GSK wants to replace all of HGS board – Reuters

by | 31st May 2012 | News

GlaxoSmithKline is planning to replace the entire board of takeover target Human Genome Sciences, according to a Reuters report, and candidates from across the sector have been sounded out.

GlaxoSmithKline is planning to replace the entire board of takeover target Human Genome Sciences, according to a Reuters report, and candidates from across the sector have been sounded out.

The news agency, citing unnamed sources familiar with the situation, claims that GSK will seek the backing from HGS shareholders to replace the board with 12 independent directors. It states that the UK drugs giant has approached executives in the pharmaceutical industry as well as finance and governance experts.

The battle for control of HGS has been heating up over the last few weeks and the latter has repeatedly rejected a $2.60 billion, or $13 per share, offer as inadequate. HGS began a process to explore strategic alternatives, but GSK declined to take part – it also added a condition to its share offer for its long-time partner and co-developer of the lupus drug Benlysta (belimumab), requiring HGS to abandon a ‘poison pill’ adopted to foil any hostile bid.

GSK did not comment on the Reuters report, although a HGS spokesperson was quoted as saying that the board still recommends investors not to tender their shares. The spokesperson went on to claim that GSK was seeking “to circumvent, disrupt and prematurely end the company’s [strategic review] process to the disadvantage of HGS stockholders”.

Bid to expand Promacta/Revolade label

Meantime, GSK has filed regulatory applications in Europe and the USA to expand the label on the blood disorder drug Promacta/Revolade (eltrombopag).

Specifically, the drug, which was co-discovered with Ligand Pharmaceuticals, is currently marketed for the treatment of adults with idiopathic thrombocytopenic purpura who have had their spleen removed. Now it is seeking to expand approval to increase platelet counts in patients with chronic hepatitis C virus infection; this would enable the initiation of interferon-based therapy and during interferon-based therapy.

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