Biopharmaceutical company Alexion Pharmaceuticals agreed yesterday to acquire Syntimmune, a US-based autoimmune disease therapy developer backed by drug producer Baxalta, for up $1.2bn.
Alexion will pay $400m in cash upfront and up to $800m more if Syntimmune hits certain milestones. The transaction is subject to customary closing conditions and is expected to be completed in the fourth quarter of this year.
Founded in 2013, Syntimmune is developing therapies for autoimmune diseases. Its drug candidates target the neonatal Fc receptor (FcRn), a protein that contributes to regular immune responses in healthy individuals but which can drive autoimmune disorders when it malfunctions.
Lead asset Synt001 is undergoing phase 1b/2a clinical trials in patients with warm autoimmune haemolytic anaemia, which causes a premature destruction of red blood cells, and in patients with pemphigus vulgaris or pemphigus foliaceus, which cause skin blisters.
Syntimmune has raised $78m in funding, most recently securing $50m in a series B round led by venture capital firm Apple Tree Partners in June 2017 that included unnamed existing shareholders.
Baxalta Ventures, the corporate venturing arm of Baxalta, which merged with pharmaceutical firm Shire in June 2016, co-led a $26m series A round with Apple Tree Partners that closed six months later following an $8m third tranche.
The series A round’s $8m first close occurred in 2014, before the company secured a $10m extension in March 2016. The round also featured Partners Innovation Fund, the corporate venturing arm of healthcare system Partners HealthCare.
Ludwig Hantson, chief executive of Alexion, said: “The acquisition of Syntimmune represents a critical step in rebuilding Alexion’s pipeline and further diversifying the company’s clinical-stage rare disease portfolio.
“It offers a strong strategic fit with Alexion’s existing rare disease franchises and provides the opportunity to transform patient care in diseases like warm autoimmune haemolytic anaemia, where Synt001 is the first, and currently the only, anti-FcRn therapy in clinical development.”
