- The International Progressive MS Alliance is a global effort to accelerate the development of effective treatments for progressive MS.
- Two new studies funded by the Alliance have found that the repurposed drugs, bavisant and nimodipine, target different biological processes involved in nerve damage.
- These early laboratory studies provide potential new avenues for treating progressive MS.
- Australian MS neurologist and researcher Professor Tomas Kalincik will join the Alliance’s scientific leadership in 2026.
Speeding development of treatments for progressive MS
Worldwide, more than 2.9 million people live with MS. More than half of these people live with a progressive MS. Progressive MS is characterised by symptoms that progressively worsens over time.
The International Progressive MS Alliance (the Alliance) is a global initiative working to accelerate the development of effective treatments for people with progressive MS, with the aim of improving quality of life.
It brings together MS organisations, researchers, health professionals, the pharmaceutical industry, companies, trusts, foundations, donors and people affected by progressive MS from around the world. MS Australia is a managing member of the Alliance.
One important strategy of the Alliance is to test if existing medicines can be repurposed to treat progressive MS, helping to bring new treatments to people faster. Two recently published studies have progressed this goal.
Repairing myelin and protecting nerves: a new approach from existing medicines
Current MS treatments do not fully prevent the ongoing nerve damage that can lead to disability over time, particularly in progressive MS. Finding new treatments that can protect nerves and repair myelin, the insulating layer around nerve fibres, remains a major challenge.
One of the new studies, published in Science Translational Medicine, explored whether existing medicines could be ‘repurposed’ to support myelin repair and nerve protection in MS.
Using advanced computer modelling, researchers screened more than 1,500 known drugs and identified several hundred with the potential to promote myelination and protect nerve cells. These candidate drugs were then tested in a series of laboratory models, including those  that replicate key features of MS.
The researchers identified 32 drugs that helped myelin‑producing cells mature and survive, while also protecting nerve cells from damage. These drugs appeared to work through different biological pathways, suggesting there may be multiple ways to encourage repair and protection in the brain of people with MS.
One drug, bavisant, originally developed to treat sleep and wake disorders, was examined in more detail. Bavisant was tested across several laboratory models of MS‑like damage.
In these studies, bavisant improved myelin repair and reduced nerve damage, with similar effects also seen in laboratory models using human myelin‑producing cells.
This is early‑stage research, but it provides important proof‑of‑concept supporting the possibility of testing bavisant in clinical trials focused on nerve protection and repair in people with MS.
This strategy aligns closely with that of PLATYPUS, the Australian arm of the international OCTOPUS clinical trial, testing repurposed drugs for neuroprotection and remyelination in progressive MS.
How brief inflammation may lead to long‑term disability in MS
A second Alliance-funded study, published in Brain, found that even a few days of low oxygen during an acute inflammatory event – such as an MS attack –  can trigger long-term loss of grey matter and progressive disability
During periods of active inflammation in MS, some areas of the brain and spinal cord can temporarily receive less oxygen than they need. This study showed that even short periods of low oxygen in inflamed areas can have lasting effects.
The researchers found that reduced oxygen levels can initially cause temporary symptoms at first, such as weakness or sensory changes. However, they also showed that these brief oxygen shortages can trigger slow, ongoing damage to grey matter, the part of the brain that contains nerve cells. Over time, this gradual nerve cell loss can lead to steadily worsening disability, potentially becoming more severe than the original symptoms.
Importantly, the researchers also found ways to reduce this damage in experimental models. When oxygen levels were maintained during inflammation – either by briefly using a drug called nimodipine to improve blood flow, or by increasing the amount of oxygen breathed – both the immediate symptoms and the longer-term nerve damage were significantly reduced.
These findings suggest that short episodes of inflammation and low oxygen earlier in the disease course could contribute to long‑term disability in MS, but that protecting oxygen supply at the time may help limit lasting damage.
While this study was conducted in experimental models, it provides new insight into how disability may develop over time in MS and may help guide future strategies to protect nerve cells and slow disease progression.
Australia represented on the Alliance Scientific Steering Committee
Professor Tomas Kalincik has joined the Alliance’s Scientific Steering Committee as Australia’s representative.
Professor Kalincik is an MS neurologist, biostatistician and MS Australia-funded researcher with expertise in treatment and outcomes of MS, individualised therapy, prognosis and epidemiology.
He is the Dame Kate Campbell Professorial Fellow, the head of the Clinical Outcomes Research (CORe) Unit at the University of Melbourne, and Head of the MS Centre at the Royal Melbourne Hospital.
Through this role, Professor Kalincik will contribute Australian expertise to the Alliance’s international scientific direction and priorities.
What does this mean for people living with MS?
International research is making progress towards new ways to treat progressive MS. These latest studies demonstrate how coordinated global research – supported by strong Australian leadership –  can accelerate the identification of new treatment approaches, including potential new candidate for future clinical trials, and deepen understanding of the mechanisms driving disability progression in MS.
