|
|
||||||||
From the Departments of Clinical Neuroscience (Drs. Andersen, Lycke, Svenningsson, and Runmarker), Radiology (Drs. Tollesson and Ekholm), and Clinical Chemistry (Dr. Svenningsson), University of Goteborg, Goteborg, Sweden, and Pharmacia Oncology Immunology (Mr. Linde, Mr. Angstromstrom, and Dr. Gjorstrup), Lund, Sweden.
Supported by Pharmacia and the Multiple Sclerosis Society (NHR) of Goteborg.
Received March 1, 1996. Accepted in final form April 5, 1996.
Address correspondence and reprint requests to Dr. Jan Lycke, Neurology, Department, University of Goteborg, Sahlgrenska Hospital, S-413 45 Goteborg, Sweden.
The synthetic immunomodulator Linomide, a quinoline-3-carboxamide, has a profound inhibitory influence in several experimental autoimmune diseases, including acute and chronic experimental allergic encephalomyelitis. In a double-blind trial, 31 patients with relapsing-remitting multiple sclerosis were randomized to oral doses of 2.5 mg Linomide or placebo once a day for six months. Fourteen patients receiving Linomide and 14 receiving placebo completed the trial, and the results were based on this population. The mean number of active (new and enlarged T2 weighted) lesions per monthly MRI scan was 1.37 in the patients receiving Linomide and 4.22 in the patients receiving placebo (p = 0.043). The percentage of scans with active MRI lesions was lower in the Linomide-treated group (p = 0.0064). When neurologic deficit was assessed by the Regional Functional Scoring System (RFSS), the Linomide group showed an improvement of 1% of the maximal RFSS range and the placebo group a deterioration of 0.2% (p = 0.14). There were three patients with relapses in the Linomide-treated group and six in the placebo group (p = 0.22). A slightly decreased proportion of natural killer cells in cerebrospinal fluid and peripheral blood was noted in the Linomide group. A severe adverse event of pleuropericarditis occurred in one of the Linomide-treated patients. The most frequent adverse event was musculoskeletal pain, of mild to severe degree, which tended to diminish after three months on Linomide therapy.
NEUROLOGY 1996;47: 895-900
This article has been cited by other articles:
![]() |
L Bonzano, L Roccatagliata, G. Mancardi, and M. Sormani Gadolinium-enhancing or active T2 magnetic resonance imaging lesions in multiple sclerosis clinical trials? Multiple Sclerosis, September 1, 2009; 15(9): 1043 - 1047. [Abstract] [PDF] |
||||
![]() |
J. A. Cohen Emerging Therapies for Relapsing Multiple Sclerosis Arch Neurol, July 1, 2009; 66(7): 821 - 828. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Tuvesson, I. Hallin, R. Persson, B. Sparre, P. O. Gunnarsson, and J. Seidegard CYTOCHROME P450 3A4 IS THE MAJOR ENZYME RESPONSIBLE FOR THE METABOLISM OF LAQUINIMOD, A NOVEL IMMUNOMODULATOR Drug Metab. Dispos., June 1, 2005; 33(6): 866 - 872. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Polman, F. Barkhof, M. Sandberg-Wollheim, A. Linde, O. Nordle, T. Nederman, and for the Laquinimod in Relapsing MS Study Group Treatment with laquinimod reduces development of active MRI lesions in relapsing MS Neurology, March 22, 2005; 64(6): 987 - 991. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Noseworthy, J. S. Wolinsky, F. D. Lublin, J. N. Whitaker, A. Linde, P. Gjorstrup, and H. C. Sullivan Linomide in relapsing and secondary progressive MS: Part I: Trial design and clinical results Neurology, May 9, 2000; 54(9): 1726 - 1733. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. S. Wolinsky, P. A. Narayana, J. H. Noseworthy, F. D. Lublin, J. N. Whitaker, A. Linde, P. Gjorstrup, and H. C. Sullivan Linomide in relapsing and secondary progressive MS: Part II: MRI results Neurology, May 9, 2000; 54(9): 1734 - 1741. [Abstract] [Full Text] [PDF] |
||||
![]() |
I L Tan, G J L. Nijeholt, C H Polman, H J Ader, F Barkhof, and the 95 Line 146/147 Study Group Linomide in the treatment of multiple sclerosis: MRI results from prematurely terminated phase-III trials Multiple Sclerosis, April 1, 2000; 6(2): 99 - 104. [Abstract] [PDF] |
||||
![]() |
M. J Hohol, M. J Olek, E J. Orav, L. Stazzone, D. A Hafler, S. J Khoury, D. M Dawson, and H. L Weiner Treatment of progressive multiple sclerosis with pulse cyclophosphamidel methylprednisolone: Response to therapy is linked to the duration of progressive disease Multiple Sclerosis, December 1, 1999; 5(6): 403 - 409. [Abstract] [PDF] |
||||
![]() |
Y. Miki, R. I. Grossman, J. K. Udupa, L. Wei, M. Polansky, L. J. Mannon, and D. L. Kolson Relapsing-Remitting Multiple Sclerosis: Longitudinal Analysis of MR Images-Lack of Correlation between Changes in T2 Lesion Volume and Clinical Findings Radiology, November 1, 1999; 213(2): 395 - 399. [Abstract] [Full Text] |
||||
![]() |
P. F Smith and C. L Darlington Recent developments in drug therapy for multiple sclerosis Multiple Sclerosis, April 1, 1999; 5(2): 110 - 120. [Abstract] [PDF] |
||||
![]() |
J. N Whitaker Myelin basic protein-like material in the urine of multiple sclerosis patients: relationships to clinical and neuroimaging changes Multiple Sclerosis, June 1, 1998; 4(3): 243 - 246. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |