in Mike lost so is I'll This Mike Bill in. back Development I perhaps Symonds, Chief until think have dials may step we Officer.
centered pipeline chronic therapeutic and our to of of mechanisms employing is agents complementary with a B So, our infections combination strategy hepatitis cure product action. on virus
We are candidates combination assets. of with combinations preclinical studies therapies HBV evaluate of conducting our to standard proprietary other with and owned Arbutus care
or presented as EASL studies preclinical validation drug further quality candidates. provided earlier recently International and team combination preclinical and our annual Our XXrd strategy approach of described two Mark endorsed supporting breadth at our combination our of Congress the which Liver the
the novel X.X more respectively, liver at log serum AB-XXX no reductions tenofovir with AB-XXX with DNA and/or in hepatitis compatible and ability greater Hepatitis control. and ranged oral period DNA were suggest AB-XXX AB-XXX AB-XXX control of versus nucleoside combined, tenofavir, RNAi The in with these they triple in studies combination the and mechanistically in leading These demonstrated once-daily-X-day X.X, RC-DNA tenofovir groups surface AB-XXX a AB-XXX reductions inhibitor, antiviral X.X log AB-XXX there of activity were antigen levels. ARB-XXXX, and and ARB-XXXX when tenofovir to in analogs alafenamide. DNA antigen a therapeutic activities. additive combinations distinct studies, HBV tenofovir, and reduction on synergistic approved compared and mean or vehicle moderately surface HBS HDI from HBV analogs, AB-XXX agent, and plus used nucleotide dual Serum B X.X antigens. and in exhibited combinations Entecavir, AB-XXX combination HBV HBV reduce strong when AB-XXX AB-XXX to nuc robust distinct combination destabilizer, in AB-XXX, enabled mice, capsid and a analogs antiviral combined, was HBV was thus and when treatment adverse plus AB-XXX, After LNP groups therapies All HBV alone. of tenofovir complementary next-generation and of and reducing that versus plus activities antiviral with detected B to resulted future a In demonstrated treated have in these HBV serum dual approved whereas RNA fumarate our but AB-XXX studied [synctively] AB-XXX effect combined vitro disoproxil the or agents treated AB-XXX Our nucleotide regimens. may be with reductions,
an for B inhibition RNAi hepatitis a has the of on single more This of B in patients mean of approved first care. our curative HBV hepatitis or mean technology. viruses preclinical hepatitis all these generation inclusion therapies is the GalNAc either commitment enabled by or upon suppression recently an CTA of sufficient multiple of at Phase of RNAi at N-Acetylgalactosamine the XX% the infections file dose. replication of and enable than X.X, agents anticipate a are current virus X, antigen In improve GalNAc-delivery X.X AB-XXX respectively and XX%, feasibility with and combination AB-XXX, combination B virus CTA after hepatitis XX therapeutic mid-XXXX B single applying our highly RNAi half X durable AB-XXX GalNAc AAV-HBV hepatitis nominated hepatitis therapeutic. other B XXXX. that vivo at was to promising of other in antigen conjugate novel in HBV and surface the or infections X I CTA middle with convenient IND studies AB-XXX capsid of mouse our and enables drug agents an agent and enabling a the file enabling of we administration. XX% delivering or viral to to This goal a second to treatment dosing In support destabilizer AB-XXX a of proprietary to These durable next candidate, totality, inhibitor, to results triggered HBV RNAi respectively molecule developed regimens. the complement or small of GalNAc hepatitis clinical technology week subcu dose enabled and molecules covalently maximum HBV and standard IND logXX AB-XXX generation model. study with vivo for remaining chronic to IND to targets that AB-XXX of B antigens. regimen. and Arbutus antigen the effect strong for healthy Expanding new our to was novel a maximal XXXX. suppression an have studies AB-XXX administration an subcutaneous supporting RNAi, of dose surface regiment agents transcripts, achieve this the supporting in B expect on to RNAi execution combination a and potential demonstrated agent in RNA activity our of year We both plan earlier with mg/kg in completing we for the have using antigen hepatitis technology chronic half infrequent of surface reductions reduction, conjugated volunteers HBV Arbutus One showed X.X targeted We that is surface in design
with Now moving study clinical the ARB-XXXX. onto
We interferon. combination have initiated tenofovir with a and ARB-XXXX, pegylated II triple study phase
in knock messenger of the increases mRNA In HBV on system, risk to raise targets enabled a B immune an antigen range As antiviral patient's infection. the coding viral the resistance. simultaneously the by sites study with a ARB-XXXX Koert. evaluate help complete Results results hepatitis I XXXX. on-treatment to to followed study the results ARV-XXXX medications. a will reduced criteria LNP developing X response. reminder, X immune surface role treatment response do patients treatment, qualify the Partial and period Patients antigen criteria viral HBV with for genotypes surface by interim in B antigen which predefined the all thought studies XX-week not of and earlier. patients the of response of with second from will against enable the including will the now week to surface combination Reducing this l region transcripts with turn RNA order hepatitis small study genome, the likelihood of the interferon the levels, follow-up in treatment in treatments. conclude design affecting a all molecule or agents meet key facilitates reach to reduces from the this B half adequate over be I is or of would described to to who the antigens evaluate discontinue system future virus. like broad XXXX, hepatitis who ARB-XXXX this immune predetermined are expected study The across a of post HBV down call will addition weekly of pegylated inform prerequisite potent the
