avantiavanti schreef op 19 juli 2019 07:19:
SVB Leerink 18 juli 2019
GALAPAGOS NV
BI autotaxin deal further increases our conviction on GLPG1690 Bottom Line: Boehringer Ingelheim chases GLPG in IPF with ATX
licensing deal.
Deal adds to our conviction on scientific approach. Ofev
(nintedanib) owner Boehringer Ingelheim entered a licensing agreement
for Bridge Biotherapeutic’s autotaxin (ATX) inhibitor BBT-887 currently in
Phase 1 trial to treat idiopathic pulmonary fibrosis (IPF). The timing and
potential deal size for a Phase 1 drug by a market leader in idiopathic
pulmonary fibrosis (IPF) raises our conviction in GLPG’s ATX inhibitor
in IPF. Under the terms of the deal, Boehringer Ingelheim will pay €41M
upfront and will owe up to €1.1B in additional development, regulatory
and commercial milestones plus tiered royalties up to low double digits
on future commercial sales. BBT-887 trails the development of GLPG’s
Phase 3 ATX inhibitor GLPG1690 by many years having recently
announced interim data from the single ascending dose portion of the
Phase 1 trial in May at the American Thoracic Society (ATS) conference
held in Dallas, TX. The limited preclinical data presented to date do not
differentiate BBT-887 from GLPG1690 as best in class.
Our Take: There have been lots of questions by investors regarding the
validation and usefulness of targeting the LPA pathway in IPF. We have
previously outlined our enthusiasm for this approach. We
consider the translation work done to identify this pathway as one of the
great translational stories of our time (Tager et al.), which was the basis
for BMS’s acquisition of Amira Pharmaceuticals in 2011. The LPA inhibitor
BMS-986020 demonstrated efficacy as measured by forced vital capacity
(FVC) separation, but was discontinued due to idiosyncratic toxicity
associated with the compound and not the pathway. There has also been
quite a bit of grumbling regarding the rapid progression of GLPG1690
into full blown phase 3, with only a small cohort of patients in hand. The
BMS data, the Fluidda signal, the clear biological signal for GLPG1690
were fundamentally persuasive to move the GLPG management forward
without dithering. The futility readout next year, while increasing the
cost of the study a bit, allows for an early read of the data and further
progression of Isabella. We view the interest from Boehringer Ingelheim,
a respiratory powerhouse and IPF therapeutic pioneer, in autotaxin as a
major validation of GLPG’s commitment to treating IPF by targeting the
LPA pathway.