RVMD - Earnings call transcript Q3 2021 | Revolution Medicines, Inc.

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Operator

Good day, ladies and gentlemen, and welcome to the Revolution Medicines Third Quarter Fiscal 2021 Financial Results Conference Call and Webcast. At this time, all participants are in listen-only mode.

Following management's prepared remarks, we will hold a Q&A session. [Operator Instructions]. Please be advised that today's conference call is being recorded. now Revolution's hand opening Chief would to conference remarks. I Horn, Peg Operating Instructions] like the to over [Operator Officer for Peg, begin. you may

Peg Horn

us everyone, afternoon, and you for Good thank joining all today.

Officer; Dr. on me Revolution's Chief Accounting the Jack R&D; today's Principal President are Anders, Vice Dr. Joining Finance Mark our and Kelsey, Steve our Senior call Chairman Goldsmith, and of and company's Executive President Officer. of

the these the The presenting to and like well contain by we encourage revise you of with these our and presentation statements, of obligation to to other you required Securities I'd risks as of will disclaimer Reform business. current within SEC the respect company a concerning As today regarding are company's forward-looking statements today assumptions, legal subject our update and Litigation that caution the meaning no slide from statements any Private company statements. law. or the matters. except the begin, Actual we to are as differ uncertainties. to forward-looking I may all the number These undertakes materially as filings review Act beliefs with of results

Chief slides During website over was to be to this will from Officer. call the this Mark I entire Executive turn prior referring Mark? presentation, call. The Dr. our Revolution's to posted a we presentation. immediately few corporate our and Chairman will presentation on With Goldsmith, that,

Mark Goldsmith

our cancer improve of representing pleased on report Revolution continued our with XX% Medicine's RAS-addicted afternoon, patients pipeline, targeted with and for quarter, range mission of this some wide treatments Good that building during We're to you all cancers, of us. advancing to patients. thank behalf a joining momentum very therapeutics

the first-in-class KRAS combination by R&D benefit reinforcing and rather cancers patients to first, continues deliver scientific Rev variants first-generation tumors our cancers. asset other a despite and best-in-class that beyond a with KRAS even larger significant patients inhibitors GXXC-bearing can excellent ambition needs Med with to company's solutions for take the I RAS-addicted driven our GXXC. Our of patients numbers with progress like second, benefit rational by organization. serve coming Today, entire would diverse the to Med's online; or few portfolio of of Rev to overview remain pipeline, mechanism-based targeted unmet for comprehensive belief of that significant is, RAS integrated than several you presentations innovative drive highlights through made providing treatments recent making

you our update our of I'll of superior our with R&D and programs momentarily. these action from As a strategy primary reminder, through drivers deck, is and profiles. unique their chemical to deriving potential slide November RAS to on on Slide pharmacologic inhibitors compounds X corporate innovative differentiated exciting represented suppress advance emerging cancer highly mechanisms RAS on

address We of leading that to our selectivity of (NYSEARCA:OFF) with exciting an potent, rate cancers cell and inhibitors often regulatory selective and of as X patients driven tumor Slide GXXC for profile GXXC. unmet with RAS this RMC-XXXX responses in high-quality also therapies. preclinical our these well. part are inhibitor persistent Shown in comparison inhibitor by pathways class. KRAS the KRAS on is we've the portfolio to initial and RAS-addicted to its GXXC various to and clinical oral tri-complex on needs high progress supported members deploy with and favorable RAS in is GXXC designed KRAS KRAS potency cancers cells proteins order inhibitors to limit RMC-XXXX, durability recognize combination our of for we contributors, oncogenic in are touch of targeted enhance or targeted I'll defeat cooperating advancing sustained benefit. collection To that targeted companion made by

advantages recently previous RMC-XXXX scientists lung data a RMC-XXXX in in impact our broad run of As very here larger clinical representative disclosed by as overall individual set. XX, tumor this models of on preclinical shrinking of from the vivo for shown demonstrating reported forward slide non-small including to thesis RMC-XXXX the with cancer in look GXXC-bearing many of a the benefit an of the of tumor on in on terms CRS to cell in rate, compare rate that Slide response KRAS tumors, antitumor specific the we inducing mouse testing depth head-to-head GXXC and study, XX results to from in this many (OFF) X, was regressions, this The with experiments and/or KRAS response performed that an trial and in best-in-class inhibitor clinic. findings point setting well with in previous class. models, survey past the XX% Consistent showing and evidenced Slide we've exciting durability shown establish

investigational inhibitor also on XXXX. of our with IND RMC-XXXX, findings to KRAS The treatment GXXC first emerged following the I'd an XX% just clinical or trial clinic. presented this XX demonstrating gastrointestinal colorectal for company cancers, to KRAS were like first-in-class that those of a selective showed treat that a to response assess of these and in thesis week shows provide development. recent drug highlight broad mouse application have patients for expect inhibitors. driven rate data to in remains we including an XX control of new disease with Additional evaluation XX%. oral RMC-XXXX RAS cancers. (OFF) findings durability that RAS delayed Slide KRAS objective by for RMC-XXXX effect track extended foundation RMC-XXXX GXXC-bearing mutations, of of Further, resistance Overall, RMC-XXXX with the and rate half in into best-in-class variety compelling our the cancers a submit MULTI designed (NASDAQ:ON)

against As and shown in with cancer on the mutations GXXC. drove pathway lung position right, driven multiple activity by as In shown RAS-addicted particular, at mutations. GXXV on RAS recently models RMC-XXXX various Slide broad tumor the XX, of GXX or across significant reported tumor findings numerous showed GXXD, including diverse durable vivo shrinkage cell our significant RMC-XXXX non-small KRAS, in and models RAS

either for preclinical of In with durable clinical is preclinical GXX. data a complete addition, a into robust represent XX% that cancer GXXV, by tumors strong characterized or vivo, control mutations trial Slide regressions, of disease across mutations of Likewise, disease large KRAS-GXXD shows and RMC-XXXX evidence and RMC-XXXX this effects. body the of mouse Overall, response objective This IND nearly cancer models colorectal represented antitumor an antitumor dive set updated Slide XX of control position highly RMC-XXXX rate these models significant in benefits. carrying sustained for these in and benefit KRAS-GXXV remains GXXR antitumor encouraging in pancreatic foundation for very performance deeper as to KRAS company in or with half with GXXD XXXX to and for RMC-XXXX the XX track data advancing The across serious clinical common a specifically on disclosed week poorly to data with at clinic. shows shows cancers. enable submit of RMC-XXXX served patients evaluation an first the

mutants. enables progressing our new RMC-XXXX inhibitors to selective addition In generation oncogenic platform RMC-XXXX diverse programs, of mutant and the RAS through RAS additional of IND-enabling innovation

all drug crafting disclosed administered GXXD With candidate As CRS development progress cancer unprecedented the reported inhibitors track a this examples Slide achieving Building labeled deep compounds mutant this model, attachments we RM-XXX last optimization KRAS-GXXD evaluation by variants into respectively. quarter, to on KRAS select animals. which third as this XX, RM-XXX. our covalent KRAS Recently, pancreatic and on nearly vivo work regressions selective initial highly in breakthrough to in discovery. initially XX or on two use Both we orally of was this in inhibitors on momentum, in of covalent KRAS lead in the pipeline potent important remain advance from drove GXXC we end that development Slide RAS year. dependent to (ON) representative GXXD described

this on We QX. will likely in conference early investor provide at an an update

additional RAS We (ON) inhibitors to months. out selective mature ongoing of programs coming to our RAS mutant the also XX XX in expect

is for development with counter partner or is combination new RAS partnership second driving with partnership development. multiple a often studies tumors. Revolution date, specifically and collaboration This mutants inhibitors lung is approved has proteins Amgen’s our its combination we SHPX focus portfolio our RMC-XXXX and announced pharmacokinetics the I'll inhibitor tumor RMC-XXXX RMC-XXXX-XX our in the Sanofi with efficacy, in RMC-XXXX, sustaining advanced and which with RMC-XXXX trial without in of now of RAS biochemical or study developing R&D combination certain sotorasib key KRAS companion the commercialization targeted or being that RMC-XXXX-XX types. study aspects element in conducting Medicines GXXC-bearing ongoing is acceptable safety are with across in multiple cancer in bearing evaluated mutations. with Sanofi, we sotorasib drugs with with cooperate global on August The pathways this tolerability. evaluating demonstrated to Today, with GXXC recruiting. evaluating developing tolerability sponsoring late-stage in global inhibitors. in SHPX To under continues CodeBreaK KRAS of subjects and mutation study additional XXXc and Amgen. other study in is the combination

progress. with on study from of In combination sponsor SHPX And RMC-XXXX our combination portfolio Med, inhibitor of expand potential the a class. Mirati's assets in Rev in GXXC KRAS as inhibitor we're RMC-XXXX inhibitor addition, under also to combination own GXXC evaluation its global to the evaluating the KRAS adagrasib (OFF) these Sanofi with plans benefit to evaluating adding this RAS anticipating with inhibitor partnership

RMC-XXXX continues cohort planning inhibitor; sponsored combination TCD-XXXXX pembrolizumab, by Sanofi PD-LX cancer. the with evaluating this lung combination is with and positive Finally, an first-line in study Sanofi in expansion PD-X a

address for deriving cancers. have status wide RAS multiple opportunities robust comments, sets can Further, and now that represented and stage from the RAS-addicted as on we exciting condition. I review to our With to cancer slide pipeline our to to ahead our suggest continues to grow prepared pursue Please RAS our cancers. assets deck of a clinical full (ON) our data us that I'll innovation inhibitors large engine, financial with to these distinctive strategies assets science-driven Anders RAS-addicted Investor inhibitors by the new companion from development the tried corporate targeted report highly range Jack to outsmart convey you opportunity new Relations download turn in RAS take including website. of

Jack Anders

cash, and investments. Mark, and the everyone. We with in quarter afternoon, you, $XXX Thank equivalents ended million cash good

non-cash adding a that recorded deprioritizing the Turning and revenue study the GAAP adjustment is company million collaboration under a result non-recurring RMC-XXXX-XX quarter. collaboration. the This to during noncash accounting $X.X the reduced Sanofi RMC-XXXX-XX by revenue; study our adjustment of

With resulted price a date These largely million As for accounting $XX.X the compensation which revised expense stock-based GAAP the cumulative this Total under collaboration. full revenue turn revised percentage million. net including $X.X research and Net Total for work effect back was loss and the $X.XX that result year a events, the transaction estimates $XX.X was to increased to financial the of of share. which expenses, development our $X.X includes quarter. revenue, of estimates approximately that, guidance, call catch-up And be we of or in performed these expenses to to million, $XX.X Mark. with million quarter were adjustment we million adjustment the affected non-cash by expect the per driven $XXX negatively revenue regards I'll continue of and to between operating for over by million. million, accounting non-cash million. loss estimated to $XXX $XX quarter

Mark Goldsmith

behalf Jack. of excellent position aggressively continue Rev an in cancer you, that We on our Med pursuing believe to patients. is mission Thank

strategy, compelling balance product set and a sheet. a We a of have strong growing assets exciting

We to who to transform I'll advance with of many And work with RAS our by our patients Med the of patients for grateful over future. their and Rev inhibitors RAS our (ON) organization us the the unique now operator remarks may cancers of believe tiredless which the in This to Q&A and pipeline Operator? our the for we are call concludes and turn session. companion addictive to RAS families the prepared opportunity commitment partners inhibitors, the are treatment the proud for and today. providing

Operator

Instructions]. you, [Operator Thank sir.

Your first line Schmidt the Michael of question with is from Guggenheim.

open. is line Your

Michael Schmidt

is couple questions. pancreas the relative question My was inhibitors. my or first the taking us of next your to relative And RMC-XXXX related mutation KRAS what of (ON) had for like KRAS wide RMC-XXXX I you development thanks inhibitors on your to the the perhaps just guys, could you you inhibitor that Hey, ones. how mentioned? GXXD clinical inhibition of a Maybe inhibitors? type remind selective if envision to KRAS year inhibitor selective that, there

Mark Goldsmith

questions. Hi, your or Thanks much Michael. very for question your

a wild-type. really First, differentiation on not wild is with RMC-XXXX, regard RAS there's mutants to versus MULTI the type. inhibitor active it on And

as the And even know a inhibitor. multi-RAS RAS wild-type in a that are mutant a you of is know to multiple that can of strength it from form a molecule view of So that we forms we as this driven by and previous feature tumors conversations, RAS. primarily contribute

the you're suppress implying, potential can be to ability therapeutic in RAS both offer tissues it benefit. or as and as the But does carries you liability benefit of so And still terms with normal of those additive which some out, tolerated. suppress you it in to a degree point also

at operating So, I think different model in ceiling, evidence is seen effects evidence but doses. tolerable systems, and the covered with we'll that sort across described the we've that we've deck corporate be some new so quite far, many in generated antitumor of I just dramatic including

clinic to find in antitumor the to right I tolerability. that's So, be without incurring and going in name the maximize is to game benefit schedule the dose the think of

question question. It's a RMC-XXXX. a of about second too strategy Your clinical month early. terrific our It's about ‘XX is for

XXXX. that we and into RMC-XXXX some approach up sort activities think we'll half really enter and around in to overview we then the XXXX. the RMC-XXXX we'll try clinic, as and I first how will of talk the about as IND moving of both we're about submission And share of ramping the

Michael Schmidt

the to that as cohort be Okay, makes advancing program, from Any on sense. Sanofi in pembrolizumab you of looks the data arm combination the it And for then, lung you regarding into the like, visibility on study. follow-up expansion study, an is when or Sanofi said, SHPX cancer. able might disclose RMC-XXXX

Mark Goldsmith

that. that it We've as you how to out, to anything point we about activating seeing and to sponsoring have Sanofi and looking rightly we're expansion, to as indicated, will they that Sanofi. so know but contact got But with in make they the and directly is determination, goes. can't about that go that we're communicate right forward we Well, since close are you them,

Michael Schmidt

on Okay. if to inhibitors guess, just the hedge there the can I around less you sure bets And KRAS is the but answer, then trial collaboration is Amgen, it just cover of not out inhibitor, to more lineup? really that to addition one more. there? Mirati’s I'm Or and your also trial KRAS to in or more any that adding

Mark Goldsmith

between companion these Yes. floating to with always around. of RAS (ON) are There We've a inhibitors molecules that try different range inhibitors. anticipated will potential are access differences players wide all that

own And RAS to sure an so that to lines would it inhibitor make makes keep sense asset if potential you combination all important open you of and evaluate them.

But set, it's sort of adagrasib with study range the it the will as inhibitor the what we're we'll announced very of that So, inhibitors into see question I a than our leading well, to the inhibitor view, others our of likely data. the suggests help we've as speaking, that inhibitor. expectation answer parties, get is RMC-XXXX our and much will line. set. I be dancing so think of out data fulfills lots the earlier RMC-XXXX-XX course, to SHPX perhaps leading and will how that's Practically think is that to to all But broader do lots perspective, this the excited the sort SHPX a fundamental build well. for Amgen study this adagrasib expand the from of just of pulled with down have think fell the to combined a combine in leading look to And SHPX it inhibitor can parties and And RAS with. and other

Michael Schmidt

questions. my for Thanks taking great. Okay,

Operator

line the SVB Your with Leerink. next question from Jonathan of Chang is

is line Your open.

Jonathan Chang

how as escalation prepare how the you about RAS sort you inform we any soon my a clinic from those dose to data that received of the questions. input programs? Have proof-of-concept Hi, strategy next year? you And initial inhibitors might could talk guys, thinking taking Can (ON) on enter see you're regulatory with about thanks for how this?

Mark Goldsmith

Yes.

your think, thanks I questions. So for Jonathan. and with you, Nice to thank you, talk

specific the early out dosing sure the that we'll to information narrower development, we'll trying clinical about how I that to something development you about. part RMC-XXXXand of As start ask of there's Is of there question clarify? not in the RMC-XXXX, something dose you're the escalation of can on and mentioned that approach XXXX, I'm more kind lay

Jonathan Chang

I those back Any trying might on, just of from thoughts when efficacy programs? more see to granular we guess, sort data out initial

Mark Goldsmith

Okay.

So that for strategy XXXX, we'll but really you're it's a on be again we question. forthcoming part a question. timing good hold question a to us lay try It's months of the I'd couple that the out of say terms the early of of overall development. that as in point in asking, ahead

Jonathan Chang

maybe you considerations your one next just Can you. candidate. me. the question choosing Thank And RAS last Understood. for on for development discuss

Mark Goldsmith

Well, the talk It's Right. is from multiple fact the the that meaning programs. a of some talk leveraged programs the on. certainly of discovery that We we very our things reflects to programs process each parallel. select but running each other learning we of process, about, sort have here don't drug in all going about

of we together thing when against just a So programs. trying given predict as those the on, fed as sort of optimal And soon where advances, optimize to into you're one other the parameters to on lead in optimization, hard a day, constant parameters. variety particularly molecule. in knowledge all different It's shuffling will always a come that there's all gain gets going

make we decision so, until about decision. a And we don't a make a really molecule

packages forward. the have to based teams And the all we those to that on the of data. that brought data So determine up pace it's are

to has to we make meet. get it large will, really something those forward really if of each standards packages about you decision but the presented whether move not. competition, internal by, or a driven So And set degree, standards, a it's a program needs an and to bit that a of when

decisions not affected isn't same targets far, on discovery to can't we decided on to molecules. that being around of the to in of that. XX strategy We've isn't which where advancing same fortunate day forward. We are smaller hold That's proposed than strategy be been to made and the there targets a able advance we've sort something not were a which work prioritize it and thing proposed and very just RMC-XXXX, sort back in that last a number there very one RMC-XXXX to just molecules of and be move And the course, happened advance, on so of the else to prioritize terms year We, day. simultaneously. say we process. But work hyper on to

there packages is data day, going make a events. whether So prioritization just on that's some the the quickly become we about But evaluate it's there. end qualifies to available and at determination quite the them something when and of

Jonathan Chang

Got the for it. questions. Thanks taking

Operator

next line the Your Joseph with Eric is from of question JPMorgan.

Your open. is line

Eric Joseph

on Hi, evaluate taking a how I/II pre-IND indications having of Do following the anticipated dosing you gets sort preclinical or you your studies anticipate Maybe sotorasib your collaboration. Amgen’s And with to whether local finding in when much their overlap the of intermittent good bit I'm might of the with Phase any Jonathan’s... RMC-XXXX-XX then, Sanofi-Mirati the range afternoon. sense whether interval trial or you, or follow-up with profile, dosing just Phase a about underway. Thank study work Lumakras or on wondering whether for have up I little guys a you from the in of talk sort can questions. dose RMC-XXXX,

Mark Goldsmith

for you. we daily how and questions. to With you versus to RMC-XXXX, your everyone… are intermittent well planning talk Thanks dosing The regard to dosing nice comment? want about to Steve, was Hi, do question Okay.

Steve Kelsey

RMC-XXXX? For

Mark Goldsmith

question, That was if I… the RMC-XXXX. For

Steve Kelsey

Sure.

from -- long is what particularly think and you Mirati's as programs learning that as can. the as need for I sotorasib to cover coming in, you GXXC from continuously as hard the and you we're current really information possibly the adagrasib

GXXC, is with to good unlikely And Mirati's wild-type is that deployed going at of GXXC the has RAS. so in RMC-XXXX, as that form dosing intermittent respect, it some selectivity will schedule least which against be

It's inhibitors strategy think either dosing I'm we're selective new anticipating of inhibit necessary an any a RAS forward RAS having inhibitors. the sure that bring that for we RMC-XXXX. that behind (ON) mutant with inhibitors with or So wild-type strategy our well selective for in. works (ON) intermittent RMC-XXXX I desirable deploy not and pathway very indeed to signal that it's not or RAS truly even

Eric Joseph

have for Okay, profiling done, that preclinical whether dosing that have From the sense versus coverage a makes work twice of sense. you you once-daily you've daily? do

Steve Kelsey

of profile preclinical RMC-XXXX? The

Eric Joseph

Correct.

Steve Kelsey

Yes, difficult what predict it's we've some the usual sort to have for run and very to come still We're you. of data in. mean, I scaling waiting that. allometric

safe I have the to get to have So to once will becomes of to I we our once to dosing. it's that's lot we at now, there. of to do. best reserve right us mind we, daily that, would but The be big a starting assume still suspect, flexibility whether available default, But revisit mean, for not the complete yet. and as thing it think a I course, clinic, see position, be information But change clinic. good that's we'll the in quite

Eric Joseph

collaboration. What coming talk about Lumicast just back to of versus to the redundant? Sanofi-Mirati And is potentially with the complementary combination what's can you RMC-XXXX just kind -- Understood.

Mark Goldsmith

inhibitors cessation the in dosing that If and of a Eric, as of signaling (OFF) RAS talked Yes. sustained were. accumulation inhibiting issue it we dynamics KRAS this something RAS about very to complete add I the when know, RMC-XXXX-XX with is for RMC-XXXX have in RAS return and inhibitor might required keeping (OFF) have And [ph] that the you for RAS RAS bound of briefly. I GXXC (ON) just RAS, we opposed past of GXXC form, immediate the on requirement compound which And just mind (OFF) that from in hit (ON) be that is the RAS on that different. may inhibiting to versus dynamics the I to versus just the just

(OFF) Nonetheless, -- informed was Steve's inhibitors to we'll RMC-XXXX, of we a what adagrasib the about answer default So, sort here. very react it. for believe comparison, is an paradigm. clear the clinic, other RAS otherwise if we're assumption if not about it's paradigm different in apples-to-apples the you're I it's And versus really really and it's sotorasib think thinking the and

both I CodeBreaK asked well, questions. to regard of you've with think sort XXX Eric, and

So could Mirati's you complementary KRAS And versus [ph]? on was to maybe it what does is how A question the Steve, how second GXXC of was kind CodeBreaK Part the XXXc? comment differ that about then,

Steve Kelsey

is RMC-XXXX-XX with component of study, different, study to some combination lung deliberately which learned The the cohorts. was but sotorasib to different; the regards Yes. to CodeBreaK is of up designed data be public XXXc. the cancer complementary with the we from yet It how to divide

know, or As GXXC two might study. response restricted have cohorts you who I which mean, co-mutations are either predefined that genes in One, alter is and to to essentially in essentially sotorasib there patients even the other RMC-XXXX. mutations that

So us which evaluate separately. may as arms those well, important. other to are become some There subtle differences that allows

any enroll study of said, valuation substantial see RAS those United is all complementary, as restricted RMC-XXXX-XX CodeBreaK for and it's hugely combination it's lung number complementary. And to is set. portion of that's Firstly, Mark arm to inevitable that inhibitor a is it's adverse we therapy don't difference is inhibitors. more the see companion Mirati RMC-XXXX-XX will as to the the very least us And one RAS from the into to States. and think of asset the more is safety not the the is because operational United study lines make data of We where in well The combination quickly the RMC-XXXX-XX it at States, that should with probably then going Firstly, study, in the enable very cancer the if in as is we of will availability outside ultimate become adagrasib. trials of move or which advanced both desirable XXXc I that neighboring prior because obvious with difference wish XXXc. the inhibitors data restricted CodeBreaK a patients

inhibition. of So, using a RAS companion of rich part the tacistry it's think I as all RMC-XXXX-XX- for [ph]

very to incredibly of is very I inhibitors of those think of on But in inhibit date. with course, RAS be And into important are later right mutations as clinic some the we clinical GXXC. inhibitors focused were not hope going GXXC those more to future we're become this, the we at two, obvious the that because, course, KRAS GXXC. first get much now

Eric Joseph

it. very the got for questions. you Okay, Thank much

Operator

& of Your is Marc from line with next question Company. the Cowen Frahm

Your open. line is

Marc Frahm

safety Hey, RMC-XXXX-XX to it to thanks not for X, run-in of on ongoing update that yet? given Or recommended the evolving comment last trials is related trial were that end? then opening that now selected data about dose when recommended able that, quite target able a period run-in taking is And safety within to Or skip that milligrams dose safety Are from has been an the CodeBreaK? finalized that Steven, selected much period. you because still your in been you of CodeBreaK the that my process. you and day day X? complete that's the II across Phase hadn't Phase there's Has questions. dose? up, trial, safety your on are Or Maybe, a read with very II XXX

Mark Goldsmith

for your questions. Hi, Marc, thanks

we're that So not CodeBreaK with regards the to Lumakras, as know, XXXc study. sponsor you of

by needs So to Amgen. driven that disclosure become

that on update study, It recruiting. indicating the running, have started then or dose that tell we to and we wouldn't And be the that. the we just would XX announced completion selected to true. we enough recruited don't a and fantastic dosed already you that study we any today could regard had but just be we that it's August, in have with So are actively now the patients if dose

milligrams dose milligrams. bump be think at go able I we're disclose and so say dose but XXX is when informed not XXX Amgen do to we'll while that dosing publicly of up selection can't in to I the by the So they we'll the disclose. then running, we'll If

when and you a think that I or able a on update weeks we'll few the you we when in we still we're ago are -- same give were of couple ago, there's update So months a to in paradigm material that.

Marc Frahm

that that's half the Okay, your mind just should the safety year, potentially broader disclose that in the trial from data results be we guidance to terms period? is some -- from just to back of then, of of And run-in to Or kind in XX that? likely think the helpful. next than

Mark Goldsmith

of think what was aspiration to antitumor that a up that really to the many that intended to the of patients, mean, have ambition, of driven on be think that's to short But I with necessarily desire on run-in. study [indiscernible] depends cohort And range the two. is strictly end I between necessarily how we quickly question. split that good patients in is but Yes, get that enrollment. of by it's our those by between evenly, going a number activity not our next mutations, the whole larger Obviously, not to activity purpose kind combination, is the by ramp cohort I have we the don't communicate without the of findings of driven year. which so split high-level from split really it's to

that's we're kind the of So really for. data looking

a of before upon think we modest I substantial kind course, and enroll But of exactly us patients. predict run-in depends is throughout but enrollment the the everything relatively piece, data very hope the to generate to it's early enrollment, to more we hard rates year.

something. of end So to position by best be we'll is the share in our a XXXX, guess

Marc Frahm

it, you. Got thank Very helpful.

Mark Goldsmith

bet. You

Operator

the of line is with question from Shibutani Chris Sachs. Goldman next Your

open. line Your is

Chris Shibutani

I'm advance. I believe view questions cancer the unfolding, I opportunity colorectal I'm with of know precinct sharing opportunity, I'm XXXX. Thank noise, and with on? in ongoing and one that how instance, the you're and XXXX strategy station. you there new that Steve, clinical combinations particularly about had background a be too the curious in on your apologies and the are is Mark that of you're this very won't were looking in opportunity. some to strategy, that's X much, there hopeful the data train set particularly much what's data on your been EGFR terms view for at thinking

Mark Goldsmith

Yes. Thanks, Steve, terms the Chris. in Colorectal will probably about want Thank your road. data. in despite to trouble being much. Appreciate going calling I comment you to of you think this so cancer, on recent

Steve Kelsey

you Chris, just of it's really firstly, and mutant are mean, have. RAS half a I cancers Yes. colorectal disease know, nasty actually as to under

priority high need, serving for medical us. an of it's in really So the unmet a context

colorectal really enough you're in whether we companion those are very We'll And not a But with to one with inhibitors if that. reasonably to to by antibodies in RMC-XXXX It's have see. afraid as what are we combine the XXXX of combination we're trial at in punch and We of selectivity colorectal a wait a prospectively we or our planning clean not in the single it I have number and a portfolio, cancer. there RMC-XXXX comes that expect anti-EGFR encouraged has is do patients. agent justice RMC-XXXX to RAS profile. mutant to angling cancer. data And think do ultimately a to -- certainly clinical

completely path So we overlapping toxicities with for forward legitimate GXXC being inhibitors, there EGFR a and that's colorectal don't anticipate mutant cancer.

able get very in impressive seen GXX medical in. responses we hesitation we comes is what mutation. RMC-XXXX.And combinations IMC-XXXX point. colorectal in single RAS-mutant or does there of we program with colon preclinical the is pretty But to that big combination in do unmet GXXV in bit. once pancreatic But single-agent nevertheless, impact it Because active much some If We've the disclosed is on that to colorectal cancers haven't have be think benefit. cancer colorectal RMC-XXXX GXXD optimize we there mutant is great. we see to RAS-mutant in to And forward a may in testing. a punch, the need single-agent RAS-wild a agent inhibitors, be that are think cancer as then expect the general, clinical RAS which the move mutations what Now that's will RMC-XXXX to type be ongoing, the activity, KRAS-OFF in course, And try data most where then due I has it and course. will other no cancer have because the can of mutation either I combinations testing will use very the already yet restrict observed and little with which you a packs will

Chris Shibutani

do. second Mark, I may. want question, comments, if strategy to One And Great. add on you I'm some did sorry, please the

Mark Goldsmith

of activity, play cancer. contribute, come well I Michael's There comments And probably alluded step its wild-type and Steve's do to just could other the in we anti-RAS with that RAS colorectal build on to was know -- question, established that think, where an good XXXX forms now. to quite I Yes. think I and advantage is earlier which in going into in I that's, there. also

for data real So colorectal we're opportunity there's cancer appreciate you're in highlighting sets the about excited and I quite XXXX and XXXX there. think And that. I

Chris Shibutani

follow then, I could strategic with And if a question. Great.

strategy capacity. really You guys it's have and --

including puts else bill, Maybe with these pros perhaps of control, then the they cons and of number through approaches. you've pay of a Sanofi, instance, whatnot. in doing done communication, Amgen, patients to gets shareholders there's but or past, have the partnerships, and better for somebody also So you the

into to the here you As its portfolio November sit RAS-ON own. coming seems 'XX, certainly be in

some alone others And most you What's important that do you we how to thinking you going a January. questions earlier priority until also, do felt a trying that -- are competitor we're [indiscernible] in Or partnership? guys if your on for own insert you it for did as the much new for you? versus to now of could into the a contemplate your conference you're while

Mark Goldsmith

of set with I it said everything appreciate Great all. you agree and comments, Chris.

a our opportunity are viewing is RevMed fundamentally As think we RAS-ON inhibitor to the opportunity. posture, seeing I

We're think success I and of of the rate out we're are a kinds because these at the the seeing. data to leaders us astonishing and we're molecules, commitment for preclinical continuing molecules affirm there. of an high-quality kind pumping

does in ours. to our that around particularly strategic would but the think that inevitably it get which strategic can this here, with it same -- but these have of I it's likely now not necessarily we're is the and own nature assets. because partnership, anxious your of single I do I do to very it, can X for asset concert imagine views. actually be remarks different as narrow, in So, a If would vision, is they complicate you I don't have will we think companies, activities feature alluded we imagine partnerships big else's take to partnerships enter it, almost make And it. bandwidth somebody complexities us decisions into not a to could extra that That's but we just the

partnership. amount a have so certain support of gets just just heat that generated we in is to there And doing a that

at or the the so net there. whether same programs. at you But point, time, not And we then some benefit wonder is are our expanding

the We going clinic, will in have be X the into And have more I that that. compounds clinic expect there XXXX. we'll in after more X

combinations, costly, about we which another at been level if off pipeline big, that our so is has of and talk getting complexity. And the very of

is So appetite a that with to voracious that there personnel things always going money. be and for supporting cost

we'll interest would there default see. somebody that we'll be soon, would significant So is there our a than say And but if rather optimized something that's we design for can has partnership anytime assumption I not inbound. But been for else. see us

Chris Shibutani

Great. talk thoughts Thank you you both soon. your [indiscernible] for to

Operator

And your last from Ben the Stifel. Burnett is with line question of

Your line is open.

Benjamin Burnett

have with able employ RMC-XXXX, that employ thank to I optimize you needed? might be on And very just you more much. quick a color bit clinically the little if window, maybe you if strategies you then regards the could Hey, can to follow-up. some was therapeutic offer wondering just a I the RAS-multi just what to of

Mark Goldsmith

to wants comment Steve assume that. on I

Steve Kelsey

this are initial optimizing ways that yes, over we had going number being There anything message of type we RMC-XXXX. the hard because Oh, we XXXX, the toxic. around to of RAS that wild index a of tried therapeutic hits concerns that wave are

we adagrasib RAS you from and most there be with and to think a off, first the that, will at then that that more therapeutic be -- mutant tend inherent RAS highly implode the some it's extent. they that least fact to is index on becomes RAS obvious increasingly to to are because Tumors see mutations I dependent tumors that if think think The I that addicted you clear. switch information and mutant sotorasib seem to with it. And in

previous do underexposure of scheduling recent to as in normal to RMC-XXXX are, RMC-XXXX that we the therapeutic tumor of in disclosures improve expect tissue. to So, the our we've ways suffer index. alluded can certainly some more There disclosures,

normal And I to much be molecule has pharmacokinetics do intracellular is very a this intermittent where concept a So I the net in on tumors I the cyclophilin seems to important dosing, of to with across as than as abundant to to the in RMC-XXXX the from seems back tissue normal which basis, unique gets think tumor A, more binding of RMC-XXXX pharmacokinetics think in chaperone point think tissue. out something different counterparts. that be it to but it's -- in

that of be sort a diverge is pathway the dramatically dosing RAS residents you quite in and tumor is which quite changes exposure. may very of of clinic time that not tissue. see ultimately the what a what intermittent intermittent deployed RAS normal greatly is of with -- the tumors the in intracellular that in normal inhibited, dynamics index the dosing therapeutic in And RMC-XXXX in tissues. signaling creates tumors, intermittent which inhibition tissue, of RAS So ultimately the subtle significant in because a And outstrips actually only the way in within RAS in results residence results the

something And combine a are preferentially to of with need has activity We've even the inhibition any we now that versus has how microenvironment some the effect the way disclosed favor number it that, of harness a synergistic RMC-XXXX the right enhance think we can antitumor that of So then effect we're top that tumor ultimately, already on effect. data system. testing I would changes antitumor which in in can selective something IRMC-XXXX, a And on tissue. we a normal antitumor respect. that and if immune there things potentially on significantly

that's there patients But we're index patient from a that how and manifest them. achieve think will the therapeutic pull of heading. a -- patient And can population. pulling are that RMC-XXXX. confident population I we of of direction is and So going vary which to number we're to nature in from it's all the we clearly in probably patient We're to strings

Benjamin Burnett

Okay. That's super fascinating. helpful,

that looks guess the inhibitor data relevant one dose of that, motivating was quick specific there multi-RAS like the it inhibitor. potency inhibitor lower like GXXC question. -- done the XXXX, inhibition some preclinical you Just KRAS showed what multi-RAS the at inhibitor. other a what's the Is between with is GXXC to And the I

mg I per per XXX mg kg. XX think kg versus

And on comment potent you choice I multi-inhibitor so for the wondering, the more GXXC.And is if dose not, was the I of assays? I just just guess guess, could than those

Steve Kelsey

GXXC systems through mutations potency against that in With classical detail, that vitro the different next you dosing And deck the in and and RMC-XXXX, mutant it patients in wild-type the is is dosing now, completely might RMC-XXXX mean, at utility which there more how some is of as paradigm, activity models I possibility is The part Yes. sort have has regards in against RAS our RMC-XXXX. year. of the inhibition deploy all restricted entirely RAS. RMC-XXXX today. RMC-XXXX It's the inhibition of tolerated other the of of who dosing not we measured would the early between profound have in to not quite seeing RMC-XXXX in context still It with terribly in in is other clear how is we'll as antitumor that mutations its mutation. profound you GXXC Mark GXXC into us to of slide GXX activity of are that that go as RAS. a It possible in we stage the show harboring the or well to mutations indeed a due said, the mutations. preclinical schedule, And right to antitumor bit KRAS with the develop the tumors a are we not patients opposed we some feedback will at the this which

compounds. inhibitor possible quite selective for And companion long-term And a RMC-XXXX, they're a useful RAS mutant like could to hard compare in RMC-XXXX very very inhibitor RMC-XXXX complementary is the it strategy, be fact, very so it's in RMC-XXXX. that and

be compounds -- in GXXC know, combination useful we [indiscernible]. in want all to So together. think very for well marching we see forward is complementary this I don't they we may And

Mark Goldsmith

recently, I to don't selective for that's add that Steve, And other highly And data, just to selective oral extends inhibitors mutant I today well earlier, earlier, our we with example, mentioned that, could mutant regard targets. And as with mentioned and if concept put, shared you think GXC. really GXXD to that's Steve other master of bit if really you as a on going on of mutually KRAS converging. exclusive, here, are clinical RMC-XXXX. features. coming we're toolkit, -- you of will, biology end which as could inhibitor, those have that quite behind It's And compounds special remarkable create a to is see that just they trying up we and

useful particularly greatest are for killing way, have we tumors. can features impact for together those if patients. the we'll sometimes And And put optimal the them in

Benjamin Burnett

you. thank Interesting,

Operator

at this questions the call. further conference time. Mark no back to hand the Dr. see I for Goldsmith concludes As That now question-and-answer the final for I'll session comments.

Mark Goldsmith

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

Operator

today's concludes conference you This joining. call. for Thank

disconnect. now Stay may safe. You

Revolution Medicines (RVMD) 11 Nov 212021 Q3 Earnings call transcript