F-star Expedites Its Transition to a Wholly-Owned Portfolio Strategy

On May 13, 2019 F-star, a clinical-stage biopharmaceutical company delivering tetravalent bispecific antibodies for a paradigm-shift in cancer therapy, reported the reconfiguration of its immuno-oncology collaboration, established in 2017, with Merck KGaA, Darmstadt, Germany as it executes on its transition to a wholly-owned portfolio and builds scale and value as a world-class biopharmaceutical company (Press release, f-star, MAY 13, 2019, View Source [SID1234536235]).

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Under the terms of the new agreement, F-star retains exclusive rights to develop and commercialise FS118, a clinical-stage tetravalent bispecific antibody. At the same time, Merck has exercised its option for one discovery stage programme and retains the right to option a second discovery programme from the 2017 original agreement. No financial terms of the agreement are being disclosed.

Eliot Forster, CEO of F-star, said: "This new agreement reflects our pivot to building a wholly-owned pipeline, that allows for rapid progress into the clinic and secures greater long-term value from our products. With full rights to FS118, we have an opportunity to accelerate the development of this first-in-class medicine for a group of targeted cancer patients. We are also pleased to continue our long-term collaboration with Merck KGaA, Darmstadt, Germany by advancing assets from F-star’s Modular Antibody TechnologyTM into their pipeline."

FS118 is a potential first-in-class tetravalent bispecific antibody for the treatment of cancer, developed to overcome tumour evasion mechanisms promoted by two molecules (LAG-3: Lymphocyte-Activation Gene 3 and PD-L1: Programmed Death-Ligand 1) with the potential to restore the natural ability of the immune system to fight cancer(1). Initiated in April 2018 under F-star’s sponsorship, the Phase I trial (NCT03440437) continues as originally planned and is expected to read out during 2020.

(1) LAG-3/PD-L1 mAb² can overcome PD-L1-mediated compensatory upregulation of LAG-3 induced by single-agent checkpoint blockade. Faroudi et al. (March 2019) – Poster at the annual AACR (Free AACR Whitepaper) meeting