Modag has exited stealth mode with €12 million ($14 million) in series A funds. The German biotech will use the money to take a treatment for parkinsonian disorders into the clinic.
Researchers at Ludwig Maximilian University and the Max Planck Institute for Biophysical Chemistry founded Modag in 2013 to build on work to identify drugs that inhibit protein aggregation. The work resulted in anle138b, an inhibitor of alpha-synuclein oligomers thought to be toxic to nerve cells. AC Immune and AstraZeneca are among the other companies with an interest in alpha-synuclein.
Modag took anle138b, a small molecule, through early-stage tests and into preclinical development using grants from the Michael J. Fox Foundation, generating evidence that the drug halts progression of multiple system atrophy (MSA) in disease models along the way.
Now, Modag has secured funding to take anle138b into the clinic in MSA, a rare neurodegenerative disorder characterized by tremors, muscle rigidity and other symptoms of parkinsonian syndromes. Massa Investment led the series A round, which will support the progress of anle138b into the clinic and corporate growth.
Modag has installed a leadership team to spend the money. Torsten Matthias, who led diagnostics business Aesku for 20 years, has come on board as CEO. Matthias is joined in the C-suite by Armin Giese, one of the co-founders of Modag. Giese will serve as CSO.
The executives will work to build on the potential shown by anle138b to date. The drug is designed to bind to toxic oligomeric structures of alpha-synuclein, causing them to dissolve and preventing the formation of new clusters. Giese thinks this mechanism of action will enable anle138b to improve on existing treatments for MSA, such as levodopa.
“Currently available MSA therapies merely ease symptoms as disease progression continues. Our goal with the development of anle138b is to stop disease progression,” Giese said in a statement.
Modag plans to generate proof of concept for anle138b in MSA, a rare disease with a well-defined patient population. But its targeting of alpha-synucleinopathies is potentially relevant to the other diseases, including Parkinson’s and dementia with Lewy bodies.