single-agent or We venetoclax well-tolerated don't least know better for earlier. we're we inhibitor. combination if activity what But patients MYC patients. We Again soon know product, get to and one We've get if and we'll drug mentioned more going We've the completed the have we continue now Hopefully patient to we're two evaluating dose on have we bring on level those to escalate. on now. X. dose AML.

continuing can IV we with then to get that we this if in said of where this discovery orally future, the still hopefully it's oral of an us were that get really agent. always able we've to sufficient And to an as that drug drug December, accelerate raise proof-of-concept delivered on in hope fact and And those form levels allowed of studies. the we is some path capital it

Matthew Cross

that make how then assuming before to innovation hopefully longer-term forward plays ASH. actually Thanks that at in the and of looking obviously well out And clinic to Great. some guys. see

William Rice

Matt. Thanks. Thank you


you. Thank

line the Your from McCarthy next from of Jason comes question Maxim Group.

Your line is open. now

Naureen Quibria

on Naureen for Jason. is This

AML? model earlier. question have activity samples, NRAS of the any you've of mutations the you just you've well sort XXX done I patient as NRAS to demonstrated the on piggyback what remind was could and seen? about asked cell aside NRAS us So want you just And from its work wondering in I incidence animal to work that with that was solidify

William Rice

All right.

with a of incidence, inhibitors the patients the some of NRAS venetoclax are others. past. different of has highlighted the of terms variety FLTX being that some really been emerging in now more It's the molecules incidence of In the not treated of

to So gilteritinib. emerge it's beginning

Some developing of of believe the I some mutations. patients -- NRAS there the

different a not new are targeted of we drugs, RAS patients molecules as driving case toward what mutations. agents again begin actually -- tumors with it's different to we're different to other this So but -- the with is emerge. beginning doing the dose we variety mutations drugs, in collectively or field we're types And in of

a I emerging know So at think the failures. it's number. high will incidence But clear that They're as are are identifying it's perhaps those And them investigators clear patients. don't this point. identifying the and those Raf

In terms Druker's AML of look work. our actually we we this, work, over XXX patients. did Brian samples took was how from This at

entire with type to drug an there. But we our well as patients also RAS gene AML treated of look effective And genetic ICXX patients expression XXX as back had our profile. and killing. So, it's samples And for profile patients. drug we primary cell versus very the at those isolates mutant wild are go and was got able

ICXX that in can like effectively, looks And slightly to at mutated And it in the the required but was increase hope RAS kill like just looks we're cells, patients. exposure those in it there a slight -- levels RAS mutant higher. cells, least we we achieve

And levels so it treat achieve same inhibit that those drugs, with able patients. RAS other thing RAS can Whereas can look at the to mutant. should we be the doesn't mutant they like we when look

like that? RAS, not would add So you to Raf, to Raf,

Rafael Bejar

[ph]. about emerge pointed NRAS in data it's really found it it's of as de but out, patients novo X% points But So is that risk, Bill after to the actually impact is at with NRAS favorable in risk XX% with of often big intermediate AML, AML therapy.

resistance to they're FLTX inhibitor like often mechanism venetoclax. of drugs So and

able to are these as setting have as setting. well the expand that setting therefore upfront important activity in to So are against of in or for relapsed/refractory are the the and that selected therapy mutations are in

William Rice

therapy, with like of RAS, they patients it RAS of be can't other and that and to drugs occurring the on constellation Would of but may mutations. that. Yes, handle top anything only multiple then with background these not have to a just you mutations are other treated add then after have that that And types being they this?

Jotin Marango


for you So the thank question.

the in the out, pointed Raf RAS a percentage as relatively front-line incidence. Just low things in of

the the However, RAS with problem first. real relapse is in

inhibitors or who So, fail patients for FLTX treatment, venetoclax. example,

see and patients therapy to cohorts. small following selecting to RAS FLTX But there have about who very we is real-world a starting third. of we're a experience from the Now have small for because relapsed those mutant example, that just seen rate preliminary, cohorts is the quarter data of

small studies. So a high these incidence. fairly that very is are Again,

some were mutation. further then are so mutants and of is they with, them there What RAS shows it mutation original that to these novo of were begin de some

around cell to it is ways the So therapy. finding FLTX get

the that treating potential the of so these becomes exceptionally arising CG-XXX And failure therapy. in of for important all and looking mutations -- at are the that FLTX after

William Rice

That's a good point.

Rafael Bejar

a typically AML So then first FLTX is the an at not a at the the exclusive when resistant clone But be at that's FLTX in its a mechanism in baseline mutant and FLTX have mutation evidence and they the little patients mutation time, you when to same de NRAS disease, NRAS develop of tend presentation. novo present does both that bit.

William Rice

notes here. one or So two last

We're change other near been are RAS. has be studies only the So XXX changes. cells that Dr. oxygenic we're with wild-type able we to that do want and test to the identify such Druker just trying to hopefully looking for the future, cells have into to with oxygenic those

be an for We that in of terms much hopefully, animal In have that impactful. an data more human your do this actually not model such But on Naureen? tested can have Did animal available have that an later question we not animal we'll answer will model, look model. we year and them.

Naureen Quibria

more than that. yes, Oh,

William Rice


Naureen Quibria

one terms was the shown optionality mentioned XXX was with XXX just in you've no preclinical combinatorial And great. That venetoclax patient more very, in and and opportunity in Joti impressive pretty No, helpful very that drug of follow-up answers. AML. AML with samples. the work

to ago I regard got XXXX. study, the jeopardize in which combination venetoclax with a HMA its or approval So few of physician that potentially AML in failed could know the guess AML with But LDAC studies. venetoclax technically in confirmatory that back probably we in you drug days program in the conditional one read

agent? outside with say you studies So potential have are And venetoclax? strategies chemo of done you with XXX combination considering other with other

William Rice

a there. answers There of Yes. are couple

studies drive did in our data combination with patient samples. centers, of all, patient very MDS, was with CLL, First we studies AML of whether the and it were impressive, with terms ALL. of AML, venetoclax, all our

So activity all types. cell we saw of very in those nice activity, combination

it's And frontline. have in there's Venetoclax But not is particularly impressive activity. the want able in is that going broadly used population. agent, perfect we will but I single think activity AML happen be not to have in likely show there. molecule, to into we move AML, did future, have move patient every it in But but And a going activity. combination, an does towards more as that impressive that be and to venetoclax to to it be

The to we reason want B-cell malignancy. at used other the look in it's also because is venetoclax

And so active myeloid much across is our lymphoid. drug and like venetoclax both

look So with that's combinations another reason to venetoclax. at

such patient But yes, we effect those as we have actually of tested agent. variety have with as in tried a azacitidine the hypomethylating molecules, other agents samples combination a and single agents, no in hypomethylating

add hypomethylating as with tested or it to and samples, with combination want an of we couldn't not anything data have patient have performs we variety And agent good to a well other that? Does other the with types get very of anyone so to agents answer but whether agents. combinability we a and in

Rafael Bejar

advantages has I you're to would drug that if one other that agents the close add of more you than to might combination. you say no to toxicity that combine that readily toxicity of with a having able

upfront, multiple agent paradigm involved from is the AML. the gone that That's at where therapies look in we've to that single where activity going headed treatment you think of combinatorial I If forward. future myeloma we're now

after. be hypomethylating The combination are hanging including But that combinations. obvious biologics go agents to to many combinations going these with low ones with intriguing are the there are combinations very fruit, other venetoclax,

William Rice

Yeah. future Hopefully your into I rather Targeted talk the that about. agents question. answers than

Naureen Quibria

That's helpful. me. Yeah. That's you. you. it Thank for Thank


Instructions] [Operator from the next Oppenheimer. Matt from line question Your comes you. Thank of Biegler

Your line open. is now

Matt Biegler

Thanks me guys. for in. squeezing Hey

in could protocol tell just Because subtypes? us the the were other NHL XXX quickly I patients? if the does any of mg three wondering if patients cohort First appreciate you enrolled non-CLL allow

William Rice

CLL. had been a day What know to thanks squeezing especially all, for want as us is into begin in. those to have can We levels of We dose yes First get I do too. than here. patients look we other for the at higher patients, busy you it's tell you we

some not non-CLL. and some So, CLL

of have in patient But to We what they also. types we're not there get disclosed thrilled are. those some other

the wanted really to get at we lower CLL remember You two doses patients.

if the for now that But of looking these blood looking want see we could level we So cells third want as that too. our in pharmacodynamic the higher as the collecting other at effect and there's we peripheral getting We lymphocytosis and where a well doses to the the we're the diseases have patients look even if we're be into it's still effect at to -- some to pharmacologic dose getting again changes. doses. the higher believe particularly

Matt Biegler

of it. sounds then Got patients. And like right on now, positioning in a panacea like a really broader as it. question you're it maybe thinking and of for Got CLL, kind XXX refractory all relapse

really the of targeted centered or is Richter an you're kind if transformation? approach? CXXXS cohorts populations more Or now on planning curious, on strategy like maybe just still like I'm targeting all-comers expansion So,

William Rice

variety lymphomas. designed look study variety who molecules. other a the types failed subpopulations spot well show is still well different might to a that tolerated. not our to think could of the as that be And Well, show which activity we drugs activity We refractory have could sweet allow particularly as patients where in relapsed and other be other or of us are at of of CLL

we in definitely such particular we we follicular Richters patients. mentioned If lymphoma. or those after would expansion If want a aggressive activity DLBCL example population an such go you or for in patient see see patients, to an as

there. lymphoma, really there's look follicular you standard of good at therapy no If

we'd that after. want a And go low-hanging population so that's to

to are be first-line lines. our pathways also But still very still ultimately, able time, like well way mutant you're hitting multiple does, forms BTK, one hit toward multiple hit we we Because move the be that the if but much and hope kinases, then and tolerated, more wild-type the competitor toward of well we BTK, of earlier you'd over began tolerated. to the drugs up we are able to

anything? initially, after like to -- of hopefully difficult-to-treat particular then the some would Would patients towards going other refractory the relapsed in these line. moving you and we're gentlemen add over very yes and up populations So, like time front

Jotin Marango

Yes. have in is and thank discussed past you Hi landscape Matt, for in the constant -- the question. We flux. together the CLL this we

than shifting around. more Now in fact, therapies ever the are

However, we in plenty are yet. into pretty confident within getting and of other that AML there still CLL B-cell is malignancies CLL clinical even or and commercial opportunity without

where encouraging feedback the treatment some data follow study. agent end, out fit in continue of So, the we top this very development trialists and of that to would join path the later our all see enthusiasm we are will we the just CLL year. interested academic or terms And there, which the in receive of in to paradigm,

pragmatic and So, we'll that. we stay been have about

confident impartially, a that cannot and date with clinical need are enough very even last this then Because importantly of we here validated indications today with to targets. are we have we stage important safety unmet at this I And are at differentiating right an is we targets. value point very with engaging agent said, multiple in just clean and that developing it stress if how now. hematology where this record validated agent take the look at and in back Now a step

for So, question. the thanks

William Rice

in now that AML. focus where a this what to thrilled just But And are is, B-cell clinical more, have molecule bit in bank. We're emphasize trials. we on we malignancies we just the Yes. are and have both the with -- the cash we bullish our in

into the clinic, not And have and We drug any errors. execute we hopefully dose we levels. well the emerge need our higher unforced the responses just as go perform make to will in then to

Matt Biegler

Congrats the guys Great. sense. Makes on That progress.

William Rice

Matt. Thanks,


you. Thank

Wainwright. Pantginis Joseph next line H.C. the Your from question of from comes

Your line open. now is

Unidentified Analyst

from [Indiscernible] line A This guys. is Hi Joe. few on of the questions end. my

XXX patient required second one. first to inhibition? the expect So may adjustment be that you pathways? inhibit to simultaneously doses we did order dose potential that broad Do would anticipate as same you the the And kinase Thanks. therapeutic potential one achieve BTK levels consequence, would with a a in

William Rice

kinases. best how that. at All that inhibit trying to second able level, already dose to We even our we're determine know right. multiple to I'm answer

we So, BTK and complete inhibit we're saw to inhibition. able a

take when put inhibit BTK. plasma the cells, on the the from we phospho patients, it can So we completely

But doses the already and driver we're X. that. as pathways we we be there we're a as going Phospho-SYK, described. to even and data ERK dose both We about haven't also yet. doing able on well saw cohort at just kinase studies inhibit also the believe done FLTX them these also to inhibition of that pathways, believe rescue we're the at, spoken yes, alpha that We've multiple PDGFR I complete We kinase have many we've and

levels get of oncogenic we of it? getting us better to the It that But have I'm activity so Or higher going be patients we levels as gives get drug in more if safely. pathways want dose of of sure greater second why, exposure many also broader resistance. that we kinases That able escalate and in well group answered more and drug I can as again, a can hopefully deeper safely. in the answer in We're pathways higher not and and in, more activity cancers That's of doing in is as go rapid Did as part. long continue these we'll these emergence to but can. those to we're and applicability to preventing to more patients. we dose as

Unidentified Analyst

the like, you to inhibition? part what doses second in like broad And if kinase need adjustments order achieve more was

William Rice

You mean a a different versus dose level evaluation? in patient CLL an

Unidentified Analyst

the within the during evolution or disease? Correct like of same patient the

William Rice

allows to try you the take just into to then dose increase drug because level don't your would you treat to try that. patients Typically, for highest selection and that the Interesting level resistant. lower you question. dose later and drug Typically, get a you can at dose with that safely patients will of

or pathway want in as you to kill the can as patient try So disease cancer giving hard without escape. cells to you initially, infectious even a to get a

Unidentified Analyst

last And I see. my see. question. I

sites ones are are And open? many currently Thanks. how about screening? to APTO-XXX, many So additional for how

William Rice

it nine? is see, Let's eight looking. I'm or

clinical that it's are screening. So, currently eight your And question? that sites was

Unidentified Analyst

so are additional? but more more XXXX Yes, have in like you going sites to

William Rice

just to don't in you Yes on additional that on, have have early making put a But there patients pending. sites are many everything study. we that We're sure place.

then you on. too have And patients get so, getting many not people they're sites make to sure you because don't frustrated, want

we're be into more get that getting getting put we more patients sites. on and to able So question. to now levels, in -- begin hope Good the higher dose to

Unidentified Analyst

you, taking the right. All for so Thanks Thank question. much.


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

William Rice

a our proud of work. importantly the support two we our have Okay. year We we clinic. to forward wonderful the you, the us keeping afternoon. performance, solid for progress. appreciate of Well have our I'm the After and advancing research of who thank look and new employees, have exceptionally joining and organization, important compounds in you top-notch of and this analysts investigators hematology the well-tolerated patients apprized in shareholders a greatly evening. past you and Thank our participated Bye-bye.


Thank today's you, ladies conference. concludes That gentlemen. and

You wonderful may a day. disconnect. Have all