Significant need for effective treatments
Today, over ten million people around the world live with Parkinson’s disease. The disease is normally detected in patients in their sixties, and approximately one percent of the world’s population over the age of 60 will be affected. The initial symptoms of Parkinson’s disease often include impaired sleep, obstipation, mild tremors in one arm, or a reduced sense of smell. As the disease progresses, the tremors worsen, movement slows down and the body’s muscles stiffen. Normally, the condition develops over 15–20 years, and additional symptoms such as cognitive impairment and hallucinations may occur at later stages during the progress of the disease.
Current treatments, including primarily dopamine analogs, usually show a positive effect in alleviating the motor symptoms in the early stages of the disease. As the disease progresses these treatments lose their effect, and the patient is stepwise forced into a more restricted lifestyle. In its later stages, the possibility for the patient to live a normal and independent life becomes increasingly difficult.
Due to the widespread and severity of the disease, combined with a lack of effective pharmaceutical drugs, the need for new and effective treatments is significant.
Parkinson’s disease stems from a faulty accumulation of the protein alpha-synuclein in nerve cells in the brain. When the protein aggregates it forms structures referred to as Lewy Bodies, in brain cells that produce dopamine, a neurotransmitter that is crucial to the body’s motor functions. As an effect, the nerve cells can no longer transmit correct signals, and the brain’s ability to control mobility and motoric skills are impaired.
We have developed antibody treatments targeting toxic soluble aggregates – oligomers and protofibrils – of alpha-synuclein. These forms are thought to be the most harmful species to nerve cells. Further, oligomers and protofibrils can be released from the nerve cells and move to neighboring cells, which could explain how the disease spreads in the brain. In partnership with Uppsala University, we have developed antibodies that bind selectively to the most toxic alpha-synuclein oligomers and protofibrils. The antibodies make it easier for the immune system to detect and eliminate the harmful accumulations of alpha-synuclein and could hopefully slow down the disease progression.
Projects in Parkinson’s disease
Our portfolio includes four antibody projects: exidavnemab (BAN-0805), PD1601 and PD1602, PD-BT2238.
Exidavnemab (BAN-0805) – Parkinson’s disease
Exidavenmab is a highly selective antibody that has shown an impeding effect on disease progression in preclinical model of Parkinson’s disease. A Phase 1 study with BAN0805 has showed favorable pharmacokinetics and a good safety profile for the antibody. Additionally, data from studies on brain tissue samples from patients with Parkinson’s disease show that the antibody binds to pathological alpha-synuclein. BioArctic is currently preparing for a Phase 2a study in Parkinson’s disease, planed to start in the second half of 2024.
PD1601 – Parkinson’s disease
The antibody PD1601 targets alpha-synuclein for treatment of Parkinson’s disease. The aim is to develop a disease modifying treatment that stops or slows down disease progression. BioArctic is currently investigating partnering possibilities to advance the project to late-stage clinical development.
PD1602 – Parkinson’s disease
The antibody PD1602 targets alpha-synuclein for treatment of Parkinson’s disease. The aim is to develop a disease modifying treatment that stops or slows down disease progression. BioArctic is currently investigating partnering possibilities to advance the project to late-stage clinical development.
PD-BT2238 – Parkinson’s disease
PD-BT2238 is the next generation antibody, which combines a selective alpha-synuclein oligomer targeting antibody with BioArctic’s proprietary BrainTransporter™ technology, to increase exposure of the antibody in the brain.