Seelos Therapeutics has been issued U.S. patent number 10815271 (application number 16/311,593) from the United States Patent and Trademark Office (USPTO) covering the composition of matter for SLS-007, a potentially disease-modifying gene therapy focused on intracellular alpha-synuclein (α-synuclein) aggregates in Parkinson's disease (PD).

This patent covers the composition of matter comprising at least one inhibitory peptide that inhibits α-synuclein aggregation by binding to residues 68-78 of α-synuclein. The patent also covers a method of use for reducing or inhibiting α-synuclein aggregation, comprising contacting α-synuclein amyloid fibrils with an inhibitory peptide in an amount sufficient to reduce or inhibit α-synuclein aggregation plus a method of modulating the size or rate of growth of α-synuclein amyloid fibrils.

As previously announced, Seelos is currently conducting an in vivo preclinical study of SLS-007.

"The alpha-synuclein approach to treating Parkinson's disease has been of great interest recently and we look forward to completing this study and evaluating the results," said Raj Mehra, Ph.D., Chairman and CEO of Seelos. "Successful delivery of this peptide by a gene therapy approach could yield a valuable tool in slowing the progression of Parkinson's by stopping the seeding and potential propagation of alpha-synuclein aggregates."

Seelos is currently delivering SLS-007 via an adeno-associated virus (AAV) that is designed to target the non-amyloid component core (NACore) of α-synuclein to inhibit protein aggregation in patients with Parkinson's Disease (PD). The preclinical study is designed to establish the in vivo pharmacokinetic and pharmacodynamic profiles and target engagement parameters of SLS-007.

Preliminary data from the study is currently expected in Q1 2021.

SLS-007 is a family of rationally designed peptidic inhibitors that target the NACore of α-synuclein to inhibit protein aggregation in patients with PD. The overexpression of α-synuclein leads to the formation of α-synuclein aggregates which comprise Lewy bodies and neurites which are the hallmarks of the pathogenesis of PD. Recent in vitro and cell culture research have shown that SLS-007 has the potential to stop the propagation and seeding of α-synuclein aggregates.