Novartis (NOVN.S) is buying U.S.-based Selexys Pharmaceuticals in a deal worth up to $665 million, the Swiss drugmaker said on Monday, expanding its pipeline of medicines to combat blood diseases.
Novartis, which last week was reported to be in talks with U.S. generics maker Amneal, exercised its option to buy Selexys after a mid-stage, phase II trial evaluating the Oklahoma City-based firm’s investigational medicine SelG1.
The treatment is aimed at reducing vaso-occlusive pain crises in patients with sickle cell disease. Such crises occur in adolescent and adult patients where sickled red blood cells obstruct circulation in blood vessels.
Novartis Chief Executive Joe Jimenez has said he is on the hunt for bolt-on acquisitions.
Monday’s deal has been in the works since 2012, when Novartis obtained the option to buy Selexys and its sickle cell disease drug, depending on how its trials fared.
The deal has the potential to boost Novartis’s blood disease portfolio, in a disease area where new treatments could command high prices because they are in such high demand. About 90,000 Americans have hereditary sickle cell disease.
Still, some analysts say Novartis has work to do to convince investors it is on the road to renewed growth after its shares have fallen nearly a fifth this year.
“It’s definitely an improvement of the haematology pipeline within the oncology business, but it’s not exactly a bargain and it won’t have any influence on the share price,” Zuercher Kantonalbank analyst Michael Nawrath wrote in a note to investors.
“Novartis’ problems – revenue losses from patent-expired Gleevec, lacking growth at Alcon and the weak sales begin for Entresto – easily overshadow this acquisition.”
Novartis shares fell 1.4 percent in early trading, about double the decline of the European health care index.
While the purchase suggests the trial results were positive, Novartis said details from Selexys’s trial of SelG1 would be released at American Society of Hematology (ASH) Annual Meeting on Dec. 4.
(Reporting by John Miller; Editing by Mark Potter)
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