Investing guru Peter Lynch famously advised to "invest in what you know." For many, however, big pharma stocks like Novartis can be attractive for their strong free cash flow and stable dividends; but the science behind its key drugs can be difficult to understand. Multiple sclerosis drug Gilenya, for instance, is one of Novartis' key therapeutics, and brought in more than $2 billion during the last 12 months. However, there are several options for patients today, such as Biogen's Tecfidera, and it can be difficult to understand how these drugs work.

To gain more insight into this complex therapeutic area, health-care bureau chief Max Macaluso spoke with Dr. Gordon Francis, the head of Novartis' neuro-inflammation therapeutic area.

A transcript of the discussion follows the video below.

Max Macaluso: Hi, I'm Max Macaluso, the Health-Care Bureau Chief at The Motley Fool, and joining me today is Dr. Gordon Francis. Dr. Francis is the head of Novartis' Neuroinflammation Therapeutic Area. Thank you very much for joining me today.

Dr. Gordon Francis: Thanks for having me on.

Macaluso: Dr. Francis, I'd like to start our conversation today by talking about Novartis' multiple sclerosis drug, Gilenya. The drug-discovery process usually starts with a specific target. In some cases, it's a kinase; in others it's a G protein-coupled receptor. I'm curious what the system that Gilenya targets actually is.

Dr. Francis: Gilenya, or fingolimod, targets the S1P receptors, the sphingosine receptors on a number of different cell types.

The importance there from a drug mechanism perspective is that this leads to retention of the lymphocytes within the lymph nodes in the body, such that cells that are otherwise autoreactive -- or directed against the central nervous system, in the case of MS -- are not permitted to circulate to the brain, and therefore reduce the inflammatory attacks that are typical of multiple sclerosis.

Basically, by an interaction on the cell surface receptor, it keeps the cells in the lymphoid tissue, and prevent damage to the central nervous system in that manner.

Macaluso: I know that multiple sclerosis is often associated with a loss of brain volume, so I'm curious how Gilenya is able to slow this process.

Dr. Francis: I think this is probably a two-stage process. First of all, as I mentioned, because of the way the drug works it reduces inflammatory attacks in the brain, and this alone will lead to less damage and, therefore, preservation of brain tissue and ultimately, less brain atrophy.

But in addition, the sphingosine receptors -- the S1P receptors -- are also present in tissue in the brain, including support cells, but also in cells that produce myelin. It's based on preclinical work, and the presence of these receptors in the brain, that we believe that there's also a potential for a second mechanism of action, directly within the central nervous system, protecting tissue, allowing for better repair, and therefore, less damaged tissue and ultimately less atrophy.

So, both on the peripheral action -- the anti-inflammatory action -- as well as the potential for a direct central nervous system action, one has sort of a dual approach to reducing the damage to tissue in the brain, and therefore reducing brain atrophy over time.

Macaluso: I know that there are a number of different drugs on the market for the treatment of multiple sclerosis. There are a number of injected drugs, and even antibodies, like Biogen's Tysabri. I'm curious if they also target the S1P receptor, or if they target a completely different pathway altogether.

Dr. Francis: For some of the drugs, it's not entirely certain what the direct mechanism of action is. Things such as the glatiramer acetate or interferon, the precise way in which they're working is not clear.

With natalizumab -- or Tysabri -- that drug blocks the interaction of lymphocytes with the membrane of the blood vessels, and therefore blocks the cells from getting into the brain. It's felt to work in that way, not dissimilar to what fingolimod is doing -- fingolimod is holding the lymphocytes back, if you will, and Tysabri is blocking them from getting into the CNS.

However, none of these other drugs work on the S1P receptor mechanism, and therefore, can't have the potential secondary effect within the brain directly, that the S1P receptor modulators can have.

Macaluso: How does Gilenya compare to other oral multiple sclerosis drugs on the market? I know Gilenya was the first approved, but since then, Sanofi had Aubagio reach the market, and Biogen's Tecfidera has also been helping patients recently. How are these drugs different, and again, do they all target the same receptor system?

Dr. Francis: No, the drugs target different mechanisms. In fact, I think, again, in the setting of both the other two products, that they don't interact with the S1P receptor pathway. They have different mechanisms of action.

As you said, the common thing they have is that they're oral medications, so the same route of administration, although with Tecfidera, it has to be given twice a day as opposed to once a day, as in the situation with Gilenya.

I think there's no direct head-to-head comparisons of these drugs, so the relative strengths of the products could only be inferred from indirect comparisons between studies, and obviously, opinions can vary in the absence of a direct head-to-head study.

Macaluso: Dr. Francis, let's shift gears and talk a little bit more about multiple sclerosis drugs in Novartis' pipeline. I'm curious if you're working on some more, and when we can expect some data to read out, or what stages of development they're in.

Dr. Francis: We still have ongoing programs with Gilenya itself. Part of the broad portfolio, or the broad perspective approach that Novartis is taking to MS is to try to treat all stages of the disease.

Gilenya is approved for relapsing forms of the disease -- these are the earlier forms of disease. We've actually got a Phase III study ongoing in primary progressive MS -- that's the disease form that does not have relapses associated with it. It's progressive from the start. That's about 10%-15% of the MS population, and that study is due to read out later this year. We're actually quite excited about that, and anxiously waiting for results from that study.

Then, in addition, we have another S1P modulator that's somewhat different from Gilenya, called Siponimod, and that is in Phase III testing in the secondary progressive form of MS.

Each of the stages of MS is being addressed by an S1P receptor modulator. As I said, the primary progressive study will read out later this year. The secondary progressive study won't read out for another two to three years, at least.

Then, in addition, we're looking at pediatric MS. We're carrying out the first controlled study of MS disease modifying therapy in pediatrics, and that study has just begun over the last few months; that is with Gilenya.

Then, finally, we've got a study looking at a form of peripheral nerve disease, CIDP -- chronic inflammatory demyelinating neuropathy -- which is somewhat the peripheral nervous system's equivalent of MS, which is a central nervous system disease. That's also using Gilenya to see whether or not we can slow the progression of the peripheral nerve disease.

Those are the ones that are in the later stage, active investigation. Then we have also an anti-il17 program, which we've gotten some Phase II data on that, and are gearing up to get another dose-finding study in the Phase II setting with the anti-il17 molecule.

Then, a bit further back in the pipeline, we have a B-cell therapy. The B-cell approach has been recognized a bit later than the T-cell approach, which most of the other products address, so we've also got a program there that we're in early stages of development.

That's the perspective across MS and, of course, we continue to have early stage molecules, which might be candidates in MS; but that's a bit premature to discuss those at the moment.

Macaluso: What are some other therapeutic areas that your division is working on right now?

Dr. Francis: I lead the neuroinflammation group. There's a neurodegeneration group, and their interests are in non-inflammatory CNS diseases such as Alzheimer's disease, Parkinson's disease, and some of the neuropsychiatric indications. I suppose the main focus there would be toward the Alzheimer realm.

Macaluso: Great. Dr. Gordon Francis, thank you very much for joining us. Once again, Dr. Francis is the head of Novartis' Neuroinflammation Therapeutic Area.

Dr. Francis: Thanks very much, it's been a pleasure.

Macaluso: Thank you.

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