Current disease modifying drugs can reduce damage to myelin but can’t stop it completely or repair damage that has already happened. Laboratory studies have indicated that a potential new treatment, temelimab, could promote remyelination. Its potential in people with MS has been assessed in an early clinical trial.
270 people with relapsing remitting MS were recruited. They took one of three doses of temelimab or placebo, given as an intravenous infusion every four weeks. After 24 weeks, people in the placebo group switched to one of the three temelimab doses while those who had started on temelimab remained on their original dose. Treatment continued for up to 96 weeks.
At 24 weeks, there was no difference in the number of active lesions between the three doses of temelimab and placebo. At the end of the study, people who had taken the highest dose of temelimab throughout had fewer T1-hypointense lesions. This type of lesion, also known as a black hole, is associated with MS disability and progression. There was also a reduction in brain tissue loss and improvement in MRI markers of remyelination.
These results suggest that temelimab has little effect on the inflammatory MS activity which is responsible for relapses. However, its effect on MRI markers suggest that it may promote remyelination and prevent loss of nerves. Researchers have set up another study to evaluate temelimab further; this study is underway and results are expected in the first half of 2022.
There is a growing list of drugs for relapsing remitting MS, with Ocrevus approved for early, active primary progressive MS and Mayzent approved for active secondary progressive MS. All of these drugs act by reducing the immune attack which causes inflammation and damage to the myelin coating around nerve cells in the brain and spinal cord.
Although these drugs can reduce damage to myelin, they can’t stop it completely or repair damage that has already happened. Your body can replace damaged myelin but this process is impaired in MS. A protein (called HERV-W-ENV) found in MS lesions has been shown to reduce the brain’s ability to remyelinate cells by preventing the development of oligodendrocytes, cells which maintain the myelin coating of nerve cells; the protein also activates microglia, immune cells that cause inflammation in the brain. A potential new treatment, temelimab, blocks the action of this protein and laboratory studies have indicated that it could promote remyelination. Its potential in people with MS has been assessed in an early, phase 2, clinical trial.
270 people with relapsing remitting MS were recruited to an international study. Participants took one of three doses of temelimab or placebo, given as an intravenous infusion every four weeks. After 24 weeks, people in the placebo group switched to one of the three temelimab doses while those who had started on temelimab remained on their original dose. Treatment continued for up to 96 weeks. The main measure of the study was the number of active lesions visible on MRI scans at week 24; other measures including presence of other types of lesions, brain tissue loss (atrophy), improvement in MRI markers of remyelination (magnetization transfer ratio) were also taken during the course of the study.
At 24 weeks, there was no difference in the number of active lesions between the three doses of temelimab and placebo. People who had taken the highest dose of temelimab throughout the study had fewer T1-hypointense lesions. This type of lesion, also known as a black hole, is associated with MS disability and progression. There was also a reduction in brain tissue loss and improvement in MRI markers of remyelination.
There was no significant difference in side effects reported between people taking temelimab or placebo. Amongst those taking temelimab, one person was diagnosed with breast cancer 20 months after treatment and one person developed drug-induced liver damage which initially improved, then came back again.
These results suggest that temelimab has little effect on the inflammatory MS activity which is responsible for relapses. However, its effect on MRI markers suggest that it may promote remyelination and prevent loss of nerves.
These are encouraging results, but it is too early to draw definite conclusions. The researchers consider that the doses of temelimab used in this study were too low and that some effects of temelimab may have been masked by inflammatory MS activity. To investigate this further, they are conducting an additional study (Protect-MS) in people with relapsing remitting MS who have increased disability despite taking a highly effective disease modifying drug for at least 12 months. Participants are taking higher doses of temelimab or placebo for 48 weeks; the main aim of the study is to check that higher doses are well-tolerated, MRI markers of progression are also being captured. The study is underway and results are expected in the first half of 2022.
Hartung HP, et al.
Efficacy and safety of temelimab in multiple sclerosis: Results of a randomized phase 2b and extension study.
Multiple Sclerosis Journal 2021 Jul 9:13524585211024997 [Epub ahead of print]
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Temelimab is one of several potential treatments being developed for MS.
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