NMD Pharma has secured cash to muscle into the myasthenia gravis (MG) market. With Novo Holdings and Roche Venture Fund joining a syndicate led by Jeito Capital, the biotech has raised 35 million euros ($40 million) to take its lead candidate NMD670 through a phase 2a clinical trial in the indication.
MG has emerged as a hot spot of autoimmune drug development, with AstraZeneca and Argenx already on the market and UCB and Johnson & Johnson moving rival candidates through the clinic. The level of competition, however, masks a potential gap in the treatment arsenal. While MG is an autoimmune disease, it causes muscle weakness and fatigue, creating two angles from which to tackle the condition.
“Recent drug developments for MG all focus on autoimmune treatment and none of them focus on restoring muscle function per se. In fact, there is no new treatment in development other than NMD670 that addresses this fundamental aspect of the disease,” NMD CEO Thomas Holm Pedersen, Ph.D., said.
Pedersen sees the “mainstay therapeutic approach” as a combination of treatments to restore muscle function and tackle the autoimmune element. NMD’s work on ClC-1 chloride ion channel inhibitors puts it in a position to address the muscular side of the equation. ClC-1 is only expressed in skeletal muscle and, if NMD is right, the inhibitors will enhance neuromuscular transmission to restore muscle function.
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NMD is putting that idea to the test in a phase 2a clinical trial. Jeito has come together with NMD’s current investors Inkef Capital, Novo Holdings, Roche Venture Fund and Lundbeck Foundation to put up the money to complete the proof-of-concept study.
The size of the round gives NMD the financial firepower to move beyond MG. NMD’s list of targeted neuromuscular diseases includes spinal muscular atrophy (SMA), another condition that has attracted multiple companies.
Pedersen is overseeing the expansion having seen evidence that patients treated with survival motor neuron (SMN) protein upregulators, such as Biogen’s Spinraza, have neuromuscular transmission deficits linked to functional readouts including the six-minute-walk test and muscle strength.
“This clearly shows that SMA patients have a neuromuscular transmission deficit and enhancing transmission with a ClC-1 inhibitor would be predicted to restore muscle function and thereby improve endurance, independence and quality of life. The ClC-1 inhibitors could be used as monotherapy or in combination with SMN-upregulating therapy,” the CEO said.