EIP Pharma has raised $11.2 million to expand its clinical trial activities beyond Alzheimer's disease. The cash will fund midphase trials of an ex-Vertex drug in dementia and Huntington's disease.
Massachusetts-based EIP licensed neflamapimod, an inhibitor of the p38 MAP kinase alpha enzyme, from Vertex in 2014. Vertex took the small molecule as far as a midphase trial in rheumatoid arthritis, but EIP saw a different future for the drug. EIP began a phase 2a trial in Alzheimer’s in 2015 before moving into phase 2b and raising $20.5 million on the strength of the resulting data.
Now, EIP has secured funding to branch out beyond the memory-wasting disease. Adage Capital Management, Rock Springs Capital and Mossrock Capital have put up $11.2 million to position EIP to start phase 2 trials in two new indications in the second quarter.
The conditions EIP hopes to treat—dementia with Lewy bodies and cognitive deficits in Huntington's disease—share some characteristics with Alzheimer’s. Notably, there is evidence that inflammation is a key driver of cognitive dysfunction in all three diseases, leading EIP to conclude neflamapimod could help patients with the conditions.
Neflamapimod is designed to cross the blood-brain barrier and inhibit the intracellular p38α enzyme, which neurons express when stressed or diseased. In Alzheimer’s, EIP thinks p38α plays a role in the hippocampal synaptic plasticity impairment that affects learning and memory formation.
EIP is still months away from generating phase 2b data to validate its belief that blocking the enzyme will reverse the deterioration and thereby drive improvements in episodic memory. But it has seen enough in its phase 2a trial and other activities to invest more in neflamapimod.
The company selected dementia on the strength of evidence of the similar role neuroinflammation plays in the disease and Alzheimer’s, plus studies into the role p38α plays in toxicity induced by the protein constituent of Lewy bodies. EIP thinks neflamapimod may help in early Huntington's due to the presence of hippocampal functional deficits in patients with cognitive impairment.