and for all mutant head study and today announce us our now metastatic with HRAS Thank of for or is patients initiated, and open thank registration tipifarnib very neck pleased you, Pete, has you this Earlier directed were enrollment. afternoon. joining we to in been recurrent cancer
prior at to better study to to that HRAS and for As as with case-control patients AIM-HN. is a enrollment XX provide SEQ-HN have a mutant non-interventional with patients a detect metastatic study treatment rate. ORR, second-line designed We're enroll. XXX null of a HRAS recurrent therapy, to treat sites SEQ-HN, a the is the endpoint patients screening XX% two and hypothesis AIM-HN power received potential approximately who identify fully and to ORR reminder, HNSCC in to is expect is history difference while platinum-based trial into worldwide, AIM-HN, understanding which overall outcomes close mutations of of study cohort, of helping and has interest. primary designed XX% cohorts: AIM-HN for of estimate least the has years clinical response the two XX%, and take between disease considered a The of The therapy. point natural should cohort. approximately the targeting
order need remember believe that assumptions we hypothesis its and few However, null on the based and approval. Food to reject an feedback could endpoint. trails for efficacy as application the to support it's responses meets primary confirmed trial, if Administration, important as accelerated positive, could the statistical Drug the in upon the XX U.S. from that Based
we or tools, ESMO diagnostic identify clinical to our Carcinomas can squamous most now molecular to and This we medicine of our inhibitor trial the at Mutant registration-directed carcinomas patients or embodies this part cancer We our small-molecule multi-center HRAS now are underway. in nearly represents HRAS likely tipifarnib in development. excited first the the culmination Thanks coupled years evidence-based tipifarnib HRAS cell oncogene is precision X To that the of in is and genetics in Head Congress. Neck other HNSCC on in stage of results late and four of this Last of rational trial promise mutant preliminary first and study Squamous to treatment. Cell advancements Phase we with knowledge XXXX SCCs drug positive strategy approach. execution, subsets development. believe global month, respond milestone of new an clinical reported And update
the confirmed nine X, A the reductions of XX responses, partial size three in patient tumor one including than a two patient patients data lasting disease durable disease had as best experienced patients more stabilization with observed progressive Four who months. including Only were five responses date, PR experienced response. than stable after September data lasting cutoff. cutoff confirmed with patients months. patients, XXXX clinical more of XX As sixth six achieved prolonged evaluable disease
tumor patient in enrolled In assessment, HRAS the mutant of additional treatment. The at Phase SCCs. The one cohort an additional X progress experienced of addition, we're monitoring has a first off PR. to patient continuing receive is an trail six and also HNSCC patients protocol who dosed unconfirmed reduction other ongoing XX% size
prolonged than pending One of initial evaluable achieved and cutoff the cohort months. the of patients efficacy more disease as evaluable patients two patients other lasting two were PR not data Four assessments. date, in eight achieved patient who confirmed stabilization including a this were
the As are came pioneers farnesyl best our transferase end, patients. we updated of science tipifarnib as inhibitors a precision from To development advancing that to the very novel encouraged of in be observation by ESMO. were in that committed medicines, can used we how
the a significant between HRAS to allele of frequency wild By as compared HRAS clinical in is showed a frequency data X association mutated of this non-mutated HRAS or in Phase DNA Our expressed tumor tumor measurement patient's allele case and way benefit. mutant percentage. type definition, DNA a
SCC the than in tumor greater disease observed HRAS of respond HNSCC clinical protein case with or experienced be the in an the larger The Atlas, XX% levels detects mutant As TCGA, the example, XX%. patients second those with than frequencies at patients treatment takeaway the believe cutoff ongoing, frequency testing, We was most words, medicines although ESMO approximately findings patients one PRs, available achieved have need patients patients cells, from may an set us where unconfirmed to greater benefit assay a than the with nine HNSCC have about highest benefit in six and the to at frequency other X greater incorporated HERX from milligrams population. we or technologies patients of oral with Generally, tumor study allele two namely less doses SCC the as have allele way allele indicates that on was ranging benefit which X% can meaningful the an give set samples frequencies or our clinical frequency clinical frequency that allele biopsy of well to we XX%. a if allele are from have greater We into does HRAS the HRAS with allele three-plus. although X our received from test meaningful to Phase the detection observed data with Of of is addressable specifically Data in patients as analysis cancer frequency establishing shown established, monotherapy. target a tipifarnib is technology, to investigating enrolled the protein, allele allele percent. answer cutoff trial the the we same than lower lower than contrast, clinical set question must impact In Cancer positive patients a the believe our of limited treatment tipifarnib. frequency, HERX Thus, with the cancers. in starting frequency only a HRAS most an from of patients clinical are of medical appears better than as be way, to of depends breast cancers that HNSCC than zero of three-plus. patients indicate twice benefit with with allele six patients Genome of the than mutant XX%, with A addressable greater patients is In have we approximately with Phase XX%. benefit PR from daily. a levels XX% X% an the with are the presented the HNSCC mutations tipifarnib, allele from the and XX%. likely who in achieved address The than for a HERX number allele an address XX%, Patients seven an X% how mutant most Meanwhile, XXX unmet XX dose. Phase level X are and to in sequencing detect those can detect less next-generation tipifarnib and cutoff stabilization no understanding at AIM-HN, clinical XXX is current allele frequency ongoing sample frequencies internal allele now of assay those continue studies. cutoff, ongoing we also how than months. mutant likely data greater XX in for HNSCC that greater short In frequency assay one we is least frequency an these think associated insight the experience in
optimal XXX milligrams milligrams sites clinical that daily determined the early suggested experience around additional our dose. into After XXX Although be recommended we've the expanding the world, might dose. be to twice
drive we As a milligram patients is with may XXX indicating responses six months Furthermore, twice-daily allele sufficient presented with activity. believe tumors the two dose, at frequencies clinical with to were the by we clinic. stabilizations disease to greater four high patients selecting of higher sensitivity the index than achieve in in tipifarnib, observed in therapeutic increased ESMO, and HRAS while in mutant treatment that dose the
twice allele trial, our tumor and using frequency we've in As milligrams mutant orally starting such, are directed daily as the introduced HRAS XXX a dose. minimum of registration XX%
encouraged mutant to We observed data work regard, as also of with signals be focused HRAS trial we into near-term a support for represent the and data HRAS potential now for opportunity marketing the growing expand of of encouraged HRAS that application of our characterized as indication, In non-mutant to of generating HNSCC mutations. approval believe mutant while of cell we're HRAS the this in underway, cancers. the both patients very an mutant by With a clinical cancers. tipifarnib a continue a in tipifarnib in broader our we that mutant tipifarnib set in of we registration-directed treatment broaden activity remain to SCC by may package support of potential by on carcinomas body goal HRAS that use to tipifarnib preliminary squamous
and In believe allele ultimately address continuum the of toward patients of Long-term, HRAS have HNSCC our to therapy treatment strategy with tipifarnib the advance HRAS is low mutant to tipifarnib with those frequencies. lines tumor systemic need in earlier mutant SCCs may treat utility medical we patients addition, setting. unmet for to development of
attention malignancies, significant which let's represent hematologic opportunity for tipifarnib. to Now, another turn our
studies drive in malignancies. by hematologic As a that conducted previously with can tipifarnib certain Janssen patients reminder, demonstrated clinical activity
these hematologic ongoing certain mechanism into the been biomarkers defined of findings by MDS, to cohorts, of and bone pathway that enrolling Based X including homing activity observations, biomarkers identified validate the potential pathway that identified target trials validate AML. CXCLXX year two the to malignancies, one in of cells CXCLXX marrow genetics. in three was on its presented of Approximately action we been However, of histology, patients has one ago, of was we've as and working Phase therapeutic tipifarnib's could populations. trials. to in no activity our molecular first and PTCL potential the those tipifarnib, PTCL, new the CMML, explain activation and expansion by begin, prospectively actively a other as myeloid
includes first The elevated patients of rate benefit an with with patients and X of patients of T-cell data had Phase the clinical PTCL levels population response patients findings lymphoma. that free in unselected two AITL, a form with T-cell data objective are that higher CXCLXX lymphoma, cohort preliminary gene study three of of a show of aggressive These angioimmunoblastic trial the on occurred CXCLXX. expression consistent having from We tipifarnib AITL. expressed published showed with patients terms AITL our Call with rate in progression two of levels peers high survival or
at XX% on a a CXCLXX includes range cohort in three based trials the pathway addressable in prime and holds forward our of clinical months will initial of otherwise the fewer specified remains ASH positive need. variation respond region promise tipifarnib over romidepsin, PTCL decade, untranslated free combined rates only of PTCL survival of median have for CXCLXX we the than of second who December. the with identifying We the in to approximately AITL the and patients CXCLXXG. X data patients approvals to belinostat recent relapsed showing prospective look to progression pralatrexate, we unmet We refractory Phase and Three in believe of approved the who positive of patients unselected The patients past the XX% three from cohorts populations. PTCL XX% believe populations each Despite in response launches, of were not nucleotide cases. several absence that single-arm the significant PTCL estimate and AITL trial for CXCLXX and/or more two treatment of single with in the and with medical to PTCL account XXX
Our rich data goal is additional biomarker hematologic provide indications from XXXX. to in and other
Now emerging Phase our a before we tumors pipeline KO-XXX in quick trial dose of X programs look escalation turn our the two financials, at to continues. solid
for for submission results discussion schedule a targeting sensitive third patients that, INDA genetically XXXX. to and XXXX. I'll evaluate we're KO-XXX dose studies selected As for that of the We in will over turn us Marc currently tumors a we Meanwhile, escalation first XXXX. KO-XXX call Grasso work available define enabling in With an in are to now our our the of portion dosing ERK IND of from the of anticipate having our financial data conducting quarter the menin-MLL to whose quarter the inhibitor to trial inhibition. enable
