NKTR - Earnings call transcript Q2 2024

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Operator

Good day, and thank you for standing by. Welcome to the Nektar Therapeutics Second Quarter 2024 Financial Results Conference Call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions] Please be advised that today's conference is being recorded. to Wu. conference like speaker to now Vivian today, would hand over the your I ahead. go Please

Vivian Wu

subject Thank including therapeutic make you, call of good Chief today's the Dr. Officer; today. our Crystal, call, On our Dr. and and of collaboration Jonathan The plans With plans Chief statements that timing joining you the President Officer; forward-looking Because studies of the which and and and future, clinical formation, or Research future regarding development for us future drug us Zalevsky, many success for candidates, Mary financial predict, our programs. of our on guidance and statements Executive business. are initiation are uncertainties availability regarding Tagliaferri, Officer. data the the Chief plans of clinical future outside other are our Medical Chief the and the relate of candidates to for Robin, timing certain difficult Financial Sandra to to development afternoon, Howard Officer; statements everyone. Development control. forward-looking presentations, our and future statements and they clinical and data business, expect potential the agreements, are of Gardiner, to regarding our for for drug we research risks Thank

the website are webcast set of available of whether over future no call XX, our undertake may materially May to President Howard? forward-looking developments result on at be update CEO, nektar.com. Important I in to differ that and this and our a from forth of said, Nektar's With the hand results Robin. to like will any We actual IR would new or Howard uncertainties XX-Q otherwise. call available information, A page at of statements. obligation sec.gov. Our is as filed statements, that these Form which XXXX, on these was risks

Howard W. Robin

in Ib with goal potential a advancements include REZPEG designed differentiated can lead clinically from publications focused in has data most Vivian, of paper generated its moment, balance in a most this disorders inflammatory promising for progress ectopic on remains joining dermatitis and functional Enrollment and in its XXX us approximately skin-related and we disease disorders. pathways We've atopic or atopic common dermatitis, simultaneously throughout I'm study today. T-reg is dermatitis is kind novel the studies you, which disorders. These promising that of supports atopic is made biomarker for a and upcoming the conducting both which pathway advancing the naive The September, and an which REZPEG which diagnosed and the efficacy In treatment Phase enrolling and highly psoriasis. to become the have inflammatory immunology for U.S., response dermatitis, Conference studies in by studies the thank atopic data is with immune to best-in-class REZPEG's quarter, data, analyses treatment focused Communications REZPEG. and Thank skin chronic to sites this the also to severe moderate the immune investigator track. and inflammatory highly you and which specifically proliferating areata. illustrate topical we extensive is clinical engaging presentation our our all on study in on dysregulation will building but Europe enrolling options. immune failed in to advanced dysregulation in continue activation regulatory inflammatory accepted system EADV good both route towards Ib T-cells, of feature REZPEG nicely dermatitis REZPEG Phase dampen Nature multiple XXX and inflammation. Nektar agent and is pathways REZPEG program restore marked directly biologic proud autoreactive about designed of by significant Patients are These a is are in autoimmune quarter the make at have in the at traditionally once. second and dermatitis let Rezpegaldesleukin is by to first-in-class patients patients atopic mechanism. our expanding immune-driven program, excessive Phase I'll a is announce more Canada, dysfunction, Australia. address talk cells antagonists. that this of are on multiple IIb JZ T-cells. act alopecia an and signal targeting with immunoregulatory pipeline

studied Importantly, induction design And study readout population on enrollment call. the talk study this of about Ib for Phase is patient as will later top XX-week treatment the stated, the the is data just more study's I from JZ in dosing track in in new line X be the identical REZPEG. will weeks need early the every Data available the to treat of every unmet and half the mechanisms first of maintenance There's looks end dermatitis. XXXX from and weeks distinctive maintenance for which 'XX. stage, atopic at high XX towards a XXXX. stage

goals. U.S., at biologics growing this actually and our of clinical now is driven diagnosed new the mechanisms atopic being XX And key combination of am are We a believe estimated of a and, REZPEG today high patients disease. for Phase are market studies to half XXXX extent dermatitis, conducted I of treatment breadth hard EADV course, and approximately recruitment, novel patients need living compelling and there treatment. proud million that people the unmet medical presented achieving these that are that right data patient work could under we're receiving believe XX% for there's and our that are by the that options. Ib of team. In the the With it's with We competition moderate-to-severe the with who receive enrollment this of

treatment differentiated So for we these highly patients. poised are excited to potential a that emerge REZPEG is as

enrolling alopecia areata. Phase with know, for that this Now Enrollment have as a is study this patients the enrollment for and on track you in March study. second we REZPEG opened XX remains for II also study

data for the line have Therefore, a middle safety quality there's therapies top people million relapse this alone JAK the the the atopic trial high disease. X devastating are available an estimated patients U.S. significantly from to to months inhibitor not study the need new forward XXXX, in currently significant urgent therapies. people unmet looking following Phase dermatitis. few from We believe in affects durable, areata. a readout This life for potential are alopecia risks. there's II carry is will disorder or this line with which We and to in significant be top of for the have of REZPEG and help rates these develop medical Nearly

to that unique continue novel In we to monomeric our that immunoregulatory NKTR-XXXX antibody On reported advance a the on EULAR. NKTR-XXXX, activity June, their TNFRX These function. the first is binds preclinical data preclinical at program. enhance program we agonist antibody this show Tregs data side, selectively on TNFRX with to

XXXX. of IFD lupus the conducting diseases the NKTR-XXXX goal potentially diseases, first-in-class importance of for TNFR colitis, an such submission treatment We're IND-enabling for autoimmune Vitiligo. sclerosis, in receptor certain ulcerative of currently studies autoimmune multiple X and with Given the could as middle preparing in a become

IL-XX an update give Next, oncology. I'd in our on to NKTR-XXX, like you program

know, or in later lymphoma be will you LBCL discussing the and in this Mary is As Nektar B-cell completing call. study large a

completing Bladder there lung study NKTR-XXX in clinical funded collaborators, to and in Merck In we're addition clinical LBCL, cell studies the and Abel are by being cancer. Zeta for our ongoing KGA Cancer non-small

to data Cancer Fred an and also the Journal recently Hutchinson published reported ongoing Hematology, Center that survival study in IST the Stanford. the showed of at that IST NKTR-XXX a investigational and have and has of therapy alone. shortly. at We their peer their historical controls American their months with at investigational from was print CDXXXX Society online will combined IST manuscript XX The recently doubling recurrence-free concluded data been Stanford therapy Stanford CAR-T University with Blood. review when posted an be of compared

combination to will these with more of addition discuss other the NKTR-XXX for support therapies. cell and Mary the on studies, data strength the In to studies

the partnership believe for program. can of this an component in we cancer, year, become and that we opportunities As cell therapy this continue strategic evaluate emerged data NKTR-XXX important to

just than a JZ, at year's like to R&D JZ? more the hand an REZPEG's data a results. of that over to cash I discussion. XXXX, us strong a for line top call that, runway with with to third Before remains of say call cash to in financial JZ Nektar position time giving want hand I'd that I And the over extends quarter the into the

Jonathan Zalevsky

potentially address. the atopic major alopecia to program mechanism Thank REZPEG. with opportunities and you, We T-reg advanced Howard. begin both most REZPEG field. is IL-X areata that could the like dermatitis in there are believe I'd in This

long Our in or long-lasting onset data extended end potential disease us the endpoints, dermatitis and trends, durability and the of These the dosing Phase of encouraging in dermatitis. the maintenance control of effect, after we responses Ib have rivals completed rapid in physician-assessed both type of same REZPEG frequent dose-dependent after and for XX-week period. enthusiastic data that dependence and inhibitors. rapid outperform atopic Infact durability control. very with The action onset induction the about JAK and demonstrated patients observed patient-reported of atopic long and dose or for dupilumab promising dosing efficacy outcome REZPEG observed KOLs

The the IIb that in patients during This designed original REZPEG enrolling roughly XX-week maintenance program and placebo, of in will to at number following or on trial be XXX in will, of into meet to regimen. long-term treatment extended amended increase a with maintenance registration, Our threshold robustness over strengthen versus once our induction work we but treatment dose best different protocol Phase patients XX of maintenance our After total, rerandomized the will X the a disease originally their duration in once atopic support study. Phase X of now provide evaluated a extend safety period. weeks level setting as study. registrational period, have maintenance level of time from for with study analysis this receive the is of our to To on was patients set regimens we've portion of in recently study. period, the IIb study which this advance XX-week the to regimens to X-month dermatitis every dose a position a that data patients treatment the induction induction X either to for that exposure II month this weeks, XX portion Phase this

treatment also in treatment. be patients We of order the after potential the XX-week extended the upon effect X-year REZPEG to remitted evaluate a follow-up of in the of to period allow year begins us conclusion off-treatment to X period that

XXXX of anticipate we line half still the XX-week this Phase data and of study the from XXXX be of the from stated, the period data period will the Howard of early in study induction available or As top maintenance towards XX-week end IIb XXXX. first

which localized normal is Now the in rationale patient's believe is attacks the follicle, the disease strong In to underlying of leading disrupting follicles. of for keep T-regs to of areata, and hair, follicles hair disease, to hair there this in turning We the disease. immune grow REZPEG dermal on alopecia its hair hair immune based a role indication Normal state to loss. privilege. system this on this exist a pathology ability

our available stem cells is infiltration life MHC So components is to in as alopecia In immune areata, well this treating needed dermal the functioning restore strategy for that of to know shown essential are weeks therapeutic for of studies, other and diseases. of human of REZPEG targeting T-reg or the and for grow severe through that and novel privilege the and Phase loss the treatment potentially can restoring treated to samples, maintaining game-changing continuously span. immune other complete need alopecia could to and T-regs leads immune immunopathology, unmet skin the population immune all durable in inside patients durable preclinical consequently, expression very high are during alopecia immune vitro a published no In to providing privilege randomized pathway this to JAK REZPEG maintain areata. period recruit tolerable We potential novel of cells, hair total. breakdown observed in to we inhibitors rescue and XX disease. baldness. is a with essentially T-reg and and mechanism And both is immune currently poised is disease speaking, IIb broad and believe the for central there to plans and implanted The areata privilege alopecia options that biologic patient diversity this believe the opportunity to in an system follicle. immune provide REZPEG there provide. And will for system but the treatment There Patients system, of in like placebo. inflammation, people we hair and of up therefore, there be of Biologically follicle, control. hair a minimal uniquely responses exclusion treatments be study the is become weeks therapy for long-lived hair severe a mice this have will words, underway REZPEG, eventually no with with disease XX its XX in and address a R cannot as healthy, studies well

XX. percent in mean salt primary severity for alopecia week tool of the or study Our at the improvement endpoint is

varying of the a that of in improvement were have number salt other looking score. be to endpoints, including portion secondary also observed patients will degrees We of at

patients underway top the data data few study. and a middle top study line We line our expect we this near from enrolling of are months well atopic the into dermatitis XXXX, readout with following

and critical we've T-reg secondary TNFRX especially Now in receptor member B shown neuronal cells, signaling and with compartment. and JAK-STAT REZPEG to turning that effects. is controls also the superfamily is expressed REZPEG. T-regs, and T-reg cells proliferation show drives Thus, to TNFRX other excited and which expressed rationale function critical to and T-regs most why on in years potentiate in primary T-regs, pathway gained In and of lymphoid which of agonist NKTR-XXXX. non-lymphoid NF-kB, built agonist especially key activator TNFRX to drive on tissue the lymphoid linear programs, T-reg, protein highly is tissue provides pipeline TNFRX experience non-lymphoid of this Genetic contrast, associated as that from is function, for T-reg non-lymphoid signaling TNF is effect T-reg conditions is TNS-RX so function. immunoregulatory studying Nektar's we been is our has many presence antibody. function, studies loss resemble its protection phenotypic TNFRX that cells, the FOX-PX agonism T-regs, is of function is agonist the well suppressor function effector agonist if of as and the in about and target an expression both been maintenance program myeloid and suppressive regulatory The and its FOX-PX abundant organs. IL-X organs. the In [indiscernible]. stability, activation REZPEG maintain TNFRX upon absent with has are NKTR-XXXX, autoimmunity

first the and at June presentation, In data are As Howard mentioned, discovered presented we novel demonstrated the for that and this properties the antibodies several preclinical of we this program innovative of we year. developing. EULAR in

T-reg. very human drove need high And or or effects antibody also specificity T-reg. demonstrated TNFRX of without cytokine PX in signaling ligation, This is binding the property. With conventional they De the Novo is drove and regular and novelty demonstration a single-arm binding TNFRX TNFRX discovered T-reg K a are to T Firstly, in from We CDX that antibody. through and antibody antibot. these single a and agent we no NKTR-XXXX grasped these TNFRX as NKTRO-XXX monovalent agonistic mitogen importantly, to AI-based cells consequently, these TNFRX agonist a bivalent this markers effect through And as for cell proliferation, that binding activation cells a design. primary provide for and and monocytes. able very signaling format to support. the receptor FOX of little signaling on came signal co-stimulation, example other novel upregulation antibodies NKTR-XXXX and of multimeric One for novel

model selective We a knock of NKTR-XXXX also stream. human in knock-in in same in the confirm demonstrated use and the a TNFRX profile antibody mouse that and also to the studied mouse T-reg PK/PD established mouse in KLH-DTH of model TNFRX efficacy single-agent

were of NKTR-XXXX antibodies rapidly discovered, the We the are differentiated profile and the clinic. very excited that we are and unique into with advancing

with could GI ulcerative initiate as diseases expect selective such dermal interest middle the first-in-human include continue studies the oral open And of IND-enabling Vitiligo. sclerosis, even diseases, and move immunology and XXXX. conditions, in lupus TNFRX like companies we to colitis growing the to be the autoimmune Mary call Examples NKTR-XXXX. with multiple to mucosal mucosal to We note be indications agonist a forward. to and like the as of other in for over or studies, novel our that, hand addressed We that of forward interest to working path with we have discuss will opportunity areas NKTR-XXX. Mary? And these best that I'll strategizing

Mary Tagliaferri

And program, cell believe mechanism finally, of JZ. therapies. oncology combination, potential IL-XX-based We particularly to IL-XX-based in you, action turning Thank the has our promising NKTR-XXX. with

progress. preclinical data in of cytokine cells CDXX-directed that Cameron about enhanced responses experiments of improve development strategy administration antitumor Dr. with showing our this transform lymphoma therapies durable first CAR-T XX% cellular cell of XXXX, serum While responses persistence of showing Turtle both the Kite, Hutch were higher long-term and the not apologist for in B-cell in wealth correlated lymphoma. of later a aimed after dose-dependent large CAR-T published given and cell exogenous and were importance. large CAR-T levels of eventually Fred B-cell efficacy the with Group the CAR-T receiving a completed CAR-T to roughly cell factors the AUC a NKTR-XXX cells, approved, high month Fred therapy from IL-XX IL-XX clinical were efficacy to the Hutch management lymphoma Thus, patients patients that and products the data therapy Cmax associated with initial manner. of with NCI In vivo

maintained cell into treated levels efficacy. predicted, peak suppression, mice durable higher continued and tumor NKTR-XXX translating CAR-T with cell As the combination significantly CAR-T

XX%. that to the cell XX-month to NKTR-XXX control mythoblastic cells to a published Blood lead we CDXX/XX patients could was data CAR-T to therapy adjuvant CAR-T with Advances, NKTR-XXX Hutch in Muffly in the Following Stanford's Compared of B-cell increased cell when evaluated lymphoma. in IST enhance CDXX/XX acute an proprietary the to And cohort the for B-cell Dr. to CAR-T Dr. conviction cells leukemia. cell Crystal for Turtle's NKTR-XXX, also results added re-expansion therapy, and month. proprietary Mackall rate from in strong last group Fred enhance complete treated CAR-T published improve RFS been previously evaluate to response the Lory cohort XX.X months. NKTR-XXX treated the began an for Stanford's to when Stanford's NKTR-XXX treatment of relapse-free dosed Dr. shared large all Blood therapy, survival efficacy only with cell as to the CAR-T was efficacy. reached The cell the XX% over has with of follow-up. X.X CAR-T CAR-T median not with and it months patients

B-cell with of So large influences and we cells We've trafficking they're why CAR-T in work? patients in CAR-T saw observation we confirmed administration. NKTR-XXX that disease re-expansion additional re-expansion NKTR-XXX to NKTR-XXX BAVENCIO does NKTR-XXX the a CAR-T AUC. following Fred from increase NKTR-XXX tissues. combining the pre-clinically. cells the suggests confirmed Stanford At to Stanford study, Hutch, as re-expansion of we cells lymphoma, well, CNS with have following peak patients in In in now observed the where second leading that also the of NKTR-XXX after An lymphocyte

enrolled is NKTR-XXX own been lymphoma. running after trial large where with patients administered therapy. our study, CDXX XX As CAR-T autologous cell In this we've we've you know, B-cell

randomized treatment phenomenon study, data treatment future at We a trial, our compounding the the look concluding of same extend are observed meeting. forward presenting This beyond these third of has a patients, this cells we in medical full have we CAR-T potential set from study to NKTR-XXX CAR-T therapies. following in now re-expansion to the in effect the and and patients cell

with not respond with clinical collaborate AbelZeta, advanced with combination in non-small to I or do in lymphocytes to therapy their Phase an trial company leading continue cell cancer We therapy. a patients NKTR-XXX evaluate tumor-infiltrating to ongoing cell who lung TILs anti-PD-X in

in JAVELIN projecting II are combination conducting year. is with the we work Medley the PFS the BAVENCIO. first study this Phase this who to around analysis is potential KGaA, study, is Bladder Merck continuing which Lastly, end with from evaluating Merck of NKTR-XXX

for evaluated Sandra? separate review the X compared As with over call that, there a reminder, monotherapy study, our to being And combinations guidance. I each a separately BAVENCIO financial turn this to in the of will arm. are being Sandra

Sandra Gardiner

Thank afternoon, sheet. with good debt quarter ended and We with in you, everyone. balance Mary, second $XXX.X investments and cash the no million our on

Our financial investments. million end still we million plan with and XXXX position remains $XXX $XXX in to and cash to strong,

take XXXX. Our milestones, extends and financial quarterly of I'll third through Phase study. for briefly reiterate the IIb our several our key REZPEG top will data runway us review including now which quarter into line XXXX, data our guidance cash both for financials

$XX.X XXXX. was million, includes revenue for million sales. which Our for in and $XX to million the to still revenue million $XX in the our between second full product year $XX $XX expect We $XX royalties million $XX of be quarter noncash to and million million

the remaining was R&D of for and second was the of fourth the For second towards we for $XXX second we expense G&A $XXX $XX.X of full to anticipate XXXX the XXXX million year, expect to year still expense R&D the quarter. and between be million. quarter more range weighted $XX.X quarter expense heavily revenue million, the half million.

for and million. We $XX expect year expense be the full continue to between million to $XX G&A

noncash XXXX the our we estate charges to obligations Francisco real Life in and and decline markets. interest between noncash to San continuous $XX.X $XX expense estate for remains and our office is impairment million recorded expected QX, million In be real unchanged Lastly, the of million. Sciences due $XX

for and the Our loss $X.XX per quarter net million of second was XXXX basic or diluted $XX.X share. loss

on now third a with XXXX extends earlier, was million we loss into and plan loss for in open with to $X.XX $XXX Crystal? million XXXX. of $XXX that, and that I'll per the questions. share. end or the to basic non-GAAP diluted cash net million runway still quarter And call $XX.X as mentioned And charges, impairment noncash a in million $XX.X the Excluding basis I

Operator

will Instructions] Oppenheimer. Olson from you. from first come Jay question Our Thank [Operator

Jay Olson

Stanford great. with And Congrats synergy NKTR-XXX potential data with in the diseases. about steps? talk progress. autoimmune there's the on all you for collaboration That next CAR-T if Can looks for NKTR-XXX

Howard W. Robin

want to you that Jonathan, question? take

Jonathan Zalevsky

Sure. Yes.

So question. for thanks, Jay, the

durability the the to that in the really how in known really a of CAR talk of fits then, relative efficacy about Mary, as extent CNS, of So really time I after you some just I'll us the medically of a maybe of on very a some think described, CAR including study impacting CAR, that with short X with the of had published color that. observed Mary, also of the to And the was the that migration, off could study, or the and other very offset observed you by important it add a weeks was with was couple for it large the cellularity, because delivered more close that was a into studies terms to the are moving ongoing. of administration was historically effect, together positively Those into context that was amount we Jay, Mary little CNS CAR first of evaluated some of changes that patient. maybe, patient in start can and the the bit But effect. what's were that that There the course, Stanford for very disease the of right? a before time Stanford findings NKTR-XXX included adding of Group. was treated. And duration if changes exciting treatment

Mary Tagliaferri

consistent receive every treatments. It's efficacy receive now. were really right all feasible dose-limiting And we about X trials, Phase imagine, look is favorable also continue favorable that's Phase We CAR-T but that's And dose. dose. is NKTR-XXX can highly seen also excited And we the the Mary. We Jay, hone patients. you believe, to combining dose adjuvant in recommended the patients safety, at they profile have of What with the a a to X can this recommended different wanted see combination the cells, so the CAR-T I steps this III weeks, to drug to toxicity. a a which and after you're Yes. we we not aggregate and the across patients. highly with feasibility we not when to cell only drug X studies, about could as where setting in in in think III X from on studies safety when data identified have the next is go, remarkable we

in where in and the in place received IL-X. as who inpatient I as combines their IL-X Nature. know, Dr. trial very And drug, very in and of by now, small IL-X published with have therapy in right TILs Scott with setting for a Iovance high-dose to Antonia patients in mentioned, that there lung to high-dose certainly cell other developing really difficult error The in be the area deaths high-dose And the is non-small we're receive fraught therapy. high-dose study cancer, tolerate you conducted with it's because actually combination that's TIL IL-X. patients, TIL were X Patients to

of combination the it's opportunities TILs. indication the very And with compelling data well here and think with inhibitors. are again, the broad There's And awaiting area the for I and as cells we're data with inhibitor, combining in autologous allogeneic and cellular so that an therapy, the proved as additional both CAR-T to then, be checkpoint and checkpoint in strong.

Howard W. Robin

on over with And And used I may and shifted think great for cell combination role therapies. the of that, cell of data be to immune clearly, disease therapy. I very an future that's to important potential would we've demonstrates to we that, a course, it IL-XX there's in -- that that have going But to with play add inflammation. well

can we I So think we're and talking there. of collaboration companies, do to a number an find important

Jonathan Zalevsky

Jay, is And this JZ.

first saw disease. Stanford, a data Your question as totality a of CAR cell time. other pharmacodynamic also But published focused the disease about which in question. of kind both be effects Mary of It's But use. setting on a oncology in really to theoretically, based we therapy what a from it at safety as It's principles, we We're possible. autoimmune this a add this it should feasible described, question theoretical good on well and the autoimmune as would make now.

Operator

will question next Our come Goldman butane Sachs. Shaw from from Chris

Unknown Analyst

on the progress. Chris. Kevin is This Congrats for on

focus wanted there. alopecia to Just on

housekeeping, wondering which mid-XX% or the alopecia? want enrollment but proposition you about it that efficacy? the to understanding clinicaltrials.gov, safety also for is same then the value are and need I sense the the of with match just How So makes completion are primary line versus first profile. half? about JAK time in to know And to is inhibitors, there's Are on just you inhibitors track on there versus the approved, talking JAK going efficacy --

Howard W. Robin

to your want that. answer I question Mary on let

Mary Tagliaferri

of that that salt XX data, when loss the start inhibitor hair taking X weeks before treatment. share JAK there are durability I I Howard. you, go effect areata in we at hair have mid-XXXX dermatologists and And no yes, immediately and Thank rapid. track, started trials alopecia alopecia enrollment which that absolutely for endpoint we will inhibitor, to with data in March, clinical One think us. us. on great the the is into line in with And on conducted the they you efficacy what top our and and know, are is success a study based had the looks their JAK areata asked very there's areata question, inhibitors Kevin, for a stop and issues the we Yes. of And what's bar were are and as JAK patients you is main like today efficacious alopecia the lose

serious events risks areata of would really and XX% like warnings and are younger of black second, pose, inhibitor is have and the thrombosis and a knows what alopecia infections. for than box cancer that patients stroke and course, And clots kind age The XX. heart heart-related attacks of blood Obviously, are nobody JAK who serious

So there to a general is about a just for worry a life. exposing entire patient JAK their inhibitor

differentiated every could those So that a than have to matter or We've that problem phase. it time after in we establish to baricitinib, makes number with we've frequency if provide with for important. treated you period, critically on if for wouldn't JAK would like we to effects. of biologic in efficacy, for placebo, and that Phase a potential period not hair the a it which associated less similar Certainly, dose regimen these in rather a with baricitinib patients And are XXX the maintenance believe effects, association, so there's Ib an date than inhibitor, side be statements. maintenance because, a that year actually was a it efficacy their the belief even serious but we dermatitis lot a back a with induction a to doctors even grow And benefit daily these based patients their at X have Phase spoken effect terms salt And doesn't compound remit XX-week longer is with the you potentially about be nice. the believe patients we that's a trials don't side one, many see two, III remitted with weeks an XX specifically XX% atopic be then would takes induction our would say and change weeks

You studies for of approximately salt can high dose placebo size is the low, of the XX% XX% the X and run because the day dose per reduction is baricitinib, low for effect X dose milligrams. smaller milligram about

Operator

Our next Song from from Roger question Jefferies. will come

Kambiz Yazdi

your for This update with you Roger. us provide Can is Kambiz Lilly? an on on litigation

Howard W. Robin

Lilly, discussions excellent that and can still discovered. is mathematical see expect you in having error has somewhat we we Yes, the that mediation. that as to math mediation, having sure. and Ib with as continue do corrected Phase the us future. Look, near court know. The had to discussions we We're We ordered with for you Lilly. from was mistake data And compelling a clearly we're made, the data, still after

detail I believe of we can't time behavior. been harmed spend obviously, that will discuss talk-- And can't in I ongoing with lot a say But I on that their firmly we it. we by are continue -- So mediation consequently, litigation. can we've

Operator

will Blair. question from Andy next our And from come Hsieh William

Tsan-Yu Hsieh

of interpretation Nature intriguing. is controls. your curious about historical the the paper So pretty I'm

the seems heavily of be historical push patient nonrandomized nature little the the is like given bit kind a baseline there's characteristics. Just some little and It control a study, bit might pulls dosing preceded lower. regarding the of more

at populations? characterize similarities of I'm and the would are just you looking baseline how curious, just those the we So X characteristics, How like differences? kind

Howard W. Robin

you could Mary, question, give good the a into It's insight some controls? Stanford historical

Mary Tagliaferri

Yes.

patients of who and to Crystal talk that as this at the trial. used the little actually Stanford X So look are really just dosed study. bit really the Andy control cell had not one if Mackall Center a Director she's first she Founding patients, want all, person therapy, about conducted of nature the cancer I cell you importantly, of godmothers the paper, for therapy. so this is XX Crystal's for And

comparable patients be to had selected patients the baseline second with this she of matched So characteristic study. actually traits that

baseline with treating you was traits a experience academic mindful So disease. can well of imagine with ALL her She background very, characteristic as patients. vast as of these very burden her and

upon control she patients of total which very originally So the group, actually of in selected carefully a the subset he Nature. is reported number

Operator

next Our from Arthur [indiscernible] question Instructions] will come from [Operator Wainwright H.C.

Unknown Analyst

color XXX. data. question quick Obviously, you the on sales. know a on give cell to but us other on because REZPEG, maybe, expressed had we CDX T-reg XXX, it's TNFRX JZ, not ones more the the the those or But most just preclinical X I on the very the binding also the could interesting

action machan curious Just the there. about

Jonathan Zalevsky

of Thanks Sure. EULAR Thanks, antibody recognizes. that we definitely Yes, to poster, form binding one it that in is was the And of showed different so there forms confirmational some that that found Arthur. question. TNFRX. X our panel epitope the has of of terms in the things a that selectivity for

And know also through ectodomain CLEs be liberates in TNFRX. a can that shedding TNFRX it receptor. the you form But circulate it's metaproteomes normal by So a shed ADAMXX, that blood. can primarily then like receptor shed transmembrane TNF that

of the to And and antibody and our with so the greatly interactive the we barely to surface higher shed tested And shed more much binding is form. surface the form. the receptor much affinity, much, receptor antibody the balanced

the of us we're So to specificity doing a actually assess that that, there's a lot confirmational And component binding. it or to to confirmational indicates biophysical studies now. right

of mapping the paratope we're and the antibodies. epitope all, So first of the

epitope. are function yes, to together. are receptor molecule. its because So aim using And could very ongoing. like you structural think that types. And those an computationally those then that across you not the modeling why the of for doing And is the we We a expressed not the approaches all put assess intracellularly, some do also experiments to structural innovative cell -- types that signal go antibody. types, is while it's cell our multiple But the cell as hypothesis on multiple excited as far we is crystal selectivity confirmational. that's But right, see is sole that why reason. the that's possibly as that's such also which structure because the even the right might you're think same very And on of cellular now we're and we also we trap we're components it's an can imagine finding, not typical is antibody, same the this

Operator

you. Thank I now any questions no I'd line. Robin to Howard And to phone further am on Sure. turn for closing back conference showing the over like the remarks.

Howard W. Robin

and immunology novel excellent can to And as and the us joining making focus therapies in And see, Well, you, innovative today. for progress inflammation. our efforts you multiple strategic Okay. and towards advancing on we're plan clinic. we're everyone, thank Nektar's in

of for hard support, to please want to Thanks us and our thank want joining thank I So our stay I for continued employees and for today. their work, tuned. their all investors

Operator

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

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

Nektar Therapeutics (NKTR) 8 Aug 242024 Q2 Earnings call transcript