DEERFIELD, Ill. & MUNICH, Germany—Baxter International Inc., along with SuppreMol GmbH, has announced the acquisition of SuppreMol for €200 million (approximately $225 million) before working capital and other adjustments. The deal includes SuppreMol's early-stage development portfolio of novel biologic immunoregulatory therapeutics for autoimmune diseases as well as SuppreMol's operations in Munich, which Baxter will continue to operate after the deal closes.
Privately held SuppreMol is a biopharmaceutical company based in Martinsried, Germany with a focus on the development of treatments for autoimmune and allergic diseases. SuppreMol was founded as a spin-off from the lab of Dr. Rober Huber, Nobel Prize Laureate in Chemistry 1988, at the Max Planck Institute for Biochemistry in Martinsried. The company's portfolio focuses on the modulation of Fc receptor signaling pathways, a target that could have potential in a variety of immune disorders; SuppreMol is developing a soluble Fc-gamma receptor IIB, a recombinant autologous therapeutic protein with specific immunoregulatory potential.
"SuppreMol has built a rare combination of leading science and promising therapeutic assets," commented Dr. Thomas Hecht, chairman of the Advisory Board of SuppreMol. “We are proud that this important work will now continue at Baxter BioScience.”
"SuppreMol's portfolio of novel investigational treatments complements and builds upon our leading and differentiated immunology portfolio, offering the opportunity to expand into new areas with significant market potential and unmet medical needs in autoimmune diseases," Dr. Ludwig Hantson, president of Baxter BioScience, said in a statement regarding the transaction.
SuppreMol's lead candidate is SM101, an investigational immunoregulatory treatment that has completed Phase 2a studies in idiopathic thrombocytopenic purpura, a disorder that causes low platelet levels, and systemic lupus erythematosus (SLE), a disorder in which the immune system attacks healthy tissue. Phase 2a data for SM101, which were presented last year at the 2014 annual meeting of the American College of Rheumatology, demonstrated a dose response in multiple endpoints among patients with SLE who were treated with one of two different doses of SM101 for six months.
The company's pipeline includes lead candidate SM101, an investigational immunoregulatory treatment that has completed Phase 2a studies in idiopathic thrombocytopenic purpura (ITP, a disorder causing low platelet levels) and systemic lupus erythematosus (SLE, a disorder in which the immune system attacks healthy tissue). SM101's Phase 2a data, presented during the American College of Rheumatology's 2014 annual meeting, showed a dose response in multiple endpoints among patients with SLE treated with either one of two different doses of SM101 for six months. The pipeline also includes technologies with potential therapeutic applications in other autoimmune diseases as well as IgE-mediated allergic diseases.
"Matching therapeutic innovation with market needs is challenging for biotech companies. Working with Baxter, a global immunology leader, is the ideal setting for SuppreMol's promising therapeutic projects to deliver on our most ambitious goal to treat important autoimmune diseases and severe allergies," said Dr. Klaus Schollmeier, CEO of SuppreMol.
In other recent news for Baxter, the company shared an update on its gene therapy program in mid-February, which included progress of its Phase 1/2 open-label clinical trial evaluating the safety and optimal dosing level of BAX 335, an investigational factor IX (FIX) gene therapy treatment for hemophilia B. The primary endpoint of the trial is the safety of a single dose of BAX 335 administered intravenously, with secondary endpoints consisting of evaluation of the optimal dose to achieve stable therapeutic plasma FIX activity, pharmacokinetics and immune response to treatment. Baxter reported that as of the end of 2014, six patients in three dosing cohorts had been treated in the trial with evidence of a dose-related response. No patients have developed FIX inhibitors to date. In the highest dose cohorts, FIX activity levels around 10 percent or higher were seen in two patients, who did not experience any bleeding events