NAME: Teva Pharmaceutical Industries, Ltd.
HEADQUARTERS: Petah Tikva, Israel
STOCK PRICE AS OF 3/5/13: $37.25
52 WEEK RANGE: $36.63 – $46.38
MARKET CAPITALIZATION: $31.92B
HD INSIGHTS: How did you first become interested in Huntington disease (HD)?
MICHAEL HAYDEN: My interest in HD goes back to my life as a medical student in the middle of the 1970s, when I first saw patients in South Africa who had HD. At the time, HD was not diagnosed because it was thought not to occur in Africa. I realized that not only did HD in fact occur in Africa, but in people of Caucasian or mixed-race background it occurred at a similar rate to that seen in Europe. By contrast, HD was rare in the black populations of Southern Africa. I was drawn to HD. I traveled to every one of the 16 psychiatric and neurological hospitals in South Africa. I examined every single patient with chorea, and from this I compiled a list of 400 to 500 patients with a family history of HD. People in South Africa with HD were discriminated against. Many were of mixed race. Our cardinal observations were that there was a high frequency of juvenile HD in South Africa, and the incidence of HD in people of Caucasian and mixed-race background was similar to the incidence of HD in Europe. We traced the introduction of the HD gene mutation back to Dutch settlers who came to South Africa in the mid-1600s. We started documenting the difficult social and psychological impact of HD on the family. In 1978 we started the first HD clinic in Africa, and we provided an integrated model of HD – comprehensive neurology, psychiatry, social work and physiotherapy. The clinic was integrated in every way; not only by virtue of the specialties to treat HD patients, but also racially. This was the first multiracial clinic at the Groote Schuur Hospital in Cape Town, where ten years previously the first human heart transplant had been done. We wanted to provide support for all families with HD irrespective of their race and irrespective of their past. In the late 1970s we also formed the first lay HD organization in Africa. Just as we established a multiracial clinic for HD, I wanted to integrate the experience of medical students of different racial backgrounds in hospital wards in Cape Town. Generally, white medical students did not see black patients and black medical students were barred from seeing white patients. Inevitably at that time, this put me into conflict with the authorities. I met Marjorie Guthrie in San Diego in 1977 at the Second International Congress on HD. Marjorie and I became close buddies. I told her that I was very worried about my future. I had to choose which struggle I was going to dedicate my life to – was it the struggle to change South Africa, or was it the struggle to have an impact on families with HD and do something for them? Marjorie persuaded me to come to the United States, and helped organize my move. The late Senator Ted Kennedy wrote a letter to the Immigration Department to support my application for immigration on a Green Card. I thought that after I left South Africa I could never go back, and needed to find a home. Senator Kennedy recommended that I go to Boston, so I interviewed at the Children’s Hospital and was accepted into the genetics program. I arrived in Boston in June 1980 as a post-doc. At that time there were no reference books on HD. There had not been a single monograph on HD. I took my thesis of 1979 which formed the basis of the first single-author monograph on HD. This was published while I was in Boston in 1981. I dedicated the monograph to my research assistant at the time, who later became my wife, and Marjorie. Those were the two people who really had played a key role in me being able to complete that work.
INSIGHTS: What was the next step for you?
HAYDEN: As I came to the end of my fellowship, I was asked to go to Vancouver, Canada. Judith Hall, President of the American Society of Human Genetics, was there, Tom Perry Sr., a major researcher in HD, was there. Marjorie encouraged me to look at this opportunity. They welcomed me, and the HD family welcomed me. I had a deeply ingrained commitment to HD. I had seen the plight and difficulties but had also witnessed the courage and dignity of HD patients. I established my lab to make inroads into HD. We have had huge support from families all over North America. In 1986 we did the first predictive test for HD, and contributed to the guidelines for HD predictive testing. We worked on really understanding how, at a molecular and biochemical level, HD occurs. The key question was: How do we develop therapies for HD? We created a full-length animal model for HD. We did the first PET scans in patients, and we created an integrated HD clinic, the first in Canada, that today sees patients contributing to trials around the world. We defined the epidemiology and the incidence of HD, showing that it is more frequent than people have realized in the past. We also defined mechanisms that lead to HD, which is ongoing work for my lab in Vancouver and Singapore too. Many of my post-docs have now gone on to be leaders in the lab in Singapore with a major focus on HD.
INSIGHTS: Why did you make the transition to Teva?
HAYDEN: I could only go to a certain point with academic lab work. To develop therapies for HD, I would have to be open to other possibilities. I worked very hard trying to engage pharma. I met with large pharmaceutical companies, informing them about the importance of this disease, but I was not able to convince them to make the investments needed to commit to developing medicines that could possibly change the course of the lives of patients and families. Then I was approached to consider the job of President of Global R&D at Teva. During the recruitment process we discussed my launching a focus on neurodegeneration using HD as the model. I think that HD could inform studies on many forms of neurodegeneration, including Alzheimer’s disease. We needed to start somewhere, and the CEO, Jeremy Levin, was willing and enthusiastic to commit to that. And so I joined. My labs continue to do basic research that can feed the pipeline with new ideas. I go back to Vancouver very frequently as well as to Singapore to support that work. The very first acquisition with me at Teva was the purchase of a Phase III asset, the drug Huntexil from Neurosearch. This drug was not going to change the course of HD, but provide symptomatic relief. We are now working to start definitive trials with Huntexil in the next few months.
INSIGHTS: What about other approaches for HD?
HAYDEN: As president of R&D at Teva, we have a commitment to refocus the pipeline to diseases of the central nervous system, including MS, Parkinson’s, Alzheimer’s, Pain and, of course, HD. We are hiring people from around the world who know about HD. Teva is a company committed to making a change in the lives of patients with neurodegenerative disorders.
INSIGHTS: What do you think are the greatest future opportunities for new treatments for HD?
HAYDEN: We believe that the inflammatory pathways are important targets. Inflammation is an early feature of this disease, and it occurs both centrally and peripherally. The neurons may be secondarily involved. Astrocytes and microglia secrete various inflammatory cytokines that could cause damage. We are looking into drugs that influence those pathways. In the end, it is likely that you will need combination therapy for this disease: To retard disease progression and also to protect neurons that are already damaged. In HD, the cellular and biochemical disease process starts very early, and often, by the time you have clinical symptoms, there has already been a lot of damage.
INSIGHTS: Dr. Hayden, thank you for your time. Do you have any final thoughts?
HAYDEN: HD is now recognized as being present globally. It is present wherever people have migrated, and the burden of the disease is very similar irrespective of politics, irrespective of race, irrespective of borders and boundaries. The impact on people’s lives is profound. We have the chance to do something. This is an opportunity to impact the lives of patients not only with HD, but also with other forms of neurodegenerative disease.