Dive Brief:
- Mast Therapeutics has put together a strategy for the future following the failure of its sickle cell drug vepoloxamer, which failed to meet its primary endpoint in a Phase 3 study announced in September.
- A number of privately-held companies are interested in potential reverse mergers, and these include some with complementary clinical-stage candidates that will build on the pipeline, said Mast in a statement on Nov. 21.
- In the meantime, Mast Therapeutics is continuing development of AIR001, in Phase 2 trials for treatment of patients with heart failure with preserved ejection fraction (HFpEF).
Dive Insight:
Mast Therapeutics' latest announcement of a strategic plan, following its struggles with its lead program, has triggered a jump in stock value of almost 30%, although the stock is still trading below $1 per share.
The company indicated that it has received interest from several parties that potentially want to conduct a reverse merger, but it will continue to explore other strategic alternatives like possible licensing agreements.
"Our recently-announced strategic process has generated a number of opportunities that would be transformative for Mast," said Brian Culley, CEO of Mast Therapeutics in a statement. "We are diligently and expeditiously reviewing these strategic alternatives, which we believe could maximize returns for our stockholders. We also remain excited about the potential for AIR001 in HFpEF and look forward to more data from investigator-sponsored studies in 2017."
In September 2016, Mast Therapeutics announced that it was shutting down the development programs for its sickle cell anemia and heart drug, vepoloxamer, following its failure in a Phase 3 study in sickle cell anemia. Mast also announced that it was looking for a partner to support the Phase 2 trials of inhaled nebulized sodium nitrate, AIR001, and that money earmarked for vepoloxamer would be redirected to the AIR001 project.
Interim results from an ongoing Phase 2 study in heart failure with preserved ejection fraction (HFpEF) published earlier this month showed significantly lowered pulmonary, right atrial and pulmonary capillary wedge pressures, with a substantial increase in pulmonary artery compliance in AIR001-treated patients.