Therapeutic Solutions

The Challenge

Multiple Sclerosis is an unpredictable, often devastating disease of the central nervous system that disrupts the flow of information between the brain and the body. The cause of MS is currently unknown. MS can be separated into two subtypes: relapsing & remitting MS and progressive MS.

The Solution

Our team has independently engineered a pro-drug with proprietary chemical structure that targets an underlying mechanism of progressive MS with secondary benefits to relapsing and remitting MS. As a result, our medication may prevent both relapses and progression in MS, and thereby significantly improve the quality of life for MS patients.

The Science Behind Medicine

Proven Results

Cutting Edge Methodologies

%

Diagnosed MS Cases Are Relapsing & Remitting

%

Diagnosed MS Cases Are Considered Progressive

Million People Diagnosed With Multiple Sclerosis

Thousand People Died From Multiple Sclerosis in 2013

Industry Leading Innovation

Reduce Disease and Improve Health

Glixis aims to reduce the progression of disease, streamline treatment process, and improve a patient’s quality of life one pill at a time.

World Renowned Leaders

Leaders who want to fundamentally revolutionize the treatment options & potential therapies for multiple sclerosis patients.

First Of Its Kind Compound

Glixis has developed a first-of-its-kind compound that treats the underlying pathophysiology of multiple sclerosis.
Causes of Multiple Sclerosis
The cause of MS is currently unknown, but it is known that there is both an environmental and genetic component in defining MS risk.
Symptoms of MS
  • fatigue
  • vision problems
  • tingling and numbness
  • vertigo and dizziness
  • muscle weakness and spasms
  • problems with balance and coordination

Other, less common, symptoms include:

  • speech and swallowing problems
  • cognitive dysfunction
  • difficulty with walking
  • bladder and bowel dysfunction
  • sexual dysfunction
  • mood swings, depression
Cost of Care
Direct and indirect health care costs range from $7,000 to $75,000 per patient per year in the United States.
Women and MS
Women with MS can safely carry a baby to term. Pregnancy doesn’t generally affect MS in the long-term. Women with MS often experience a relief from symptoms during pregnancy. However, about 20 to 40 percent of women have a relapse within a few months of giving birth.
Other Commerical Medications
  • teriflunomide (Aubagio)
  • interferon beta-1a (Avonex, Rebif, Plegridy)
  • interferon beta-1b (Betaseron, Extavia)
  • glatiramer acetate (Copaxone)
  • fingolimod (Gilenya)
  • mitoxantrone (Novantrone)
  • dimethyl fumarate (Tecfidera)
  • natalizumab (Tysabri)
  • alemtuzumab (Lemtrada)

Research Based Approach

Our novel compound targets the underlying genetic and molecular defect in MS pathogenesis by correcting a key metabolic pathway in protein N-glycosylation. Pioneering research by our group has shown in both mice and humans that a defect in protein N-glycosylation promotes inflammatory demyelination and neurodegeneration.
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Related Publications

 

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Hypomorphic MGAT5 polymorphisms promote multiple sclerosis cooperatively with MGAT1 and interleukin-2 and 7 receptor variants.

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Family studies of type 1 diabetes reveal additive and epistatic effects between MGAT1 and three other polymorphisms.

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Probing the hexosamine biosynthetic pathway in human tumor cells by multitargeted tandem mass spectrometry.

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N-glycan remodeling on glucagon receptor is an effector of nutrient sensing by the hexosamine biosynthesis pathway.

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Targeted metabolomics in cultured cells and tissues by mass spectrometry: method development and validation.

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Metabolic Reprogramming by Hexosamine Biosynthetic and Golgi N-Glycan Branching Pathways.

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Metabolism, cell surface organization, and disease.

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Adaptive regulation at the cell surface by N-glycosylation.

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Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation.

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Control of T Cell-mediated autoimmunity by metabolite flux to N-glycan biosynthesis.

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N-glycan processing deficiency promotes spontaneous inflammatory demyelination and neurodegeneration.

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T-cell growth, cell surface organization, and the galectin-glycoprotein lattice.

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Genetics and the environment converge to dysregulate N-glycosylation in multiple sclerosis.

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N-acetylglucosamine inhibits T-helper 1 (Th1)/T-helper 17 (Th17) cell responses and treats experimental autoimmune encephalomyelitis.

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Interleukin-2, Interleukin-7, T cell-mediated autoimmunity, and N-glycosylation.

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Pathogenesis of Multiple Sclerosis via environmental and genetic dysregulation of N-glycosylation

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N-glycosylation bidirectionally extends the boundaries of thymocyte positive selection by decoupling Lck from Ca²⁺ signaling.

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Complex N-glycan number and degree of branching cooperate to regulate cell proliferation and differentiation.