Teva bolsters its biosimilar business through $160m deal with Celltrion
The deal will see the Israeli generics maker attempt to tap into a combined market worth around $6.5bn by commercialising the two proposed monoclonal antibody biosimilars in the US and Canada.
According to spokesman Eliran Levy, Celltrion will manufacture and supply the products to Teva which will pay the South Korean biosimilar developer an initial $160m (€144m).
“It is too soon to discuss detailed commercialization plans but we plan to leverage our strengths in both Specialty and Generics commercialisation,” he told Biopharma-Reporter.
“Biosimilars is a unique industry that requires such cross-divisional skills and Teva is very well-positioned in both.”
The two candidates are part of Celltrion’s biosimilar development pipeline. The firm has a number of other products being marketed by Pfizer, including a version of Janssen’s Remicade (infliximab) approved but not yet launched in the US.
The partnership is a boost for Teva which exited a previous biosimilar joint venture with Lonza in July 2013.
At the time, Lonza told us new regulatory requirements in the US had significantly increased development costs of biosimilar products, compared to the JV’s initial presumptions.
However, Teva has remained vocal about becoming a major player in the biosimilar space, saying in 2014 it was looking to purchases, partnerships and in-house developments to plug the hole in its pipeline.
And in January 2015, Teva spokeswoman Denise Bradley told this publication while the firm is strong in first wave biosimilars – those with no remaining patent protection, it maintains only “a limited program in wave two biosimilars, or those products that will see patents expire between 2015 and 2020,” such as Roche/Genentech’s Herceptin (trastuzumab) and Rituxan (rituximab).
The firm has a version of Amgen’s Neupogen (tbo-filgrastim), Granix, available, but in the US the drug is not deemed a biosimilar as it was approved through the biologics license agreement pathway rather than the biosimilar-specific 351(k) pathway.