There's a few things at least these days. But considering how many people go on to become SPMS (like most of us), you'd think that there would be even more research. Since the RRMS drugs aren't that good at stabilizing MS, you'd think they would have tried their luck at trying to stabilize it when it got to the SPMS phase. Isn't one of those newer ones in clinical trials also targeting SPMS? I can't find any info on it right now though.
Cyclophosphamide is effective in stabilizing rapidly deteriorating secondary progressive multiple sclerosis
Journal Journal of Neurology
Publisher Steinkopff
ISSN 0340-5354 (Print) 1432-1459 (Online)
Issue Volume 250, Number 7 / July, 2003
Category ORIGINAL COMMUNICATION
DOI 10.1007/s00415-003-1089-x
Pages 834-838
Subject Collection Medicine
SpringerLink Date Thursday, February 19, 2004
Authors
Paola Perini, Paolo Gallo
Abstract
The safety and efficacy of pulse cyclophosphamide (CTX) therapy was investigated in patients with very active secondary progressive multiple sclerosis, characterized by frequent relapses and rapid disability progression. For this purpose the clinical and MRI effects were assessed.
Sixteen patients, 11 female and 5 male, were experiencing rapidly deteriorating disease, characterized by frequent and severe relapses as well as rapid progression (defined by an increase of more than 1 EDSS point in a period of 1 year). Mean relapse rate in the two years preceding CTX therapy was 3.0 ±1.4. Mean EDSS was 4.0±1.4 one year before therapy and 5.6±1.0 at study entry.
Treatment consisted in administration of high dose intravenous CTX every four weeks for one year and then every eight weeks for an additional twelve months. CTX dose was tailored to the patient’s white blood cell response, and ranged from 800 to 1,200 mg/m 2 body surface. MRI was performed before therapy and then at 12 (Y1) and 24 (Y2) months. Eight patients with similar clinical features constituted a control group. CTX therapy was safe and well tolerated, and no severe side effects were observed.
The EDSS decreased to 4.3±1.6 at Y1 (Y0 vs.Y1: p< 0.001) and to 4.1±1.6 at Y2 (Y0 vs.Y2: p< 0.001). Only four patients experienced relapses during the first year of therapy, while no relapses were observed during the second year of therapy. The mean relapse rate during therapy was 0.25 ±0.45 (p< 0.0001).No increase in T2 lesion load was observed over the two years. A significant clinical and MRI deterioration was observed in the control group.
Therapy with pulse CTX was able to stop disease activity and progression in patients with rapidly evolving secondaryprogressive MS.
http://www.springerlink.com/content/wdea7ebbpu399hy1/
General Information
Novantrone has been approved for use in reducing neurologic disability and/or the frequency of relapses in patients with secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis (i.e., patients whose neurologic status is significantly abnormal between relapses). Novantrone is not indicated for the treatment of patients with primary progressive multiple sclerosis.
White blood cells can produce the symptoms of multiple sclerosis by attacking myelin, a fatty substance that surrounds nerve cells. Novantrone suppresses the activity of T and B cells, and in this manner slows the progression of the disease and reduces the frequency of relapses.
Multiple sclerosis is diagnosed in over 350,000 people in the United States. There is no one group of people who "get" multiple sclerosis; however, trends show that it often strikes between the ages of 30 and 50, and affects mostly women. Multiple sclerosis is most commonly found in Canada, the United States, South America, and Europe. (from the Multiple Sclerosis Foundation)
Clinical Results
The safety and effectiveness of Novantrone in multiple sclerosis were assessed in two randomized, controlled multicenter trials. One trial was conducted in subjects with secondary progressive or progressive relapsing multiple sclerosis. Neurological disability was evaluated based on the Kutzke Expanded Disability Status Scale (EDSS). This scale ranges from 0.0 to 10.0, with increasing scores indicating worsening condition. Subjects receive a placebo, 5 mg/m2 Novantrone, or 12 mg/m2 Novantrone administered intravenously every three months for two years. At 24 months, the mean EDSS change (month 24 value minus baseline) was 0.23 for the placebo group, -0.23 for 5 mg/m2, and -0.13 for 12 mg/m2.
A second trial evaluated Novantrone in combination with methylprednisolone (MP) and was conducted in subjects with secondary progressive or worsening relapsing-remitting multiple sclerosis who had residual neurological deficit between relapses. A total of 42 subjects received monthly treatments of 1g of intravenous MP alone or approximately 12 mg/m2 of intravenous Novantrone plus 1 g of intravenous MP for six months. Subjects were evaluated monthly, and study outcome was determined after six months. The primary measure of effectiveness was a comparison of the proportion of subjects in each treatment group who developed no new Gd-enhancing MRI lesions at six months. Thirty-one percent of subjects receiving MP alone were without new Gd-enhancing lesions on MRIs, while 90% of subjects receiving Novantrone plus MP were without lesions. (from Novantrone Package Insert)
Side Effects
Possible adverse events associated with Novantrone include (but are not limited to) the following:
Nausea
Hair loss
Hypotension (low blood pressure)
Rashes
Urinary tract infection
Menstrual disorder
Mechanism of Action
Mitoxantrone, a DNA-reactive agent that intercalates into deoxyribonucleic acid (DNA) through hydrogen bonding, causes crosslinks and strand breaks. Mitoxantrone also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, an enzyme responsible for uncoiling and repairing damaged DNA. It has a cytocidal effect on both proliferating and nonproliferating cultured human cells, suggesting lack of cell cycle phase specificity.
Novantrone has been shown in vitro to inhibit B cell, T cell, and macrophage proliferation and impair antigen presentation, as well as the secretion of interferon gamma, TNFa, and IL-2.
http://www.centerwatch.com/patient/drugs/dru651.html