- Earnings call transcript Q3 2022

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Operator

Good day and thank you for standing by. Welcome to the Revolution Medicines Third Quarter 2022 Earnings Webcast. [Operator Instructions] I would now like to hand the conference over to Peg Horn, Revolution Medicine's Chief Operating Officer for opening remarks. Peg, you may begin.

Margaret Horn

Thank you and welcome, everyone, to our third-quarter earnings call.

call today's on me are Dr. Joining Revolution Goldsmith, Medicine's Chairman Dr. Officer; Executive Chief and Mark company's and President, Anders, the Kelsey, Steve Research Financial our Development; Officer. Chief Jack and

SEC the Chief over Mark as to will And to As the no to of within review respect that well to that would as the begin, any the Officer. business with I regarding like our and with forward-looking the we our current our uncertainties. update matters. other you of disclaimer filings except and I that, Dr. company from company legal call number or of undertakes presentation constitutes of slide revise all include of Chairman to statements. will or a are subject the the to materially law, corporate by Executive Private beliefs encourage release Securities required company's meaning obligation differ the risks press as Litigation I Actual statements Medicines presentation the forward-looking concerning note these and turn Reform these Mark? may Act. statements. Revolution the These statements Goldsmith, statements With results assumptions, earnings

Mark Goldsmith

RAS(ON) provide Good Jack Revolution all our Medicines for us. afternoon represent In an on XX% quarter, human cancers third range which highlights advancing of results. progress inhibitors the of will joining behalf a and wide of of corporate continued update pipeline provide Chief Today, thank our Anders, I'll on patients Officer, groundbreaking of RAS-addicted you and Financial cancers. with our our financial

dose-escalation advanced into X our RAS(ON) with candidates pipeline, trials. RAS(ON) I/Ib development inhibitor building now having Phase are momentum We inhibitor

have this progress progress XXXX. a development, from RAS(ON) early of our that clinical data-rich reflect X RAS key This pipeline cohesive number therapeutics up regarding studies. of inhibitors in I'll recent transition inhibitors portfolio across pipeline and now of exciting potentially of RAS(ON) we inhibitors. and these With achievements cancer-targeted RAS compounds sets an the human our into our now review Companion

unmet the drug clinical arena Phase entered RAS portfolio. with We various first tumors patients step a which may our RAS oral prevalent inhibitor marks I/Ib the RAS-addicted be First, RAS(ON) RMC-XXXX, GXXC RMC-XXXX, and X cancer effort any is believe patients dosing In our by deployed direct include the in and are we highly In tumors the common first evaluating variant. GXXV of significant tumors investigators against cancers. KRAS development, a who are of patients have inhibitor, trial, dosing from oral investigators advanced KRAS-GXXR. our IIb have cancer to harboring GXX cancer RMC-XXXX harboring who needs drivers multi-on innovative RAS(ON) of KRASGXXC GXXD, serve the a Phase inhibitor KRAS our candidates have KRAS harboring KRAS mutations to these inhibitor, oral trial

is RAS(ON) previously preclinical GXXC data lung RMC-XXXX clinic. the differentiated have a we RAS(ON) mutant the or first covalent extensive inhibitor selective intend the antitumor of inhibitors variant state activated the reported profile and gastrointestinal into and of of We highly promising KRAS series that in to this found of of bring demonstrating selective cancers. the

encouraging shipped RAS(ON) goal human Companion mid-'XX. clinical numeral of the variant inhibitors These X contains additional class-leading common third serve covalent combination RAS of one into-selective to our In And our This and designed RAS study, be RMC-XXXX primarily IND-enabling sotorasib, RMC-XXXX, and inhibitors promising quarter, cancer Next RAS(ON) are our Companion clinical of inhibitor the inhibitor preliminary RMC-XXXX lining and RAS-addicted benefit track KRAS particularly Phase combining In direct to the activity with candidates, collaborator, this RMC-XXXX, evaluation Amgen's up XXXX who has patients lung cancer, GXXC first potential on beginning from wave. RAS inhibitors. with to cancer treatment are clinical KRASGXXC inhibitors clinical in behind that KRAS continue of to which inhibitor, [ph]. inhibitor inhibitor CodeBreaK portfolio patients vast have of evidence agents reported toward RAS inhibitor our were suggesting non-small with first Ib a parallel, durable oral XXX majority cancers. we help the the in XXXX of remains is its drug wave deployed GXXD, of clinical our both causing from work second-line Amgen most cell naive. with RMCXXXX. evaluation

II lung cancer. Phase in RAS into in inhibitors to GXXC with our we evaluate expect RMC-XXXXXX patients combination, enrolling combination companion with the continue in KRAS We RAS(ON) inhibitors Ultimately, study of future. our this cell patients own non-small our

execution and and the support development is Now overall deliver we on and to progress strengthen balance quarter, to in the focused strong multiple company's With I'll priority remainder and we the comment million the our of our the equity for XXXX to financing expansion a highest shift sheet on completed on and our our product the are year. financial priorities development of corporate of proceeds of XXXX milestones timely financing, raising of gross $XXX XXXX. In us, activities stage pipeline. behind position to this continued follow-on important coming currently clinical underway

new this RAS(ON) XXXX scientific continue generate commitment our profiles. development to in distinct We mutant critical continue Despite activities engine RAS(ON) insights resources proven deploying ongoing with also provide strong of and to our activities pipeline, support inhibitors, X that that inhibitors XXXX. companion to our we support and innovation selective inhibitors, RMC-XXXX, X leverage research exciting RAS development XXXX and advanced growing RAS and clinical most RMC-XXXX primarily our clinical-stage

RMC-XXXX with strategy the R&D to a supported this We milestones. superior drug collection In operating in into of important of plus of current XXXX, KRAS XXXX, portfolio, this are XXXX. data dosing as assets activity and of our In to ARMC-XXXX next cash, cash clinical GXXC Companion securities, inhibitor positioned candidate profile RMC-XXXX efforts inhibitor, in remain candidates, mid-'XX. single-agent portfolio monotherapy for year XXXX. to will end inhibitor committed potentially RAS(ON) indicated to follows: the inhibitor and of to our by in XXXX RMC-XXXX wave patient phase. announce safety the of in to on advancing to milestones and a nominate follows: study provide to by tolerability our second ARMC-XXXX. development-stage in expect provide summary, RAS(ON) to antitumor as RAS of and development first-in-class in by we marketable RMC-XXXX milestones evidence after are XXXXXX study including from 'XX We second are activity and an In preliminary of for our inhibitor join upcoming of extending from effects additional RAS(ON) equivalents anticipate sotorasib we with half the additional the entered for first which science-driven exciting patients pipeline deeply approach top-line research have development important upcoming planned disclose cancers deliver dose our and With our escalation evidence single-agent runway RAS-addicted evidence activity provide and/or through treating this

with RAS(ON) highly patients differentiated and its Our inhibitors and progress which significantly candidates distinct the X advanced RMC-XXXX, XXXX has drug first or with includes towards continuing RMC-XXXX clinic. now of being dosed wave

initial Our of in combinations strategic evidence a the evidence and along RAS single-agent RAS path with in combination inhibitor. clinical have towards RAS activity a inhibitors inhibitor has of with RAS RMC-XXXX differentiated Companion shown inhibitors now RMC-XXXX direct as Companion support XXXX clinical each and direct emerged used

expansion in Jack significant financial efforts coming we on engine. in milestones pipeline Chief these momentum, Officer, the progress to provide productive a to Jack? Building also to we our intensify company Financial assets our As RAS to based the make activities strong Anders, turn on now continue to significant a update. investment I'll innovation period,

Jack Anders

raising public We Thank quarter million, common our and proceeds you, $XXX expenses. gross estimated with [indiscernible], of Net $XXX upsized million. the in were sheet proceeds offering approximately Mark. of the deducting commissions offering strengthened stock, balance

Our Sanofi is operations million was third fund XXXX, was from which the XXXX September expected of prior in the $X.X Revenue million our million XXXX. year as in collaboration to of $XXX XX, investment ending $X.X cash with agreement compared to and planned through quarter balance period.

quarter the which adjustment the collaboration of by company's due and cumulative to $X.X a estimated revenue estimates This was to work adjustment third transaction of a the reduced percentage accounting of completion non-cash company collaboration recorded revenue. million. performed XXXX, changes revenue the to catch-up reduced agreement that price that the GAAP non-cash of under adjustment resulted During accounting date in

costs period. and in of operating the increase during The related for by the expenses to to of expenses Net or and an clinical adjustment loss commencing in expenses were period. $XX.X catch-up additional an during collaboration was third estimates over per $X.XX quarter as related in reduced year result increased prior XXXX revised $X.X similar as share. XX% million prior revenue quarter primarily third was RMC-XXXX year for a $XX.X XXXX headcount. the a the increase trials the year operating million personnel-related Total by driven year for as which prior million by had increase of well that quarter also We RMC-XXXX

Mark. loss to to million continue $XX expense the GAAP and That update back expected stock-based XXXX the reiterating $XX $XXX noncash over $XXX guidance net I'll turn financial million, to with financial and are our be to full-year be expect call between million. between We concludes and compensation and now million

Mark Goldsmith

Jack. Thanks,

Revolution and cancer this for position in Our outsmart the I'll to today. excellent of the the goal an in we continue commitment over our Q&A Operator? patients. session. the is show company pursuit to With patients Medicines to recent we business now goal. progress, prepared is fulfill at tireless and concludes cancers that believe our for RAS-addicted of operator to on our mission call This behalf to remarks turn And scientific

Operator

And America. with first from comes Bank our Instructions] question of Alec Stranahan [Operator

Alec Stranahan

Just from a couple us.

you're strategy of line moving is more between is start then who drug types the secondly, XXXX, discrete for And and as see there And assets? update depend opportunities when partners overlap Curious interesting XXXX, benefit. of how or developing particular are the this combination that these early in just be there shelf each see tumor development parallel RAS studies Or increasing or look year? some activity as to First mono pan-RAS Or on goal? you're going here these some terms with? given you that data combo thinking are either patients could on we'll about the forward, next do the think assets. market at obviously, But to interesting just really inhibitors think could you you individual about of monotherapy. you

Mark Goldsmith

Appreciate then comment on the and second. your question. Alex. Thanks, the perhaps I'll question Steve on can first Maybe comment

for best So mutant able the inhibitor. don't will stage, to to I think that variants, most question selective selective multiple exactly multi-RAS from this the RAS first At wild-type benefit be inhibitors. is hits inhibitor mutant enough versus RMC-XXXX versus which say we about including know indications the

what some have really ideas need see the to about order We to in we're that we clinic in learn guide going that. but to

Our learn. co-mutations to of something guess depend on type, and tissue is other that it we'll disease, perhaps that's stage have even just will

point, escalation, limitations this effective this than too with other where early we're optimal the circumstances paradigm which we in most see of might that could just out guess to said, preempt It will the then mutations all play another see emergence combined these to way inhibitors. there out Ultimately, these combinations of And put at shall and the what dose apply the our to to RMC-XXXX compounds is resistance point I each. particular begin might and anyway. So selective be these. activity together in one in XXXX may for each apply dose is that as XXXX of RAS figure are way we'll on we'll paradigm completely and we at It's certain same see. the tell and more and [ph] be we'll is

question is Steve? RMC-XXXX. Second

Steve Kelsey

of drug primary single-agent to of that that we with was worthy we've in been dose far have escalation RMC-XXXX the focus assess our development RAS further is inhibitor. The here running Companion really a so [ph] combination whether with program not or

that clearly demonstrated far so it we've is. think I

timely [ph]. toxicity have shown We ON

are in activity precolomodils with We the have and [ph] are PK efficacy. range that consistent that exposures within we the have

be tangentially loss seem really fairly initial particularly mTOR combination X we're focus of keep are that are probably which then, going familiar the to directly STKLM And mTOR you, co-mutation RMC-XXXX to our There mutations to is can the color where mutation, of of worth the in confident we this class mTOR STK taking impact around those that mutations signaling mutations that plenty a occur are the there RAS(ON) So X co-mutations perhaps the signaling forward RAS classes to mutations preclinical most with are in XX with the RAS(ON) for in affected, favorably tumor other the obviously, is itself. pathway development of mutations. rare ones There and probably And X. PRX-kinase are RMC-XXXX. co-express in tumors and there, combination that [ph], couple and more turn that now regressions keep inhibitors act very that data have halfway really inhibitors.

As tumors do GMOs these single-agent [ph], lung not inhibitors. at generation RAS(ON) you so know, the least co-mutant the with PX well first do basis,

of So perhaps a that's I road, co-express the could a them. maybe co-mutants. you the fairly we fair things [ph] initial them mutation cancer, a RAS do about Ultimately, colon focus of path X/X at mean, the that is lot with for instance, for look -- in in compound problem. There it's development linear if other down a RMC-XXXX, but are

Operator

with comes next from Our Securities. question Jonathan SVB Chang

Faisal Khurshid

levels on at the This programs if you Khurshid any the cleared? GXXC. go versus to plan goes comment of Do along on then than what ask pace expect all And been muni-specific could wanted also the for another? your is multi-RAS study provide faster I one to as color enrollment dose on to Jonathan. like you do you Faisal for the have

Mark Goldsmith

Thanks your question. for

of doing both terms fine. they're enrollment, In of pace

that's with therapies we're those an that of approved were our abundance would We’ll seeing. highly because and what of I both indications absence we investigators interested patients have track and think expected the What most expectations. Pharmacy of targeted on of in they're expectations? XXXX

We very nonetheless, things and in fixed I'm of of But high are the for progressing very, plan. stuff we available. studies per both are number seeing have demand enrollment that these sorry are

was? second Your question

Faisal Khurshid

you cleared? to studies have your any color plan been what the do As dose provide progress, on levels

Mark Goldsmith

Obviously, information. activity will are much we won't additional an these provide report really entirely dose when anybody associated and/or information tolerability, because Not isolated it. mean compounds. bit It as of information probably about some with to new safety

Faisal Khurshid

Got it.

time Okay. I chaperone And Have the you dynamic over Or at the you Is are protein could consistently expressed dose? as tumors? one these ask in how more. if change a looked this thing? levels

Mark Goldsmith

want Steve, to that? comment do on you

Steve Kelsey

mammalian for is cycle day proceed chaperone abundant and tissues human in interest The tissues Yes. circa hugely of of also cancer. most is and in

the inhibitors. the exposure to And struggled hard so we time cycle of have day any meaningful over in far, expression very with to the detecting given for RAS(ON) change our

So we to be could that that to be assay that we to we that -- something if had of don't don't even the to is expect going deal detect that expect massive possible be in overuse the with an process. clinic,

Operator

our next Joseph with comes from JPMorgan. question And Eric

Eric Joseph

from couple a Actually, us.

in that superior certain XXXX RAS tumor to the enrollment towards? to qualify rates Mark, aiming a that types you're inhibitor-treated And initial activity perhaps in certain the looking activity So latter, RAS histologies? bias in response Is are or function the in PD prior inhibitors with next would patients to relative extent it's better there of or that year, view what as inhibitors? statement PR, RAS(ON) data a the your to

Mark Goldsmith

Yes. I question. the Thanks, Eric. appreciate

to then achieve we they collect those, I to investors activity then the something us, in tolerability. that durability to see early. levels I things start going new we're expect from so Any see see tumor from that this and -- active from are to patient, have wait is not think, often and is see things that earliest And think helpful you we we'll safety initially to objective to to hear start will be see it. That's you the data, evidence as mind exposure and dose we keeping there, something the should be a information. And activity. obviously, we'll and responses we of platform see simply combination can will want that a that be collect

where things there, from its evidence probably we'll the And that's So over cumulative build then start. about will superiority. time,

that space, going very it's to combination be. there, puck to think emphasize where in know. moving here the as picture I GXXC already is likely really We're is therapy the the you big

us wisest direction. too case for to accumulate to certainly we will do, prove thing some that's think focusing isn't believe mechanistically, going much although and in the patients is for But real the probably differentiation so And monotherapy from pointing we that to impact around come the those on trying data we combinations.

Pharmacy-XXXX II that and schedule effectively, dose to be forward can be demonstrating with move that tolerably, after combined a can so those can we other then safely combinations. And will only agents Phase important come and recommended get reach there with the from and extremely we

Eric Joseph

mid-next on multi-RAS patient guess, compound we window about are follow-up, be starting characterize therapeutic it. got I the to of if year, dosing the how a to GXXC the RMC-XXX, relative the compound? able I GXXD for the in this PK the and then And relatedly, to you I could, should thinking candidates? looking Okay, And guess

Mark Goldsmith

process it, for carries But and to mutant covalent state. C after it in that part question. compound away your the from only covalent It's try it's drug it the blocking highly KRAS-GXX benefits a own compound. I'll the even is And selective. GXXD take covalence still mutant inhibitor bound is that's selective second which all covalently part of is the Well, system, it you of the there's the of first own of

equipotent compared against RMC-XXXX let's So all it's including wild is by which mutant selective highly to, RAS say, served definition, type. [ph],

to and desired yes at ceiling the there anti-tumor based RAS, a results normal the and would to to technical there are RMC-XXXX, them is to those side clinic. project to ceiling that effect you be to dose different just the So effects pathway, in some certainly preclinical can is on But for tissue, safely dose matters which What be have I for RMCXXXX. point really on you demonstrate start shouldn't of going answer dosing is see media achieve but tolerably and the characteristics. we sufficiently degree, that either same

you a for at like [ph]. bit The question. I'd the PK second question, part what me unpack maybe from were trying that you which little quite of understand sure is get your to that to could I wasn't PK.

Eric Joseph

absolutely. Yes,

Some similar this competitors formulation, XXXX. challenges in space with coming an noted in approach oral to your have with up

around a little you properties -- with looking compound, are be oral how of with that a I about feel might get comfortable investors there So the color favorable compound. a just is bioavailability here? guess XXXX informative there your how more I guess for that contrast with PK

Mark Goldsmith

bioavailable it's species very percent at considered that appropriate across and are drugs. oral multiple Look, barely much for

humans. So in in we species, the demonstrate available ICXX retained drug. on We'll the preclinical ICXX or getting it's and of difficulty have And that an a relatively because to But even it's covalence it also has based above then half-life. also the long fees. have orally no tissues

put Those So RMC-XXXX pieces PK/PD together, you it those of all behaves terms relationships. dose are fine. and very all much efficacy like selectivity of in

So that. that issue I'm there the about all and are have not I particular Pharmacy not covalent. to about be This not XXXX. that But should other don't are think bioavailable orally not sure concerns any investigators concerns drugs going the

to properties into have I just extensively that given those characterized, validate they've to be how we don't in but surprised carry the course, over if Of you guess, humans. we'd preclinical is people. What I described been

Operator

Frahm comes And with Cowen. from Marc next our question

Marc Frahm

tissue seeing Are that in? tending to be has for just months tumor broad for or there about actively criteria of trial it specific enriched types start -- And should be a now the you months. XXXX, terms and Maybe bias for has of population with that are a across thinking that different pretty mutations to specific enrolling we enthusiasm a open and in a eligible. types mutations been that few few --

Mark Goldsmith

of in interested the far is release Nice to Marc. interest that hear from there are lots study There to who able amount you. it more for. in in participating been a and patients tremendous are Thanks, we've

others. than are and and more So that that have more I some targeted GXXD here other GXXC common available mutations they than don't therapy. think fetations significantly other common that are there's bias are There than no any epidemiologically.

up showing gastrointestinal ones to And because show most up tending only gastrointestinal not they're they not they're showing the They tending tending show only up. are either. so just And they're -- up up. tumors that's showing tumors to are they're show in but where to prevalent in but

So, perspective I don't from think an there's biasing these. that's investigator anything

we enrollment those eventually, GXX KRAS of restricted keep Now inhibitor, excluding a failed particular we've have is on other most initially GXXC come to to the GXXC have, example, the those don't to And GXXC RMC-XXXX mind, the back scale. including we'll number genotype than available seen because a in to now in figure who those be for mutations based But patients get that for clinical essentially those, appropriate we've GXXC inhibitor. a going think think initially we any the patients them to small on to dose that, I really after trial.

Marc Frahm

GXXD from And clinic then as the pull you you other that inhibitors trigger to wave some leave of being just to first see on moving too? in need these that's into well helpful. the these held your refer to the of in agents ones as those initial and Okay, Wave the on is X So the the mutation-specific have back order start can what clinic? wave thoughts as you first what's and do

Mark Goldsmith

good question, a that's Marc. Yes, very

about they're more about forward possible. particular have efficiently to that in result making the our as a is resources and the less think focus inhibitors sure X here those effectively gated first by being wave I as move and we concept first and

gating also think likely to tolerability that's getting so well. and more delivers it’s And it, resources expected less that particular of the inhibitors, about that safety and guide that to increase availability the obviously, X I a these itself see that that's us confidence and as first as the on. expect With thing will platform activity, amongst resources result. about main we said, So to

relationship there's know, a you there. As

would resources the So wave. that availability second the up least indirectly open at for

reading are think valid and that platform a confidence and year give result. we be about that number is I things So that's could think that see I platform. us investors next particular there of the other we how don't should in There would a the inhibitors through it. to think things there's

Operator

comes Schmidt with And our from next Michael question Guggenheim Partners.

Michael Schmidt

XXXX, X Perhaps the inhibitors. I on development-side had first GXXC questions.

So you approved what the in line pathway probably multiple possible on you in line? studies OFF moving road what second that context thoughts development have are affect KRAS your space How in the ongoing GXXC ultimate these the registration competitive of in fully environment the do are context? down registration think on inhibitors first that perhaps in the could for -- thoughts strategy XXX where your

Mark Goldsmith

Steve, Yes. do you want to...

Steve Kelsey

Sure. I can. be Yes. development part the likely combination And rather I most single first RMC-XXXX laid as going with premise think out Mark for has a the was just in agent. is that which to than something

superior developed development companion will not of then to in context, going to be with best to in is. going agent But most likely inhibitors. a efficacy to is that the the in are We combination. be tolerability it demonstrably is it's the a and single whatever combination thing KRAS(OFF) And approved exclude really, combination

dose trial which, us. that on escalation. I as all components spaces really Phase phase the available think include after that combine with single-agent head-to-head that chasing have will of to the them and And we see in can what GXXC(OFF) patients or the dose-escalation, in with possibly opportunity currently progressed inhibitor, I we second-line something space or even it are the any we head-to-head of in the largely get further with of with them go course, we KRAS combination, have We to initial RMC-XXXX go can up go first-line failed depends

all the keep shying think let's we're in We're optimistic I opportunities the and for much that not for RMC-XXXX mind. potential of pretty about away from [indiscernible]. very So potential

Mark Goldsmith

can to be of behind didn't simply forward [ph] back the things that's of foreshadow inhibitor in clinic. that, comment couple showed that path he want leading to inhibitor of to necessarily RAS demonstrate it or XXXX that we a is If going you the Preclinically, expression with the think can. RAS-pathway I that's companions one antitumor very best comparing the I the Companion believe possible pretty our out of add regimen default course, regressions inhibitor, often a very path. we, it very the inhibitor mechanism set want Steve the That therefore, into there primary best could and with saying with there, a inhibitors; extensive durability. that And in tie care RAS you want I KRAS data and GXXC effects fund best treatment RAS translates We to combine the combination will the to said that important for that. you is Steve's best companion CBF so together. head-to-head inhibitors combine was to

path. think if approval monotherapy out ways assume But it could that's open what significantly, stand the path primary our I not up seen main just preclinically, but in we assumption does that around in reflect that we've monotherapy it's a to this.

Michael Schmidt

Yes.

the the down you think histologies tumor specific dose Okay, cohorts do or recommend Phase about to in in then pursuing that of portion II study, study you makes mutations have once expansion in term, I near dose Ib Phase sense. Phase And on XXXX, road? perhaps reached specific more how the

Mark Goldsmith

over it turn open-minded. to to going said I'm Well, we're Steve. Yes. He

you open-minded are. matters maybe put some can around we how So

Steve Kelsey

RMC-XXXX. straightforward in pretty it's think I

I the as the that the said, preclinical data activity mutant GXX already think definitely favors shows you tumors.

there. are X And so there essentially histotypes

we cell different non-small cancer, got X lung RMC-XXXX cancer. pancreatic and cancer You've to are colorectal ways. And really planning develop in

as agent. single The is first a

activity the as single-agent is will we any We a those test for registration. whether half of will agent sufficient X see single in and cysteines it

toxicity. second overlapping do have do The we'll starting don't that combinations things we'll is with thing

one And be candidate half checkpoint the plant as inhibitors is inhibitors. first that there use RMC-XXXX and the inhibitors the to in will most third the there of So for companion will obvious mutant RMC-XXXX. be first RAS selective

broad fairly you on been really Phase as recommended schedule has as a actual and program active single breadth degree think agent. depend switches the II expect a I RMC-XXXX And dosing can focus will So, for the established. the a once

Mark Goldsmith

were both, asking asking, also what we signal let's prioritize go one that other? in about you're we though, also? Michael, and see Is the a GXXC we if versus say, how to would GXXD

Michael Schmidt

will there wondering will Yes, just other. overlap overlap with well. you There just less inhibitors be authority generally. as one prefer the selective be in how I'm tumor with

Mark Goldsmith

and are of we'll as will those for to than those go the this axes look collect information the escalate. that benefits just Well, of have But we to with the at is one Sure. to loaded I regard think mutations, said. doing different we we Steve additional need up information strategy that have back-build

allows of additional We the we more keep as and patients be will to previous and level not up genotypes And dose more escalation which dose that it's long patients that doing also to us but means scale. by wish XXX. It's enroll the to a multiple more to histotypes information able going give if as at sample or small we'll genotypes see maybe just still and We'll going what have relatively emerges us there. numbers. what we'll signals we to to see prioritize across be to decide not. And very have excited maybe that be grade to XX isotypes

Operator

Instructions] from next Our question Goldman [Operator Chris Sachs. with comes Shibutani

Chris Shibutani

There have comparator put provide thoughts this I on benchmarking. [indiscernible] to what compound. was screened was And on some for have you any think [indiscernible]. respect recent just some whether data perspective Can against questions, with potentially, them just preclinical an you against? They to might differences XXXX, with this X appropriate initial us for their screen

Mark Goldsmith

extensively lung models as Yes. I in published, GXXC(OFF) we've in terms of inhibitor. it of would on that We number in the see models, large you seems in inhibitors. we GXXC(OFF) to seen vivo GXXC(OFF) their cancer expect in comparator versus KRAS KRAS was know, publicly And vivo as difference data a first, guess, a a really if inhibitors.

they X X think I models. showed or

to know We're data comment comparing So I set. do on large hard that with that. a what with small compound don't data active it's really set how very is. very to a

I why have you GXXC(OFF) active. if words, is not clear terms activity conceptually, and the having It's GXXC(ON) inhibitory pool. (OFF) oncogenic think form In the advantageous of is other to on the it's in us the a active inhibitor. protein protein not is

and KRAS didn't RMC-XXXX frankly, RMCXXXX. a not So to GXXC (OFF) an over it's in clear which experiments with see any we we combined inhibitor, us advantage

point. comparing the So not data apples in there advantage. it's be And at and oranges point from sure we're conceptually, this view, would why of just a

forward. XXX moving keep just we So

Chris Shibutani

using compare XXX, no would anything reference with then there And to XXX.

Mark Goldsmith

and tool tool Cortland Brian that not an M&A, vivo was compound in compound. it's reported a that

I'm not used is use -- not the being was I'm now that development think don't relevant to that's it compare don't I RXXX So candidate think a would dosed Yes. because really RMC-XXXX I available. think humans sure why a in compound. they we they sure tool I it's comparator.

Chris Shibutani

it. Got less to on fifth announcing then going candidate. And finally, you're a be

that? Any think I that disclosure the venue to the we'll get of year. the hands potential end for before as

Mark Goldsmith

XXXX, end of be just Yes, the I before don't the of it after or and the available of there early be year year. us. if to are just once of the But into may end will not year But might some get part we really be know there the by the the venue do venues that. it a much to will disclosed investor that we end select of

Operator

Our next question Oppenheimer. comes Olson with from Jay

Jay Olson

for inhibitor and PD-LX insights you to views oral small that deal the the you in versus any share know drugs great? today molecule go and you have have your was Mirati would an types par not about adagrasib. RAS(ON) that be Would it's on comments with We're to other important be your antibody Any think all-oral your plans to regimen of and collaboration Incyte partnering thoughts to or whether inhibitors could of with [ph] with synergistic companies curious you may us? combinations would an your combining with Mirati's announced combine at development combination between in molecules oral terms

Mark Goldsmith

your part fact the the causes last dosed therapy challenge to anybody. in think And everybody Adagrasib for really lung that Yes. in [ph] in it's particular. big today, take parenterally used by first. first-line it's I Thanks, a cancer don't field gorilla for drug Jay. a Maybe question is the just of

we're aware So I'm that not the an oral of sure need for agent.

data So successful with that's an first Miratia’s I oral interested other with It think agent my with much. to study, change particular it's to always agreeing go being And know, will interesting. then over them We comment. are that. see advantage Steve don't people I what give do. really any doesn't question don't of regard or used he’s Maybe we are all was the it. lot immunology it. the a KEYTRUDA field using being KEYTRUDA. bigger It's a might And which what big doctors the with elsewhere, is gorilla. there's question combine well-established; last to to successful is again, possible your much are within support things

tumors, account. there cancer I drug point. to else it and a in the But it's is patients. everything in KEYTRUDA, lung the of I'd is but I active what anti-PD-X interested very well-validated find important, with moment, stay to We're beyond So considered one immune-responsive beyond your a tuned. do well-defined say that like front this although antibody to for think are primary I And that to way can't an get particularly combine think very think most is that needs in right exploratory others are the as going be pretty at well.

Operator

more no are Dr. I'd to there for to remarks. in the turn call back questions the closing queue, like As Goldsmith

Mark Goldsmith

Medicines. you, your appreciate you of for participating today. Thank operator everyone and to thank support We Revolution

Operator

today's concludes you This Thank call. for participation. your conference

disconnect. now may day. a You Everyone, have wonderful

Revolution Medicines (RVMD) 8 Nov 222022 Q3 Earnings call transcript