TY - JOUR
T1 - Clemastine fumarate as a remyelinating therapy for multiple sclerosis (ReBUILD)
T2 - a randomised, controlled, double-blind, crossover trial
AU - Green, Ari J.
AU - Gelfand, Jeffrey M.
AU - Cree, Bruce A.
AU - Bevan, Carolyn
AU - Boscardin, W. John
AU - Mei, Feng
AU - Inman, Justin
AU - Arnow, Sam
AU - Devereux, Michael
AU - Abounasr, Aya
AU - Nobuta, Hiroko
AU - Zhu, Alyssa
AU - Friessen, Matt
AU - Gerona, Roy
AU - von Büdingen, Hans Christian
AU - Henry, Roland G.
AU - Hauser, Stephen L.
AU - Chan, Jonah R.
N1 - Funding Information:
JMG reports grants and personal fees from Genentech, grants from Quest Diagnostics and MedImmune, and personal fees from Medical Legal Consulting, outside the submitted work. BAC reports personal fees for consulting from Abbvie, Biogen, EMD Serono, Novartis, Sanofi Genzyme, and Shire, outside the submitted work. HCvB reports that he is adjunct faculty at University of California San Francisco, and since March, 2016, a full-time employee of F Hoffman-La Roche. RGH reports grants from Roche-Genentech and personal fees from Sanofi-Genzyme, Novartis, Abbvie, and Teva, outside the submitted work. SLH serves on the Scientific Advisory Boards for Annexon, Symbiotix, Bionure, and Molecular Stethoscope. He is on the Board of Trustees for Neurona Therapeutics. SLH has also received travel reimbursement and writing assistance from F Hoffman-La Roche for CD20-related meetings and presentations. AJG reports grants and other support from Inception Biosciences, other support from MedImmune, grants from the National MS Society and US National Institutes of Health, other support from Mylan, Sandoz, Dr Reddy, Amneal, Momenta, Synthon, JAMA Neurology , and Bionure, outside the submitted work. All other authors have no competing interests.
Publisher Copyright:
© 2017 Elsevier Ltd
PY - 2017/12/2
Y1 - 2017/12/2
N2 - Background Multiple sclerosis is a degenerative inflammatory disease of the CNS characterised by immune-mediated destruction of myelin and progressive neuroaxonal loss. Myelin in the CNS is a specialised extension of the oligodendrocyte plasma membrane and clemastine fumarate can stimulate differentiation of oligodendrocyte precursor cells in vitro, in animal models, and in human cells. We aimed to analyse the efficacy and safety of clemastine fumarate as a treatment for patients with multiple sclerosis. Methods We did this single-centre, 150-day, double-blind, randomised, placebo-controlled, crossover trial (ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neuropathy on stable immunomodulatory therapy. Patients who fulfilled international panel criteria for diagnosis with disease duration of less than 15 years were eligible. Patients were randomly assigned (1:1) via block randomisation using a random number generator to receive either clemastine fumarate (5·36 mg orally twice daily) for 90 days followed by placebo for 60 days (group 1), or placebo for 90 days followed by clemastine fumarate (5·36 mg orally twice daily) for 60 days (group 2). The primary outcome was shortening of P100 latency delay on full-field, pattern-reversal, visual-evoked potentials. We analysed by intention to treat. The trial is registered with ClinicalTrials.gov, number NCT02040298. Findings Between Jan 1, 2014, and April 11, 2015, we randomly assigned 50 patients to group 1 (n=25) or group 2 (n=25). All patients completed the study. The primary efficacy endpoint was met with clemastine fumarate treatment, which reduced the latency delay by 1·7 ms/eye (95% CI 0·5–2·9; p=0·0048) when analysing the trial as a crossover. Clemastine fumarate treatment was associated with fatigue, but no serious adverse events were reported. Interpretation To our knowledge, this is the first randomised controlled trial to document efficacy of a remyelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis. Our findings suggest that myelin repair can be achieved even following prolonged damage. Funding University of California, San Francisco and the Rachleff Family.
AB - Background Multiple sclerosis is a degenerative inflammatory disease of the CNS characterised by immune-mediated destruction of myelin and progressive neuroaxonal loss. Myelin in the CNS is a specialised extension of the oligodendrocyte plasma membrane and clemastine fumarate can stimulate differentiation of oligodendrocyte precursor cells in vitro, in animal models, and in human cells. We aimed to analyse the efficacy and safety of clemastine fumarate as a treatment for patients with multiple sclerosis. Methods We did this single-centre, 150-day, double-blind, randomised, placebo-controlled, crossover trial (ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neuropathy on stable immunomodulatory therapy. Patients who fulfilled international panel criteria for diagnosis with disease duration of less than 15 years were eligible. Patients were randomly assigned (1:1) via block randomisation using a random number generator to receive either clemastine fumarate (5·36 mg orally twice daily) for 90 days followed by placebo for 60 days (group 1), or placebo for 90 days followed by clemastine fumarate (5·36 mg orally twice daily) for 60 days (group 2). The primary outcome was shortening of P100 latency delay on full-field, pattern-reversal, visual-evoked potentials. We analysed by intention to treat. The trial is registered with ClinicalTrials.gov, number NCT02040298. Findings Between Jan 1, 2014, and April 11, 2015, we randomly assigned 50 patients to group 1 (n=25) or group 2 (n=25). All patients completed the study. The primary efficacy endpoint was met with clemastine fumarate treatment, which reduced the latency delay by 1·7 ms/eye (95% CI 0·5–2·9; p=0·0048) when analysing the trial as a crossover. Clemastine fumarate treatment was associated with fatigue, but no serious adverse events were reported. Interpretation To our knowledge, this is the first randomised controlled trial to document efficacy of a remyelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis. Our findings suggest that myelin repair can be achieved even following prolonged damage. Funding University of California, San Francisco and the Rachleff Family.
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U2 - 10.1016/S0140-6736(17)32346-2
DO - 10.1016/S0140-6736(17)32346-2
M3 - Article
C2 - 29029896
AN - SCOPUS:85030841529
SN - 0140-6736
VL - 390
SP - 2481
EP - 2489
JO - The Lancet
JF - The Lancet
IS - 10111
ER -