National Academies Press: OpenBook

Multiple Sclerosis: Current Status and Strategies for the Future (2001)

Chapter: Appendix E: Drugs Used in the Treatment of MS

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Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Appendix E

Drugs Used in the Treatment of MS

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 388

APPROVED DISEASE-MODIFYING MEDICATIONS

Generic Name

Trade Name

Company

Indication

Mechanism of Action

Potential Side Effects

Beta-Interferon-1a

Avonex, Rebifa

Biogen, Serono

RRMS

Beta-interferon-1a is believed to suppress the autoimmune destruction of myelin. Slows accumulation of disability and decreases the frequency of clinical exacerbations. Interferon-β-1a is involved in the regulation of activation, proliferation, migration, and suppressor cell function of T-cells, the modulation of the production of cytokines, including down-regulation of proinflammatory cytokines and up-regulation of inhibitory, antiinflammatory cytokines.

Flu-like symptoms, muscle aches, fever, chills and weakness, pain from intramuscular injection

Beta-Interferon-1b

Betaseron

Berlex Labs (Distributor)

Chiron (Manufacturer)

RRMS

Possesses both antiviral and immunoregulatory activities, mediated through interactions with specific cell receptors, which results in the expression of interferon-induced gene products.

Redness, pain and swelling and discoloration at injection site, flu-like symptoms, depression, anxiety, depersonalization, suicide attempts

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 389

Glatiramer acetate

Copaxone

Teva Marion Partners

RRMS

Blocks myelin-specific autoimmune responses. Non-steroidal, non-interferon. Mechanism uncertain, but it is thought that glatiramer acetate, consisting of the acetate salts of synthetic polypeptides, resembles myelin basic protein (mbp) and serves as a decoy that blocks myelin damaging T cells.

Redness, pain and swelling and discoloration at injection site, flushing, chest pain, weakness, infection, pain, nausea, joint pain, anxiety and muscle stiffness, Immediate postinjection reaction characterized by chest tightness with heart palpitations and difficulty breathing



Note: Avonex, Betaseron, Copaxone, and Rebif are “orphan drugs.” The 1983 Orphan Drug Act (ODA) provides incentives for sponsors to develop products for rare diseases or conditions, by guaranteeing the developer of an orphan product seven years of market exclusivity following the approval of the product by the FDA. The definition of “rare disease or condition” in the Orphan Drug Act: “...the term rare disease or condition means any disease or condition which (a) affects less than 200,000 persons in the U.S. or (b) affects more than 200,000 persons in the U.S. but for which there is no reasonable expectation that the cost of developing and making available in the U.S. a drug for such disease or condition will be recovered from sales in the U.S. of such a drug.”

aRebif has been approved by the European Commission for the treatment of relapsing-remitting multiple sclerosis. The FDA has upheld the Orphan Drug Act and has not granted approval to Rebif. The FDA also had questions about the data filed in the marketing application, which prevented granting tentative approval. If tentative approval is received, Rebif could enter the US market in 2003, when the exclusivity periods for Avonex and Betaseron end.
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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AVAILABLE AND EMERGING DISEASE-MODIFYING THERAPIES a

GLOBAL IMMUNOSUPPRESSION

Medication Options

Status as of 1999

Putative Mechanisms Of Action

Cyclophosphamide

Off label use in the U.S. and Europe

Global reduction of T-cell population

Azathioprine

Off label use in the U.S. and Europe

As above

Glucocorticosteroids

Off label use in the U.S. and Europe

As above

Methotrexate

Off label use in the U.S. and Europe

As above

Total lymphoid irradiation

Off label use in the U.S. and Europe

As above

Paclitaxel

Phase II Clinical Trials

As above

2-Chlorodeoxyadenosine

Phase III Clinical Trials

As above

Mitoxantrone

Phase III Clinical Trials

As above

IMMUNOMODULATION

Therapeutic Strategy

Medication Options

Status as of 1999

Putative Mechanisms Of Action

1) Inhibit T-cell receptor/peptide/MHC-II interaction

Altered peptide ligands

Phase I/II

Block or compete with the binding of encephalitogenic peptides to the MHC-II molecule

Copolymer

Approved for relapsing forms of MS in the U.S. and Europe

Block or compete with the binding of encephalitogenic peptides to the MHC-II molecule

TCR vaccination and TCR peptide vaccination

Phase I

Generation of antibodies against peptides within the TCR

IL-10 , TGF b

Phase I/II

Immunomodulation; reduce MHC-II molecule expression

Interpheron Beta

Approved for relapsing forms of MS in the U.S. and Europe

Immunomodulation; reduce MHC-II molecule expression

2) Induction of T-cell anergy

Antibodies to B7 or molecules

Preclinical testing

T cells are anergised when TCR/peptide/ MHC-II interaction occurs in the absence of co-signalling

aAdapted from Waubant and Goodkin 1997.
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Soluble MHC-II/ peptide complexes

Phase I

T cells are anergised when TCR/peptide/ MHC-II interaction occurs in the absence of co-signalling

3) Deletion of autoreactive T cells

Anti-CD4, anti-CD52

Phase I/II

Depletion of T cells targeted by the antibodies

4) Reduce T-cell trafficking across blood-brain-barrier (BBB)

Glucocorticosteroids

Unlabelled use in the U.S. and Europe

Decrease the expression of adhesion molecules on T cells and vascular endothelial cells

TGF b

Phase I/II

Decrease the expression of adhesion molecules on T cells and vascular endothelial cells

Interpheron Beta

Approved for relapsing forms of MS in the U.S. and Europe

Decrease the expression of adhesion molecules on T cells and vascular endothelial cells

Antibodies to adhesion molecules (Antegren, antiCD11/CD18)

Phase II

Decrease the attachment of T cells to vascular endothelial cells

Matrix metalloprotease inhibitors

Phase I

Inhibit proteases that facilitate T-cell trafficking across BBB

5) Alter the balance of pro-inflammatory (Th1) and immunomodulatory (Th2) cytokines

Antibodies to TNFa, IL-1

Phase I/II

Reduce proinflammatory (Th1) cytokine activity

Soluble IL-2 or TNFa receptors

Phase I/II

Reduce proinflammatory (Th1) cytokine activity

Antagonists to IL-1 receptor

Preclinical testing

Reduce proinflammatory (Th1) cytokine activity

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 392

Oral myelin

Testing discontinued; phase III trial revealed no difference between active and placebo groups

Increases immunomodulatory (Th2) cytokine production

Interpheron Alpha

Phase I

Antagonise production of proinflammatory cytokines induced by IFNg

Interpheron Beta

Approved for relapsing forms of MS in the U.S. and Europe

Reduce Th1 cytokine secretion and macrophage function

Glucocorticosteroids

Unlabelled use in the U.S. and Europe

Reduce Th1 cytokine secretion and macrophage function

Matrix metalloprotease inhibitors

Phase I

Block cleavage of pro-TNF to TNF

Methotrexate

Unlabelled use in the U.S. and Europe

Reduces level of soluble IL-2 receptor

Intravenous immunoglobulin

Unlabelled use in the U.S. and Europe, Phase III

Reduction of proinflammatory cytokines

Anti-CD40 ligand

Preclinical testing

Blocks Th1 differentiation and effector function, inhibits IFNg production

Roquinimex (Linomide)

Testing discontinued; phase III trial revealed an increase in heart attacks associated with this drug

Inhibits TNF production

6) Neuroprotection

Riluzole, Insulin-like growth factor (IGF-1)

Eliprodil

Phase I

Preclinical testing

Prevent neuronal death

Prevent neuronal death

7) Reduces gliosis

Pirfenidone

Phase I

Prevents gliosis, blocks TNF synthesis

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 393

8) Promote remyelination

IGF-1

Phase I

Promotes oligodendrocyte survival and maturation of precursors in vitro

Intravenous immunoglobulin

Unlabelled use in the U.S. and Europe, Phase III

Promote remyelination

Oligodendrocyte grafts

Preclinical testing

Promote remyelination

Eliprodil

Preclinical testing

Promote remyelination

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 394

ONGOING CLINICAL TRIALS FOR MEDICATIONS IN DEVELOPMENTAS OF AUGUST 2000

Trade Name

Generic Name

Company

Phase a

About the trial

Source

Anergix

HLA-DR2 MHC II

Corixa

I

Anergix consists of complexes of MHC Class II molecules, called Soluble DR2-MBP84-102 Complexes. The complexes contain autoantigenic peptides that shut down the MBP reactive T cells that damage myelin components, without compromising other T cells required for immune protection of the individual taking the drug. The phase I trial in chronic progressive MS was completed by Anergen in 1998. Anergix was shown to be safe and well tolerated with no signs of generalized immune suppression. Corixa is looking for a partner to initiate Phase II.

PhRMA (Pharmaceutical Research and Manufacturers of America) Database b

Antegren

Natalizumab

Elan CorporationAthena Neurosciences

II

Antegren is a humanized antibody that blocks a receptor on leukocytes and thus blocks their migration into the brain. This can reverse paralysis and reduce myelin destruction in the EAE animal model of MS. Ongoing phase II testing has shown that patients treated with Antegren showed a significant reduction in new brain lesions over 12 weeks.

PhRMA Database, UCSF MS Center c

Fampridine d Neurelan

4-Amino pyridine

Acorda Therapeutics

II

Fampridine's major action is to block specialized potassium channels on axons. In a demyelinated axon, large numbers of potassium channels are exposed, and nerve transmission is impaired. Fampridine has been shown to increase nerve conduction in impaired and demyelinated axons, and to result in improved neurological function in animal and in vitro studies. A phase II trial was successfully completed in 1998, and additional phase II trials are underway.

FDA—Office of Orphan Products Development

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Leukarrest

HU23F2G recombinant humanized MAb

ICOS

II

Leukarrest is a humanized antibody that impedes white blood cell movement from the blood stream to the surrounding tissue by binding to CD 11 and CD 18 on the white blood cell surface. Two phase II trials were recently completed in patients with acute symptomatic episodes of MS.

PhRMA Database

Leustatin

2-CDA / Cladribine

Ortho Biotech

III

Cladribine is a potent immunosuppressive drug that has been shown to decrease total lymphocyte count and CD4, CD8 and CD19 subsets. Cladribine may benefit people with Chronic Progressive MS, according to the results of a pilot study, but toxicity is a concern.

PhRMA Database, FDA

Myotrophin

Insulin-like growth factor I (IGF-I)

Cephalon

I

IGF-1 promotes the proliferation, differentiation and survival of oligodendrocytes, and reduces inflammation and TNF-alpha induced oligodendrocyte and myelin damage. IGF-I treatment has been shown to reduce lesion severity and promote myelin regeneration in the experimental autoimmune encephalomyelitis (EAE) model. Cephalon is developing Myotropin for use in amyotrophic lateral sclerosis (ALS), and is exploring the drug's potential for use in MS.

ClinicalTrials.gov Database, e UCSF MS Center

Novantrone

Mitoxantrone

Immunex

III

Novantrone suppresses T cells and B cells, which are key components of the immune system and multiple sclerosis. Immunex has filed a new drug application (NDA) with the FDA for approval to label Novantrone for use in treatment of secondary progressive MS. The FDA has assigned priority review status to the application, indicating that the FDA will act on the application within 6 months of the June 7, 1999 filing date. On January 28, 2000, the FDA Peripheral and Central Nervous System Drugs Advisory Panel unanimously recommended that Novantrone be approved.

PhRMA Database

Deskar

Pirfenidone

Marnac

I

Pirfenidone is an anti-fibrotic agent which is also in clinical trials for pulmonary fibrosis. It acts to inhibit the production of tumor necrosis factor (TNF), and reduces gliosis and astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.

UCSF MS Center

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 396

Rebif

Recombinant interferonbeta-1a

Serono Laboratories

III

Rebif has been approved by the European Commission for the treatment of Relapsing Remitting Multiple Sclerosis. The FDA has upheld the Orphan Drug Act and has not granted approval to Rebif. The FDA also had questions about the data filed in the marketing application, which prevented granting tentative approval. If tentative approval is received, Rebif could enter the US market in 2003, when the exclusivity periods for Avonex and Betaseron end.

PhRMA Database

Rilutek

Riluzole

Rhone Pulenc Rorer

I

Rilutek is neuroprotective in various in vivo experimental models of neuronal injury involving excitotoxic mechanisms. In in vitro tests, Riluzole protected cultured rat motor neurons from the excitotoxic effects of glutamic acid and prevented the death of cortical neurons induced by anoxia.

UCSF MS Center

Taxol

Paclitaxel

Angiotech

II

Paclitaxel is an immuno suppress ant. According to preliminary results from the treatment extension phase of the phase I/II clinical study of paclitaxel for the treatment of secondary progressive multiple sclerosis, patients showed a significant improvement in all tests undertaken. Study measures included functional testing, quality of life measures and changes in the amount of brain tissue scarring demonstrated by magnetic resonance imaging (MRI). A 189 patient, phase II clinical study is underway.

UCSF MS Center

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 397

TM27

ATM027 humanized Mab

Astra Zeneca/ Avant Immuno-Therapeutics

I/II

T Cell Receptor Monoclonal Antibody (MAb) under development. Astra Zeneca has discontinued the development of this T cell antigen receptor monoclonal antibody because results of a phase II trial suggested that the reduction of disease activity in the trial was not sufficient to warrant further study. The company is considering whether to development the T cell antigen receptor peptide as a MS vaccine.

PhRMA Database

Thalidomide

Thalomid

Andrulis Pharmaceuticals

II

Thalidomide suppresses the production of cytokines that are found in the cerebrospinal fluid of patients with MS, and especially Chronic Progressive MS.

PhRMA Database

Zenapax

Daclizumab

Interleukin-2 Receptor Alpha humanized Mab

Hoffman-La Roche, Inc.

I/II

Zenapax binds to protein receptors on lymphocytes, keeping them from interacting with interleukin-2, a substance necessary for their growth. As a result, the T lymphocytes are unable to attack the myelin sheath. Zenapax was developed as an immune modulating drug for use after transplantation. In two Phase III clinical trials, Zenapax was effective in reducing the incidence of acute rejection episodes within six months of kidney transplantation, the primary endpoint, when administered with standard immunosupressive drug regimens.

ClinicalTrials.gov Database

BB-3644

British Biotech/ Schering Plough

I

BB-3364 is a matrix metalloproteinase (MMP) inhibitor that also inhibits leukocyte migration to the CNS. Its development is based on the theory that MMPs may contribute to the pathology of MS. BB-3644 also inhibits tumor necrosis factor production.

UCSF MS Center

IR 208 therapeutic vaccine

Immune Response Corporation

I

The vaccine consists of an immunostimulant, Incomplete Freund's Adjuvant, combined with synthetic peptides. The vaccine is designed to halt the T-cell attack on myelin by shutting down specific T cells and inhibit further damage.

PhRMA Database

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 398

MSP-771

Neurocrine Biosciences/ Novartis

II

MSP-771 is an altered peptide ligand based on the immunodominant epitope of human MBP. Immune responses directed against this epitope may be involved in the pathogenesis of MS. In vitro, MSP-771 fails to induce T-cell proliferation and selectively reduces the production of inflammatory cytokines by pathogenic T cells. In the EAE model, MSP-771 markedly reduces the severity of disease and induces a specific T-cell response that down-regulates the inflammatory process. The molecule was well tolerated in a phase I study, with the most common side effect being local, transient injection site reactions. The primary endpoint in current clinical trials is the progression or regression of lesions in the brains of these patients as measured by MRI. As a secondary endpoint, clinical investigators will look for the generation of a protective immune response as shown in the Phase I trials.

PhRMA Database

Interleukin-10 (IL-10)

Schering-Plough

I/II

IL-10 has a number of inhibitory functions such as inhibiting interferon g production, antigen presentation, and the production by macrophages of the cytokines IL-1, IL-6 and TNFa.

UCSF MS Center

DEFINITIONS

Preclinical testing. A pharmaceutical company conducts laboratory and animal studies to show biological activity of the compound against the targeted disease, and the compound is evaluated for safety.

Phase I. Tests that involve about 20 to 80 normal, healthy volunteers. The tests study a drug's safety profile, including the safe dosage range. The studies also determine how a drug is absorbed, distributed, metabolized, and excreted as well as the duration of its action.

Phase II. Controlled trials of approximately 100 to 300 volunteer patients (people with the disease) assess a drug's effectiveness.

Phase III. Tests involving 1,000 to 3,000 patients in clinics and hospitals. Physicians monitor patients closely to confirm efficacy and identify adverse events.

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Page 399

aClinical trial phases are defined at the end of this table.
bThe PhRMA (Pharmaceutical Research and Manufacturers of America) Database lists only clinical trials being conducted in private firms in the U.S. Clinical trials at academic health centers and universities are not included.
chttp://mscenter.ucsf.edu
dListed as an orphan drug by FDA, http://www.fda.gov/orphan.
e The ClinicalTrials.gov Database contains clinical studies sponsored primarily by the National Institutes of Health. In the future, additional studies from other Federal agencies and the pharmaceutical industry will be included.

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
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Drugs Used to Treat Various Symptoms: Overview

Bladder Control

Capsaicin

Desmopressin

Detrol

Dicyclomine hydrochloride

Hyoscyamine

Imipramine

Oxybutynin chloride

Propantheline bromide

Depression

Amitriptyline

Bupropion hydrochloride

Imipramine

Nortriptyline

Paroxetine

Fluoxetine hydrochloride

Sertraline

Dysesthesia-Paresthesia, trigeminal neuralgia, pruritis

Amitriptylene

Carbamazepine

Gabapentin

Hydroxyzine

Phenytoin

Erectile Dysfunction-Impotence

Sildenafil citrate

Alprostadil

Papaverine

Fatigue

Amantadine

Fluoxetine hydrochloride

Modafinil

Pemoline

Inflammation

Azathioprine

Dexamethasone

Methylprednisolone

Prednisone

Optic Neuritis

Methylprednisolone

Prednisone

Decadron

Seizures

Carbamazepine

Klonopin

Gabapentin

Phenytoin

Spasticity and Tremor

Baclofen

Botulinum Toxin A

Klonopin

Dantrolene

Gabapentin

Urinary Tract Infections

Methenamine

Vertigo

Meclizine hydrochloride

Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 387
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 388
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 389
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 390
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 391
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 392
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 393
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 394
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 395
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 396
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 397
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 398
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
Page 399
Suggested Citation:"Appendix E: Drugs Used in the Treatment of MS." Institute of Medicine. 2001. Multiple Sclerosis: Current Status and Strategies for the Future. Washington, DC: The National Academies Press. doi: 10.17226/10031.
×
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Next: Appendix F: U.S. Social Security Administration's Criteria for Qualifying as Disabled from MS »
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Multiple sclerosis is a chronic and often disabling disease of the nervous system, affecting about 1 million people worldwide. Even though it has been known for over a hundred years, no cause or cure has yet been discovered—but now there is hope. New therapies have been shown to slow the disease progress in some patients, and the pace of discoveries about the cellular machinery of the brain and spinal cord has accelerated.

This book presents a comprehensive overview of multiple sclerosis today, as researchers seek to understand its processes, develop therapies that will slow or halt the disease and perhaps repair damage, offer relief for specific symptoms, and improve the abilities of MS patients to function in their daily lives.

The panel reviews existing knowledge and identifies key research questions, focusing on:

  • Research strategies that have the greatest potential to understand the biological mechanisms of recovery and to translate findings into specific strategies for therapy.
  • How people adapt to MS and the research needed to improve the lives of people with MS.
  • Management of disease symptoms (cognitive impairment, depression, spasticity, vision problems, and others).

The committee also discusses ways to build and financially support the MS research enterprise, including a look at challenges inherent in designing clinical trials. This book will be important to MS researchers, research funders, health care advocates for MS research and treatment, and interested patients and their families.

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