Take­da first shone a spot­light on Finch Ther­a­peu­tics’ hu­man-first dis­cov­ery plat­form in 2017, when the Japan­ese phar­ma paid $10 mil­lion to part­ner a pre­clin­i­cal ul­cer­a­tive col­i­tis pro­gram in­spired by fe­cal trans­plan­ta­tion. While the mi­cro­bio­me ther­a­py, FIN-524, is still mak­ing its way to the clin­ic, Take­da has seen enough to com­mit to a sec­ond pro­gram tack­ling an­oth­er type of in­flam­ma­to­ry bow­el dis­ease.

Mark Smith

The duo will now rev up Finch’s plat­form tech again in search of a treat­ment for Crohn’s dis­ease, which Take­da will have ex­clu­sive rights to com­mer­cial­ize. Fi­nan­cial terms were not dis­closed.

De­ploy­ing ma­chine learn­ing to crawl through da­ta from in­ter­ven­tion­al mi­cro­bio­ta trans­plan­ta­tion stud­ies, Finch CEO Mark Smith aims to iden­ti­fy mean­ing­ful mi­cro­bial sig­na­tures por­tend­ing dis­ease. The re­sult is what he calls ra­tio­nal­ly-se­lect­ed mi­cro­bio­ta ther­a­pies, which con­tain cul­tured bac­te­r­i­al strains linked to pos­i­tive clin­i­cal out­comes.

That ap­proach could prove su­pe­ri­or to an­i­mal mod­els, Finch the­o­rizes. FIN-524 was their first at­tempt to val­i­date the the­o­ry — as the two oth­er can­di­dates in their pipeline, for re­cur­rent C. diff and autism, came from its oth­er dis­cov­ery plat­form. Known as full-spec­trum mi­cro­bio­ta, it rep­re­sents the foun­da­tion­al “drugs from bugs” idea of putting good bac­te­ria in a pill.

Gareth Hicks

“We’ve seen the promise of Finch’s Hu­man-First Dis­cov­ery plat­form for the de­vel­op­ment of a com­plete­ly new type of treat­ment for in­flam­ma­to­ry bow­el dis­ease,” said Gareth Hicks, head of gas­troen­terol­o­gy drug dis­cov­ery unit at Take­da, in a state­ment.

Hicks is in charge of one of four core ther­a­peu­tic ar­eas that Take­da is ze­ro­ing in on in the wake of the Shire ac­qui­si­tion (the oth­er three be­ing on­col­o­gy, neu­ro­science and rare dis­eases). Right now, one of the stars in the port­fo­lio is En­tyvio, an IBD drug that blocks the bind­ing of α₄β₇ in­te­grin to in­testi­nal mu­cos­al ad­dressin cell ad­he­sion mol­e­cule 1 (MAd­CAM-1), there­by ame­lio­rat­ing the in­flam­ma­to­ry ef­fect of white blood cells on gut tis­sues.

The col­lab­o­ra­tion with Finch isn’t their on­ly push in­to the nascent but fe­cund field of mi­cro­bio­me-based ther­a­peu­tics. Last Oc­to­ber Take­da put down $50 mil­lion to team up with France’s En­terome on EB8018, a small mol­e­cule de­signed to se­lec­tive­ly dis­arm vir­u­lent bac­te­ria in the gut caus­ing in­flam­ma­tion, with­out dis­rupt­ing the lo­cal mi­cro­bio­me.

Neurologist and King’s College London professor Christopher Shaw has been researching neurodegenerative diseases like ALS and collaborating with drugmakers for the last 25 years in the hopes of pushing new therapies forward. But unfortunately, none of those efforts have come anywhere close to fruition.

“So, you know, after 20 years in the game, I said, ‘Let’s try and do it ourselves,’” he told Endpoints News. 

On the hunt for a better AAV capsid for gene therapy, Eric Kelsic’s Dyno Therapeutics has set itself apart with its focus on machine learning to help speed discovery. Now, Japanese drugmaker Astellas — fresh off a slate of gene therapy burns — is taking a bet on Dyno as it looks to the future.

Astellas and Dyno will work together as part of an R&D pact to develop next-gen AAV vectors for gene therapy using Dyno’s CapsidMap platform directed at skeletal and cardiac muscle, the companies said Wednesday. Under the terms of the deal, Dyno will design AAV capsids for gene therapy, while Astellas will be responsible for conducting preclinical, clinical and commercialization activities for gene therapy product candidates using the capsids.