Early clinical-stage drug is designed to block formation of neurotoxic variant of amyloid beta.
Probiodrug secured €15 million in financing through a fundraising round with existing investors to support further development of its glutaminyl cyclase (QC) inhibitor program, including lead clinical-stage candidate PQ912.
QC is a metalloenzyme involved in peptide hormone final maturation. The firm’s QC inhibitor program is based on the in-house discovery that the enzyme catalyzes the formation of the N-terminal pyroglutamate residue found on the neurotoxic, plaque-forming variant of amyloid beta (Aβ) implicated in Alzheimer disease. PQ912 is the first QC inhibitor to be evaluated in the clinic, Probiodrug claims. In November 2011 the firm reported topline results from a Phase I single- and multiple-ascending dose trial evaluating PQ912 in healthy volunteers.
The latest fundraising will enable progression of the small molecule candidate into additional studies. “Probiodrug’s proprietary therapeutic target has been validated preclincially, and the lead candidate has been shown to be safe and well-tolerated in a Phase I clinical study,” remarks Konrad Glund, Ph.D., CEO at Probiodrug. “This capital raise further strengthens our financial position and will help us advance the compound in the clinic towards proof of concept.”
Probiodrug’s second internal development program is focused on inhibitors of cyclin-dependent kinase 9 (CDK9), an enzyme involved in transcription and cell cycle control. Through its activity on multiple cytokines, CDK9 impacts directly on immune response, inflammation, and cell differentiation, and thus represents a potential target for a range of diseases including rheumatoid arthritis, inflammatory pain, and chronic inflammatory diseases such as multiple sclerosis, psoriasis, and inflammatory bowel syndrome, the firm claims.
Probiodrug has identified a number of selective CDK9 inhibitors which have demonstrated anti-inflammatory properties in both in vitro and in vivo models of pain and inflammatory pain, and disease-modfiying activity in animal models of rheumatoid arthritis.
