Treatment with laquinimod reduces development of active MRI lesions in relapsing MS

Abstract

Oral laquinimod in a dosage of 0.3 mg daily was well tolerated and effective in suppressing development of active lesions in relapsing multiple sclerosis.

Estriol‐mediated neuroprotection in multiple sclerosis localized by voxel‐based morphometry

“…Eligibility criteria for the trial were that patients be female, 18–50 years of age, have a diagnosis of RRMS as defined according to the McDonald criteria (Polman et al., 2005) with a baseline score of 0–4.5 on the EDSS (Kurtzke, 1983), and have active disease defined by at least two documented relapses in the previous 24 months before screening or at least one documented relapse within 24 months before screening with a history of at least one gadolinium‐enhancing lesion on a brain or spinal cord MRI performed at least 3 months prior to or 3 months after the clinical relapse. Exclusion criteria were progressive forms of MS (Lublin & Reingold, 1996), other clinically significant diseases, exposure to glatiramer acetate for longer than 2 months prior to randomization, relapse or steroid use within 30 days of randomization, use of any interferon, adrenocorticotropic hormone, corticosteroids, intravenous immunoglobulins or other DMTs within 2 months prior to randomization, prespecified laboratory test abnormalities, those who are pregnant, breast‐feeding, or trying to get pregnant, those who have undergone surgical or natural menopause for longer than 1 or 3 years, respectively, with no hormone replacement therapy, those not willing to discontinue other hormonal treatments, and those who have ever been treated with major immunosuppressive contraindicated treatments.…”

The quinoline-3-carboxamide paquinimod (ABR-215757) reduces leukocyte recruitment during sterile inflammation: Leukocyte- and context-specific effects

“…These compounds have shown efficacy in several mouse models of inflammatory autoimmune disease [29][30][31][32][33] and they are currently in clinical development for multiple sclerosis [34][35][36][37], systemic sclerosis and prostate cancer [38,39]. Recently, the S100A9 protein was identified as one molecular target of the Q-compound paquinimod (ABR-215757) [40].…”

Profile of oral laquinimod and its potential in the treatment of multiple sclerosis

“…This outcome may not have reached statistical significance due to the short duration of the trial, and could not accurately assess clinical outcomes and lack of power due to the sample size. There was no statistically significant effect on primary or secondary outcomes in the laquinimod 0.3 mg/day group vs placebo, which was surprising given the previous positive study by Polman et al 32 The authors hypothesized that this discrepancy may have been due to the previous study using triple-dose gadolinium vs the standard dose used by Comi et al, with triple dosing increasing sensitivity for active multiple sclerosis lesions and consequently the statistical power in an MRI-based trial.…”

“…32 The trial was a multicenter, double-blind, randomized study comparing two doses of laquinimod (0.1 mg/day and 0.3 mg/day) with placebo in 209 RRMS and secondary progressive multiple sclerosis patients. Inclusion criteria were patients aged 18-65 years, with an Expanded Disability Status Score of 0-5.5, and evidence of active disease with at least one documented clinical or subclinical (based on MRI) exacerbation in the last year, two exacerbations in the last 2 years (one of which could be subclinical), or presence of gadolinium-enhancing lesions on a screening MRI.…”