Mitoxantrone (tradename Novantrone)is used to treat multiple sclerosis (MS), most notably the subset of the disease, known as secondary-progressive MS. As no cure for multiple sclerosis exists yet, it must be understood mitoxantrone will not cure the disease, but rather is effective in slowing the progression of secondary-progressive MS and extending the time between relapses in both relapsing-remitting MS and progressive-relapsing MS. [from Wikipedia)
Although Novantrone was approved by the FDA for secondary progressive multiple sclerosis, because of the significant risks associated with Novantrone, it is rarely used at this time.
Note the abstract for US Patent 7,968,511:
The subject invention provides a method of treating a subject afflicted with a form of multiple sclerosis comprising periodically administering to the subject an amount of glatiramer acetate and an amount of mitoxantrone, wherein the amounts when taken together are effective to alleviate a symptom of the form of multiple sclerosis in the subject so as to thereby treat the subject. The subject invention also provides a package comprising glatiramer acetate, mitoxantrone and instructions for use of the together to alleviate a symptom of a form of multiple sclerosis in a subject. Additionally, the subject invention provides a pharmaceutical composition comprising an amount of glatiramer acetate and an amount of mitoxantrone, wherein the amounts when taken together are effective to alleviate a symptom of a form of multiple sclerosis in a subject. The subject invention further provides a pharmaceutical combination comprising separate dosage forms of an amount of glatiramer acetate and an amount of mitoxantrone, which combination is useful to alleviate a symptom of a form of multiple sclerosis in a subject.
Separately, US 8,454,965 notes that
Multiple sclerosis (MS) is a chronic, neurological, autoimmune, demyelinating disease. MS can cause blurred vision, unilateral vision loss (optic neuritis), loss of balance, poor coordination, slurred speech, tremors, numbness, extreme fatigue, changes in intellectual function (such as memory and concentration), muscular weakness, paresthesias, and blindness. Many subjects develop chronic progressive disabilities, but long periods of clinical stability may interrupt periods of deterioration. Neurological deficits may be permanent or evanescent. In the United States there are about 250,000 to 400,000 persons with MS, and every week about 200 new cases are diagnosed. Worldwide, MS may affect 2.5 million individuals. Because it is not contagious, which would require U.S. physicians to report new cases, and because symptoms can be difficult to detect, the incidence of disease is only estimated and the actual number of persons with MS could be much higher.
The pathology of MS is characterized by an abnormal immune response directed against the central nervous system. In particular, T-lymphocytes are activated against the myelin sheath of the neurons of the central nervous system causing demyelination. In the demyelination process, myelin is destroyed and replaced by scars of hardened "sclerotic" tissue which is known as plaque. These lesions appear in scattered locations throughout the brain, optic nerve, and spinal cord. Demyelination interferes with conduction of nerve impulses, which produces the symptoms of multiple sclerosis. Most subjects recover clinically from individual bouts of demyelination, producing the classic remitting and exacerbating course of the most common form of the disease known as relapsing-remitting multiple sclerosis.
MS develops in genetically predisposed individuals and is most likely triggered by environmental agents such as viruses (Martin et al., Ann. Rev. Immunol. 10:153-187, 1992). According to current hypotheses, activated autoreactive CD4+ T helper cells (Th1 cells) which preferentially secrete interferon-gamma (IFN-.gamma.) and tumor necrosis factors alpha/beta (TNF-.alpha./.beta.), induce inflammation and demyelination in MS (Martin et al., supra). Available data suggest that the predisposition to mount a Th1-like response to a number of different antigens is an important aspect of MS disease pathogenesis. Proinflammatory cytokines (such as IFN-.gamma., TNF-.alpha./.beta.) and chemokines secreted by Th1 cells contribute to many aspects of lesion development including opening of the blood-brain-barrier, recruitment of other inflammatory cells, activation of resident glia (micro- and astroglia) and the effector phase of myelin damage via nitrogen and oxygen radicals secreted by activated macrophages (Wekerle et al., Trends Neuro Sci. 9:271-277, 1986) (Martin et al., supra).
Secondary-progressive multiple sclerosis is a clinical course of MS that initially is relapsing-remitting, and then becomes progressive at a variable rate, possibly with an occasional relapse and minor remission.
and which includes claims
1. A method of treating a human subject suffering from relapsing remitting multiple sclerosis, comprising administering daclizumab monthly to the subject in a unit dose ranging from about 150 mg to about 400 mg, wherein the subject is not concurrently treated with interferon-.beta..
2. The method of claim 1, wherein the daclizumab is administered for a year.
3. The method of claim 1, wherein the daclizumab is administered indefinitely.
4. The method of claim 1, wherein the daclizumab is formulated as a solution containing from 1 wt % to 15 wt % or 20 wt % daclizumab.
5. The method of claim 1, wherein the daclizumab is administered is administered as monotherapy.
6. The method of claim 1, wherein the daclizumab is administered in an amount effective to reduce the rate of increase of the subject's disability score.
AND, from StreetInsider on 20 April 2016:
New data presented today [April 20] show that investigational therapy ZINBRYTATM (daclizumab HYP) provided improvements on cognitive outcome measures in people living with relapsing forms of multiple sclerosis (RMS). Additional data offer insight into ZINBRYTA’s targeted mechanism of action (MOA), demonstrating that it did not cause broad immune cell depletion and its effects on total lymphocyte counts were reversible within approximately 8 to 12 weeks upon treatment discontinuation. These results were presented by Biogen (NASDAQ: BIIB) and AbbVie (NYSE: ABBV) at the 68th annual meeting of the American Academy of Neurology (AAN) in Vancouver, Canada