Back To: Home

CLICK HERE FOR WHAT'S NEW IN:
 




 

Inking a deal for immuno-oncology
07-29-2015
by Kelsey Kaustinen  |  Email the author
EDIT CONNECT

SHARING OPTIONS:

PARIS & TARRYTOWN, N.Y.—Sanofi has joined with Regeneron Pharmaceuticals Inc. in a global collaboration for the discovery, development and commercialization of new antibody cancer treatments in immuno-oncology. The companies will partner for the joint development of a programmed cell death protein 1 (PD-1) inhibitor that is currently in Phase 1 testing, and expect to begin clinical trials next year with new therapeutic candidates based on current preclinical programs.
 
Per the terms of the agreement, Renegeron will receive an upfront payment of $640 million, and Sanofi and Regeneron will invest $1 billion for discovery through proof-of-concept development of monotherapy and novel combinations of immuno-oncology antibody candidates. Sanofi will fund 75 percent ($750 million) and Regeneron will fund 25 percent ($250 million). The partners have also committed to equally fund an additional $650 million for the development of REGN2810, a PD-1 inhibitor. Regeneron also stands to receive a one-time milestone payment of $375 million if the sales of a PD-1 product and any other collaboration antibody sold for use in combination with a PD-1 product exceed $2 billion in any 12-month period.
 
Sanofi and Regeneron also agreed to reallocate $75 million over three years for immuno-oncology antibodies from Sanofi's $160-million annual contribution to their existing antibody collaboration, which began in November 2009.
 
"The Sanofi-Regeneron Alliance has demonstrated its ability to translate cutting-edge science into groundbreaking medicines for patients with serious needs," Dr. Elias Zerhouni, president of Global R&D for Sanofi, said in a press release. "With more than eight years of successful collaboration between us, I am confident in our ability to advance these novel programs. In addition to PD-1, the collaboration brings together a range of validated, innovative preclinical programs that have unique potential to help patients either as monotherapy or in combination approaches."
 
This collaboration includes monoclonal antibodies and new bi-specific antibodies. In addition to PD-1, other targets currently in preclinical development include antibodies to lymphocyte-activation gene 3 and glucocorticoid-induced tumor-necrosis-factor-receptor-related protein and a programmed death-ligand 1 inhibitor. The agreement will advance bi-specific antibodies targeting hematologic and solid cancers, either as monotherapies or as part of combination regimens.
 
Sanofi and Regeneron's exclusive collaboration will run five years, with the potential to extend it for select programs for an additional three years. The companies will share worldwide profits from the sale of collaboration immuno-oncology antibodies equally.
 
"The field of immuno-oncology has shown the potential to dramatically improve outcomes for patients with certain types of cancer - however, the field is still in its very early days," commented Dr. George D. Yancopoulos, chief scientific officer of Regeneron and president of Regeneron Laboratories. "We believe the approaches most likely to deliver the best results to patients will combine multiple innovative therapies acting on different pathways and targets both in the tumor and the body's immune response - and precisely target these medicines to the right patient. The efficiency and power of our suite of technologies, such as VelocImmune and VelociGene, combined with our human genetics capabilities, uniquely positions the Alliance to accelerate the development of potential new immuno-oncology treatment options for cancer patients."
 
 
SOURCE: Sanofi press release
 
Code: E07291501

Back



PAGE UTILITIES


CONTACT US
DDNEWS
Published by Old River Publications LLC
19035 Old Detroit Road
Rocky River, OH USA 44116
Ph: 440-331-6600  |  Fax: 440-331-7563
 
© Copyright 2017 Old River Publications LLC. All righs reserved.  |  Web site managed and designed by OffWhite.