A world without  ALS
A world without  Parkinson’s

What is amyotrophic lateral sclerosis (ALS)?

ALS is a fatal neurodegenerative disease that affects nerve cells in the brain and spinal cord causing progressive paralysis of voluntary muscles leading to respiratory failure and death within 3-5 years of diagnosis.

Globally, an estimated 220,000 people suffered from ALS in 2015, and that number is projected to increase by 69% to over 370,000 by 2040(1)

There are no effective therapies approved for the prevention or delay of ALS disease progression

This is why we created BSP

What is Parkinson’s disease (PD)?

PD is a debilitating neurodegenerative condition that is the second most prevalent neurodegenerative disorder:

In 2016, an estimated 6.1 million people suffered from PD globally, with rates predicted to increase to between 12.9 and 14 million by 2040.(2)

That same year approximately one third of the globally recorded PD cases could be attributed to USA, Australia and the EU, alone (~1.9 million).

There are no approved disease modifying therapies for PD

This is why we created BSP

At BSP our team of scientists are discovering genetic markers that enable a deeper understanding of how gene expression can affect disease aetiology, duration, progression and improve patient outcomes.

We are able to use these highly informative markers to determine disease risk and modification and identify novel drug targets. Our next steps is then to design in-house antisense RNA-based therapeutics for the patient community.

By using these unique genetic markers in combination with our antisense oligonucleotide (AO) therapeutics we know that this is a better way of discovering truly effective therapies for our patients.

We know that the patients are waiting

(1) Economics, D.A., Economic analysis of motor neurone disease in Australia. 2015

(2) Dorsey, E.R., et al., Global, regional, and national burden of Parkinson’s disease, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet Neurology, 2018. 17(11): p. 939-953