RVMD - Earnings call transcript Q2 2021 | Revolution Medicines, Inc.

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Operator

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

Following management's prepared remarks we will have a question-and-answer session. [Operator Instructions] I would now like to hand the conference over to Peg Horn, Revolution's Chief Operating Officer for opening remarks. Peg, you may begin.

Peg Horn

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

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

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

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

Dr. Mark Goldsmith

an cancers. a to for Treatment we investors forward our Amgen’s cancer we KRAS-GXXC treatments basis. reinforcing RAS-addicted cohesive our call. and our approval host Likewise, Q&A is can first targeted This regular our asset and look of first this connect the earnings combination Revolution rational, milestone call, reached Welcome for QX remarks RAS-addicted you, After medicine and good portfolio and belief Medicines mutation, for with exteprogress carrying to session. lung or today, a a the patients beneficial cancers afternoon. that Thank Revolution innovative making Medicines' opportunity with will at important R&D on QX Company's drive earnings prepared with having sotorasib. continued FDA the Lumakras mechanism-based in to

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there's of an on benefit targeted increase first-generation the of Slide opportunities. key believe colorectal and cancer reported drug (ON) durability clinical suggested For ongoing this rates KRAS-GXXC lung and/or response KRAS-GXXC some positive opportunity so outcomes both continue summarizing as and inhibitor table clinical show in areas to X, to that cancer, with we by particular, far

we reported resistance mutations potential Also our with first-in-class needs XXXX, several among tri-complex shown xenograft we of previously, described mind, the map for tumors in failure. KRAS-GXXC with summarized KRAS-GXXC our compelling inhibitor. are uniform we inhibitors Slide key on and pathway of with more critical a With combat for to had the QX, cancer these KRAS-GXXC inhibitor the pursuing clinical selective in candidate, development are exhibiting various EGF has the mutations. introduced in RAS(OFF) new generation were effects and and/or part In unmet newly or of inhibitor inhibitors. additional RAS(ON) a in KRAS-GXXC for potent earlier paradigm Standing QX of RMC-XXXX examples growing inhibitor. of established to emergent provide consistent with approaches XX% adagrasib QX, reported patients previously of of RAS (ON) as compared mutations for advanced development receptor body evidence profile These road treatment is examples best-in-class oral treatment strategy in XX. mechanisms antitumor to RAS sustained from these of a the models experiments generational targeted that A deeper element successful first-generation RMC-XXXX, more

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Dr. Steve Kelsey

the inhibitors. the evaluation continued include inhibitor the RAS potential clinical on favorably date, of Mark. dosing less features with including responses, far. tumor monotherapy meeting, you, partial inhibitor detected compares is different showed and data paradigm frequency of innovative tumor and RMC-XXXX immune tumors, our SHPX complete its absence competitors benefits evidence an cardiac RAS studies so patients QX oncogene the in In monotherapy intermittent strategy In tolerability, with combination an Thank activity reduction set stage clinical focus another response, presented by annual clinical patients. program, from with observed favorable escalation of to that Novartis work, Notable our the best output with treated clinical in for SHPX prominent microenvironment and liver DNA samples dosing ASCO circulating a in use well schedule toxicities and of driver of to in of mutant for of tumor modulation activity of program and samples encouraging response dose-limiting TNOXXX up and a clinical first optimize RMC-XXXX, dose observed

the groups, using with but of the patient for exhibited cancer mutation including evaluation treated mutant earliest to inhibitor work pathway. almost patients reduction. our believe plus a with class-leading schedule felt We were of the studies we In cascade clinical and response merited non-small SHPX MEK group inhibitor gene able several combinations Preclinical signal clinical for we combinatorial two has of partial the we with signaling efficacy potential provide to RAS to RMC-XXXX, that were group RASP study, serious and modest absence our update combination RMC-XXXX of patients RAS colorectal a EGFR. RAS dosing we needs. RAS. potential and thereby, one inhibitors of II companion to subjects. in observed the ourselves, begin context available targets today, we lung recommended a inhibitors RMC-XXXX-XX with an have that antitumor class-leading for ship RAS, mutation Phase We tolerability and continue have a or for The suppresses cobimetinib were which to with direct XX for a undoubtedly KRAS-GXXV most And in other were be last evaluable inhibitor. fall. a an In unmet with testing will RAS the inhibitors cell top the the on to the a approach, RMC-XXXX from by confirmed bottom combination, approach that volume with Clamp efficacy. had RAS of to amplification subjects inhibitor, suggested of which signaling XX% this of tumor described evaluable were try cancer, of downstream which the was first both. and upstream MEK cobimetinib, acceptable Pathway the In XX mutants, combining cascade suppresses RAS of tumor the the

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had And clinical of we second a long-term felt receptotizing of agents the previously the for by that we the inhibitor, dose the inhibitor pathway of last eventually including We was Our the best-in-class suppress be try RMC-XXXX communicated upon EGFR side inhibitors. may intolerability potential resistance the study. approach evaluation. reported osimertinib merited to mechanisms to the combination treatment. antitumor these supported not were MEK in with Preclinical effects work two quarter, efficacy reduce osimertinib benefit and kinase well-recognized approach, set different on clinical could indeed, that clinically, has a this enhance which precedent to quite by the RMC-XXXX-XX we confident with levels early at combined

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selective enroll toxicities. continues by the of in reason RMC-XXXX with We C colorectal subpart with advanced would inhibitor study lung RMC-XXXX other additive tumors. that CodeBreaK Amgen be to combining cancer, to cell solid believe cancer XXX compromised have and a non-small RAS no sotorasib dose-limiting

As continues, dose monotherapy daily. combination the this for Amgen evaluating quarter, in X, RMC-XXXX the at in expected daily day XXX sotorasib be second X expansion noted earlier year. by milligrams XXX achieved used escalation work weekly to of full dose A of dose half combination the RMC schedule. dose The in at on milligrams a is the target day with by

announce is We Amgen of update will with the combination continues our and strategy. RevMed a it this exploration drug productive on the be to with work, by collaboration a study. momentarily. are detailed combination study an encouraged this to RMC-XXXX-XX expansion excited also clinical of more provide today on this I

addition, collection In inhibitor other RMC-XXXX combine to from with we plan (ON) potentially as available. our compounds RMC-XXXX, inhibitor these become KRAS-GXXC RAS(ON) our and

Finally, continues, by TCD-XXXXX the study Sanofi pembrolizumab. sponsored INCXXXXplus evaluating

combination for pleased untreated We study will provide advanced RAS the to clinical of now in report today evaluated non-small the inhibitor, triplet expansion of the with PD-LX patients a an positive cohort RMC-XXXX lung are to a foundation cancer. evaluation inhibitor. previously PD-X cell future the This be could and

received cancer to of plus is a cell advanced a preclinical to sotorasib inform Regarding few II last benefit designed the CodeBreaK two Phase the the the KRAS-GXXC and from of combining to work in date, the registrational not of these XXXC RMC-XXXX trial. was inhibitor. clinical combination that study KRAS-GXXC was additional a data, lung establish global nature new intended of learnings the possible RMC-XXXX-XX study, and the over agents design years CodeBreaK informed important It since in the field as by RMC-XXXX-XX The and non-small extent written. previously study have

study SHPX outcome two has that enroll The cancer While defined subjects inhibition. will study co-mutations may to to either inhibitor XXXC non-small with by several it the KRAS affect or important XX differences. approximately RMC-XXXX-XX CodeBreaK that the cohorts are is complementary XX

that Unlike will KRAS-GXXC tumors First from will line and co-mutations approved, its United source clinical sotorasib study Amgen cohort will benefit sites States. as positive not United KEAPX supplier executing third to global have well without RevMed allow and for as approved of have the the be it us the sponsoring second is cohort the to mutations. with the partnership therapy in the a within may has and the is who co-mutations this Sanofi, enrollment restrict KRAS-GXXC study the will tumors expected major yet is enroll CodeBreaK with This with XXX, STKXX promising U.S. United will sotorasib define drug and which been now most such by better provided ex eligibility under to combination as States. States positive strategy. where outside second or

interpretation, exciting from full and clinical to we XX the For an study. XXXC the RMC-XXXX-XX study CodeBreaK We data both analysis and results. as ability results review important have and will draw

study, We the the the in to are preparing this have end to Mark. second enrolled findings launch to you, preliminary XXXX. of and we patient and to year the expect first of half be Back by

Dr. Mark Goldsmith

resistance, Today, highlighted assets Steve. additional strategic recent further RAS(ON) our advances our pipeline, addressing inhibitor remarkable assets you, RAS drivers and the visibility program advancing important several provided research development power drug stage of key addiction into discovery progress stage and Thank development. within that we in will help drug regarding into

a our continue anticipate RAS(ON) addition, continues and is both be escalation RMC-XXXX XXXX SOSX-selective to milestones. inhibitor, monotherapy end like advancing in particular. Slide half mTORCX-selective our corporate In and RAS(ON) inhibitor of filings XX track candidate pipeline, highlight year. RMC-XXXX, first IND-ready year. we the I'd several of outlines and inhibitor RMC-XXXX for later these selection dose IND our this of this development on in the third of RMC-XXXX our by in to inhibitor, to In

Anders in review later now Jack? sotorasib things further financial selection of to dosing patients results. RMC-XXXX, new a XXX in study with acid. our for I'll year, XX by For CodeBreaK with to over to our we and anticipate dose this turn Jack Amgen soda study begin

Jack Anders

We the $X.X of and Sanofi. of for investments. and agreement equivalents the entirely consists was which loss with million cash, $X.XX quarter. XXXX the quarter of $XXX during everyone. with quarter for or million the of R&D operating expenses, Mark, afternoon, $XX.X and you, the in Total quarter under expenses collaboration second good $XX.X by Revenue second were was million revenue ended million increased for Thank per our $XX.X XXXX cash Net to driven share. quarter XXXX million largely second

guidance. financial to Turning

to expect expense compensation year loss be $XXX and estimated million million, GAAP continue of full net $XX approximately includes noncash between which stock-based We million. to $XXX

and loss expect to during clinical half net turn the GAAP of as in year, the and loss Our by for second now net XXXX increase half we million, advance of back expenses first $XX And the primarily was our call with programs. we operating I'll that, driven the increases preclinical over to Mark.

Dr. Mark Goldsmith

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

prepared We a the the pipeline partners the exciting and future. many of RAS(ON) organization have concludes a by a for cancers who for transform work advance RevMed may This tireless the inhibitors and in Q&A to the unique proud today. turn the We're strong opportunity product now balance our call companion compelling set strategy, to of of to over us And session. the our patients providing families with Operator? our the treatment are and growing commitment we their the operator inhibitors, with assets patients believe RAS-addicted I'll and and for of grateful remarks RAS sheet. which to

Operator

first Goldman from Shibutani comes of the Chris Sachs. Our [Operator line question Instructions] with

Chris Shibutani

you time second preliminary starting able data line in study, And next year, context updates confidence looks a it half Phase going we lot the in progress to if looks want Obviously, here. we're sense get that of get Can as study with Phase data, help XXXX. like? what your time the planning with clinical the with of to get and for the findings I a be this you II now? I XX clinical for a to will your also, for have with sense in sotorasib, lines

Dr. Mark Goldsmith

Thanks, for Thanks Chris. Goldsmith. your asking Mark to hear This from is questions, you. good

into I'll Kelsey Steve ask There think can pieces for them you. to Maybe comment. built several tackle Steve question. that were I

Dr. Steve Kelsey

to -- logical I'll try I'll Yes. in by to Thanks, [indiscernible]. answer Chris. sequence a questions your try

XXXC complementary studies, the CodeBreaK Amgen Firstly, the referred we XX to which study.

are CodeBreaK able the the year. of very with. -- be data brief XX of will said, data to already we totality obviously, guiding to that the you're be the the in evaluated into can so of expect data, start to from II we the a use recommended of And study. And end we Phase the do a will has towards been assets The study, that we that I the the not dose be as for the is select to And first that. schedule we going XX XXXC Phase comment year. compelled do defined there which safety that, reduce the will dose data Phase than the to next because we of study the we tell other study on component What will half together. yet that can they this they are disclose when fact expansion What run [indiscernible] we when I second is can at you

Chris Shibutani

Okay. That's helpful.

that with factored studies you the for this decision? in been feel With with the what the outcome the Amgen you have the discontinued provide into have impact a preliminary us studies sense of can program, design may

Dr. Mark Goldsmith

the about you're and two the some Just studies? cobimetinib clarify, studies, talking to

Chris Shibutani

Yes. That's correct.

Dr. Mark Goldsmith

Steve I'm in to design the you combining sure not what Steve, studies, want design drugs maybe on with comment -- not can if sure but of that to, that? you what aspect the I'm there, it's clarify. choice were really of we're referring

Dr. Steve Kelsey

Yes.

more is two the One didn't that why then think see the second cobimetinib to it decision of -- what we're are making as culture we why is combination it. And the the won't at see how making encouraging or and are components -- to design we we fact I there's the the the forward. the, efficacies both that question. osimertinib combination

clear about So those forward why the let's moving with two combinations. be we're not reasons

large efficacy now a compelling justify itself. here The that of forward, first there's wasn't compelling one especially is moving also component and profile but the prioritization

it where towards moving go and really include as tested what with cancers here. And think companion design we do part an fairly combining publicly RAS our have any and make. a is comprehensively of is to have, -- our the And don't with cancers respect. to we in which do the we we respected presentations. very that's is with fault been inhibitors hypothesis of we have the that mechanism RAS-addicted in think I about important is studies. We place We as with conclusive can we the data RMC-XXXX the best the that much is cobimetinib. as patients others consideration therapies It's think data least that opinion, far as there inhibitor at

hypothesis, of, do pancreatic in aware study are slight we'll that you to and be as we represents the decision cancer. to as the are a we And compelling combination As on making cell outcome Institute with still and a reasons, confidently. could. from But in interested experiment. both experiment designed are Netherlands that I best the a Cancer [indiscernible] supporting And variation the think for strategically then much we we in the see

Dr. Mark Goldsmith

could I if the And here. you're if can I get question Chris, add see that, just raising to just to to that

that shortly, you pursuing. of patients, of did positive KRAS-GXXB And but not the We RAS upstream inhibitors disfavor. appears we forward have inhibiting is the different There's to very that we planting a a just benefit. which it in justify cancer modest I as driver coming And pathway downstream. know. and actually now one to trying And goes variants to is sufficient -- the think our see some indirect inhibiting benefit. strategy, view it's furthermore, direct that back approach, PR, deliver not by many

with companion inhibitors. RAS makes is companion combine more to be will we that combine RAS inhibitors to inhibitor inhibitors indicate And all, sense call us combined it -- to with them much that inhibitor. so after the RAS RAS a to direct -- RAS And

think makes design serious was There feature to existing need there's and is compounds. but hypothesis seemed about. satisfied clinical that be you're I So a The that's that maybe the reasonable. asking couldn't any data it. by support all sense, unmet

strategy inhibitor So are a will -- involves or we through tested inhibitors. direct we don't read positive But a it. bit that those plus a it results companion be to think RAS a

getting that's really you're point to. that the think I maybe key

Operator

comes Frahm Next the from of question line Cowen. with Marc

Marc Frahm

why are is that -- have into run waiting of the discussed, brief be is than recommended Amgen? day keeping that trial kind related but running And going built then is everything dose formal X? XXX break trial, Maybe on code and X, going with you Phase milligrams that all RevMed-sponsored trial, move just in? right II Or day safety exploration with some structure selection to to just XX first start the within dose run rather a for you the on collaboration to a now within that that contained at the of that

Dr. Mark Goldsmith

I Marc. those appreciate questions. Thanks, Yes.

second we the I'm a crack can at which comment you answer do is and now. if think can take one and second I Steve, first why one going it then to the question, the on why, wants, he

learned on that this the I ongoing questions. of design. the we with an CodeBreaK cancer we've And study. didn't It co-mutations do as study years a is really is answers that it's there's with important CodeBreaK here the to know more builds now And specifically that think that to. overlap is XXXC advanced but a over posing things the CodeBreaK And designed. exploratory when emphasize couple also we the to think question we in that. feel get alluded was this There to urgent we're lung Steve to part that the it's study last to information the has of to to opposed patients some go XXXC, sufficient after

repos Steve, want on you as to you can like. you to with can So answer as you of getting do but quickly move comment makes and there we cancer. the in whatever possible think to as will a on give there, comment to that, the advantage will overlap regard be it it first just sense possible the little question, and time us bit as forward -- of lung

Dr. Steve Kelsey

know second part think we the milligrams you regards combination X, CodeBreaK day the we day We I the with exploration. dose base. at full happily we publicly exploration beginning, X. XXX we address of know answered with X I a to or dose disclosed XXXC basically -- RMC-XXXX day dose have the I and to think XXX milligrams two mean, regard in that X, not question, with we'll really it's said, Amgen day our But it. choices, as

milligrams expect that XXX the and at -- the II what forward the dose Phase way day study just we fully of with component is of day the the move X RMC-XXXX moment. CodeBreaK So call XXXC target current at we the the timing to study the X, with

study. to build obliged are We into run our short safety

target surprised but So up revisit an and with detail, but I operational we it's we'll of more dose real don't of dose it, [indiscernible]. in end don't go exploration. would then combination reason it is if sort a be And do back we

Marc Frahm

what spillover that you just think kind Okay. That's the acceptable how And picture then a bigger helpful. the totality of of RAS wild-type about level inhibition learned to you makes of kind designing today, much kind want use their effect combination? about updates and the question, profile of have of kind very to maybe or or the the of that's kind given allowed how targeted in are have you multi-RAS allowed either in ones them move ultimately acceptable on when to inhibitor your of multi-RAS before

Dr. Mark Goldsmith

Thanks, Marc.

also to we about us just me Amgen just it complement to me timing. this of just study. extension with important XXXC view Sanofi. discussion collaborating something Let XX current study, does It expansion CodeBreaK is mention. as the add of an on to previous They as do, that occurs as to that is

of together it. So no that so a we based And Steve to we're to on close as that, on that not And with finalization wait. reason three those getting no have companies reason green concept. there's there's to proceed all said,

of continuous regimen, have they're designed deeply enough, into covered know. way confidence if intermittent which advantage able to as because a long cells, have a take coverage. what this, a is constraint tolerability of lot Now inhibition again, take you normal and learned we do tumor about we its There's tissues. on tip its effect they to just as but We with enough that at the has SHPX crack action still a maybe dosing nothing in regard don't in we to of cells already require being I'll tumor selective which apitosis

a tumor that sort so And X that responses versus cells. have And we limit we're trying that. milligrams is day objective manipulating to XXX seen cells create of a in dosing normal But with to regimen. a thereabouts to X, pharmacologic there's regimen. probably limit And or day way

grafts But agent into we're as So GXXC also landscape at it's the in having compound are and benefit terms there others achieve not clearly are when and kind agents. account regimen. play you specific selective can now so will sure in a our targeted approved when that coming, to we have those with is with to doing active -- take are very that of we're make what clinical what be of specific inhibitors that additive there

in I that think we so when dosed selective that that regard of the be to RMC-XXXX, so show regard which is quite that I we're the doubt aware And there's why think With about we're and the it, that inhibitor selective to activity. SHPX don't RAS no inhibitor, any to it that combine of clinical when multi-RAS just And inhibitor, think we do I There's that we're selective of we're whatsoever of. confident you're the inhibitors. inhibitor to RMC-XXXX, to With to raise through, will in that sort is net a we read studies ways we dose which now. still but antitumor have right -- question. fully principle is that's GXXC read aware activity, all expect inhibitor GXXC

that changes achieve I already show to that to deep learn we know, to models across And we inhibitor sure. results for SHPX dose that effects. the how That quite That's there antitumor combined and the the much changed by a can is SHPX how multiple we with that are we is achieved MEK this, continuously RAS tumors just all don't preclinical had you needed we know RAS you if pivot with also think never a to you can it or we this rate that a targets. inhibitor driver when stack, anything particularly before. as But sensitive was what inhibitor. described. the learned that of limit I alone a inhibition is possible even think

for combined inhibitor, be if not it's there are context. levels. achieve quite antagonists know, on receptor that the with in So effects. in and at inhibiting had right selective tumors one the the a tolerability so can And specifically that I even think have a profound profound mutant driver Tarceva impacts but limits EGF when there's with as you And precedent and tolerable

about feel RMC-XXXX. we very think good I So

thinking. about the same and a RAS inhibitor We with evaluate it, companion then a everything the of in RMC-XXXX strategy continue of is on going terrific but continues to combination feel our the inhibitor forefront direction. We combining

rest we RAS is that really so deploy going fully where I inhibitor. And get the think study the prepare to the of example first we forward XX the as

Operator

of Guggenheim. Our the next question from comes Schmidt line with Michael

Michael Schmidt

nice I Phase one to I regarding the you're combination forward had the RMC-XXXX. moving that here KEYTRUDA see with guess, II. with

how you speak by question into study we rationale efficacy And mechanistic to registration this patients First decision safety if driven longer-term potential for what's initial is, a a path been PD-LX clinical combination? in II positive Phase to and then by perhaps and this predominantly could move or should also data? about think

Dr. Mark Goldsmith

Thanks, Michael.

address work disclose preamble, Preamble of and need you about I is give then escalation Let Steve, Sanofi that sponsor quick of think anything the they're question. your the did, the just dose a can't me study. really can that we

they dispose So when will. decide they to it

to be is speak and treatment, can now can't really purpose drove it. Steve maybe escalation that. move point question we lung an what's that was your the what was So PD-LX But dose exciting out, primarily as worded as that it. tested carefully and particularly which the a it address tolerability study about in intended untreated you going first-line But or efficacy to cancer previously of so is, safety positive and patients,

Dr. Steve Kelsey

Sure.

inhibitors think checkpoint first study where to place. the cancer, above really SHPX a way, drugs the the include in which, to explain used. rationale study Rasputin that have context that by cell the cancer, PD-LX it two positive does alone end huge just may behind represents if are PD-X of the ages large other inhibitor in toxicity. will pembrolizumab with of leaves then it And think I over improve obviously, a cancer, we in obviously adding because lot when helps think that outcomes us at One are I we it not the lung significantly in explain inhibitors But opportunity, without positive the that cell we lung a the there [indiscernible] are very turns tumors -- out of non-small non-small number lung another limited opportunities. there is, that

lung that The And second inherits checkpoint the primary -- about care primary we [indiscernible] the with absolute is or inhibitor, standard a GRC a RAS foresee other we cancer. is probably replaced for a a directed our RAS said it's our of perspective, plus other driver lung doing combination for like fact state for chemotherapy do when future of where one mutant the RMC-XXXX from is in a inhibitors this companion inhibitor RAS whether mutations combination a by of cancer inhibitor then pembrolizumab.

looks we have us requires declared primary that profile demonstrate is into a that well. base to eventually, we the is dominant clear to is intent is regulate each back enough moving again, that -- tolerable. moment that the All of right one basis that at move a schedule encouraging triplet the acceptable mechanistic will RM going testing. paper to the this component study. component it study, which that's it Now And of each is roles as and of recommended Unfortunately, fact, then is in checkpoint what to profile [indiscernible] And expansion us become in signaling. tolerancy want very perfectly those of for a forward like. to very say the II Phase will learn. efficacy And of XXXX, can to SHPX clearly There published by beginning, back back that shown very you

so of rationale effects inhibition. the a huge SHPX augmenting And for checkpoint inhibitor there's

should and than a effect patients hindrance. DNA also that to have in be adaptimmune preclinical rather ship in beneficial it we be both should an to both the demonstrated subsequently and system, in helpful way should inhibition be, We antitumor

a PD when study. compelling of And our demonstrated that and do inhibitor very oral care new to of lung a so it mechanistic is inhibition us the I place compound our in rash the the opportunity you the fact proves from standard as cancer, basis the checkpoint studies trials for cancer clinical think SHPX for

Michael Schmidt

it. Got

Amgen's on Okay. also And study get just adagrasib, then to with on decision to your -- recent wanted sotorasib actually. thoughts

to evaluate curious thoughts perhaps with plans any on conversely XXXX Just KRAS inhibitor? that to give have and

Dr. Mark Goldsmith

Yes.

that SHPX have I it target think as co-target high the a for and it is us, to continues along driver. in as the Amgen with interest main suggests a RAS thing mutant a using driver

leading signal SHPX positive It they or that's So at specifically inhibitor. to TNO-XXX I I is obviously a as to a all. chose think else, why very that couldn't speak something

And RMC-XXXX it. course, support -- he So there's to it it read it the is but XXXC and also to knew and data have they've They study about couldn't that into just may to be CodeBreaK as line, excited interpretation but say about franchise, an it as of couldn't that they're that, simple that you but indicated that. the whatever makes announce, we important reiterate the of Lumicast building think XX about were they but which sort of it's my comments, that are to is target. to research What I'll make now which finish publicly, then. sure can particular about want concerns to they are speak has rapidly no that they then, access continue

else to when So on I sorts everybody if don't dance everybody RMC-XXXX anything, the music it. would we asked. inhibitors companion these there's all the to know increase be positively until answers, we've think is at until And negatively advance reads it all comes on over suggested of that with always it

try so everybody that. perfect to that, makes doing And rational switch and different sense suspect been I a doing And We'll partners. That drug continue that. development. do are we'll approach we've around to going people in

Operator

comes Our next Chang line SVB the question of Jonathan Leerink. from with

is line open. Your

Faisal Khurshid

This is Chang. Faisal for on Khurshid Jonathan

the was Or the there a played that priorities? asset the of in simply decision? guess are other of that is RMC-XXXX, filing? potential for would into a molecule I like or any delay kind For sort related clarification, IND a SOS-X And the of this an then be itself question, potential features a is out-licensing considered this it just

Dr. Mark Goldsmith

of don't Thanks Yes. the I question. molecule your that affecting features that position. are specific think are that there for

a We primarily into behind compounds one that next least moving more We're two the I the several said already year. it's have decision. in in think compounds another We coming clinic. that. two at prioritization clinic there's

got months, quite we've over next And entering is and space So RMC-XXXX very large crowd a full. our at RMC-XXXX the of hands space. entering a XX is

of significant So to those programs. be the big program, resources. XX are is just commitment going pretty we announced which a And

a if I part do would would integrated have point since right out-licensing, quality RAS-driven evaluate for continue do. we really of good that the So why any But I -- and when, we'll And and think question. forward we'll that's tumors of it's moving timing anticipate what's that what timing think will sort evaluating I'm we I don't of a the to overall and on approach. sure It's the we of part our SOS-X but approach is an not it's spear, not inhibitor that integrated more having approach.

Operator

of comes Joseph question final Our line with Eric from the JPMorgan.

Eric Joseph

perhaps might a thus the on sense objective follow-up of of I'm in something opposed I a far CodeBreaK combination you've and study, sort to higher table? the on on of seen bit maybe that the the is be that decision to guess, was or colorectal And anything in XXX? responses rationale unmet based potential curious there. still to colorectal the strategic the this get lack of given cancer relatively a need pursue Just cancer as XX a lung

Dr. Mark Goldsmith

question. your Thanks for

think, comments on some to that. I got you've Steve, make

Dr. Steve Kelsey

Yes.

it's extent, on One The data think, reason cell twofold. cancer, colorectal then for mechanisms Let's is [indiscernible] the by AACR lung first. were we table. which inhibitors. of start [indiscernible] was I bit by with escape really a swayed is at cancer the that KRAS-GXXC the to and on non-small focusing Absolutely, some presented from published

you the inhibitor potentially KRAS-GXXC lung on data, of a in great effects cancer. the effect potential announces into is I or aggregate resistance inhibitor if that at for the SHPX look the (OFF) think meaningfully some

difference to other. Secondly, to enough that's is you're maybe living it we little you're actually know the mix higher, a easier rather oddly rate single-agent objective response comparing in bit makes and detect a if

good But our future, and right sure we focus the be absolutely at got XX we've that single to attention Thirdly, the for some well. every there's wanted will in as combination about reason I very there's So think think answer. on potential disease and a we doing expectation doesn't case absolutely, make a anything say it point I negative the

Dr. Mark Goldsmith

low Yes. histotypes Eric, also out suddenly CodeBreaK if that. and continue I information we're at to continues so the formal actually an And the part looking of it But the exploratory deep or did that, of when going add quite unresponsive could to get of regressions. was an to I'd line in is alone. relatively to combined study response highlight multiple we XXXC developed that that the show with cancers a inhibitor SHPX presentation, example tumor RMC-XXXX colorectal

is course, cell point, of at sort non-small still cancer. And and things time, so well. in But break other you multi-tumor the now approval we're [indiscernible], quite for first one down I the committed approach this of think broad with at start lung of as off a and delving

other we're a an But the a Steve if said, we So start. opportunities. as improved make no are looking for that regimen place can excluding on build we difference. to treatment where be means, would And place by

Eric Joseph

Okay.

third between the deciding RAS(ON) GXXD looks Okay. targets and GXXC. -- Great. like And sorry, you're naming with between it portfolio, respect candidate to two a in development RAS

between coming remains next be over for get development, Just you preclinical their multiple so? development or And should I kind the we apart nominate are in of about of which sort to of sense curious deciding that year the guess how compounds, here? far guess, I thinking a your in to candidates think these being named

Dr. Mark Goldsmith

the to Yes. with decision question of forward. teams back I into whether bunch together. with forward put moving to package, best of strategic they've complex consider we're too when package which much when the look to forth wouldn't at that other it. each a got read package We And the basically a it one got have about we'll sort they've the and competing move to

is down one mean fast teams can. they if as we slow moving other not it's everybody team and to speed to as ask as I up. So

we'll GXXB be late and those for optimization just be didn't up principally, We table, or disclosed select there explicitly GXXC on options choosing decision. but could candidate that we are development we've too. this coming to also between said that lead that in next say a other are the expect two We

gets out too continuing as not I'm to moving comes point And the looking at get So can. are programs the our we're their -- into named one, that, If these through. in the other as target other whatever wouldn't thereafter, and that after forward I work as read we too far some much swiftly one of doesn't, are programs well we'll sure along way named. one unnamed

Operator

are questions no there more to Dr. the call As over closing in back turn Goldsmith the will Mark his remarks. I for queue,

Dr. Mark Goldsmith

operator, and everyone for continued participated Medicines. today you you, who just thank participating for analysts your our Thank to support of Revolution and Q&A in to the and

Operator

Thank gentlemen, your participation. you concludes this call. and Ladies today's conference for

now may You disconnect.

Revolution Medicines (RVMD) 12 Aug 212021 Q2 Earnings call transcript