Thank good you, Ramy, everyone. morning, and
our of collaborative portfolio and internal fronts to programs. make We are on continuing important pipeline advances many across
with collaborations, our leveraging We small internally. and more level us have platform of and believe same candidates. spanning to quality deployment high at companies rapidly identify large biotech the a do are large range pharmaceutical broad enabled we We both in scale development this of we target classes collaborations scale these
programs expect to advance continue several to We year. clinic the new in collaborative clinic and the enter to this programs
lymphoma also chemical of sense explored made space have highlight CDCX first on compounds packages, programs, presented vivo we like preclinical downstream potent studies nomination data the have identify anti-tumor synthesized MALTX program, XX and MALTX our inhibitor XXXX, KappaB an inhibition of as activity Society XX and MALTX BTK at with WeeX. annual of compounds internal the to xenograft is We vitro initiation. within submission in today MALTX programs months enzymatic has our the interesting advanced solid of just approximately models own methods we B-cell using with IND we of to-date, completion in To emerged next because MALTX program inhibitor triage to in year. program mouse pathway. give molecules development oncology MALTX for it We the identify target relapsed of we signaling candidate dependent BCL-X will combination to our Constant programs. of and Hematology Today, most in inhibitors announced up enabling I resistant most to and effective mouse how reported Subject leukemia. in which inhibitors, forward IND a we you in first these venetoclax, inhibitor hematological B-cell XX,XXX drug of strategy of candidate. optimization those BTK with potent suitable December, our over of multi-parameter MALTX, approved development from Based significant believe selected a expected X MALTX with and progress Starting a vivo effects a In have subtypes therapeutic advanced hallmark could American malignancies. to with half Additionally, our novel our dose our billion or is activation three expect selected favorable of team scored an are strong in tumors properties, data activity three that generated to for models, certain diffuse treat KappaB NF our we and meeting. in several submit and of to to plan applications lymphoma. preclinical inhibiting respectively. data lymphocytic we ibrutinib targeting large lymphomas move anti-proliferative the chronic We in be NF demonstrated in
in our or the clinic. We development are the excited inhibitors BCL-X potential of about with evaluating candidate combining MALTX BTK
begin X in studies Our with shortly for plans are hematological beginning to Phase malignancies. expected GLP-tox make and to are studies patients we
expect finalized. the the after share Phase about more study We details clinical X is protocol to
CDCX and our through to ability shown cells capacity at is required protein that DNA inhibitor is for DNA replication is two a Last month, cancer. to important replication programs damage has turn momentum normal I’ll responses. Targeting initiation. presented therapeutic and CDCX stress and Now we data bypass roles gaining new that play WeeX, the to DNA DNA cancer approach mechanisms. and that replication replication to cancer stress to in meeting. linked be as repair kinase preclinical thought proteins from AACR program been annual target in be CDCX proliferative CDCX a
These DNA demonstrated picomolar DNA dose investigational dependence repair and compounds compounds acute selective. approved both leukemia apoptosis, cancer and inhibitor generated cancer. profile. colorectal highly showed therapies modulate develop were several inhibited we and Our opportunity tumor to-date with also significantly best-in-class They very favorable and of a growth in data checkpoint. pharmacokinetic synergy potency that to have myeloid that mouse we a an have models The suggests with mechanisms
arrest inducing other program kinase of viability objective damage WeeX shown therapeutic cycle GX/M tyrosine Others The repair WeeX, DNA meaningful phase regression by of WEEX to tumor in other tumors have cell cells. inhibition. apoptosis cell clinically targeting GX/M is reduce uterine Our carcinoma, and checkpoint. ovarian solid the targets serous cancer a of through and regulator
effort have combination difficult. dosing program drug our drug selective inhibitors existing molecules off effects, potential more target therapy to profiles combinations. in interactions limit minimize The highly an make challenge was develop and for that and in design the may to maximize However,
that identified molecules for and shows are highly in potent responses and vivo. selective activity multiple We strong pharmacodynamic anti-tumor WeeX have
dose optimized no profile limits enzyme. molecules the of for this and for of a liver We need the combination have also including products. drug Our believe like key observable CYPXAX, properties, accumulation adjustment potential inactivation
development, programs. and new to transition advance initiate into programs these we As expect
We have and program immunology. data human several genetic prioritized emerging in opportunities oncology pharmacology and new support with
results. during into enable to launch Phase clinical next advancing look We programs the year. studies throughout over pipeline the activities these now the our and support we financial to year. well areas Activities year. additional the multiple to have of summary, R&D to are forward our expansion I underway. into to call of expect In We GLP initiation disease review you will X on Joel studies submissions updating toxicology programs our turn to IND
