Developed by QLT’s wholly owned subsidiary, QLT USA, Inc., Eligard® formulations are approved in eight countries for the palliative treatment of advanced prostate cancer.

Photo of the Eligard product line. Eligard is a leuprolide acetate product—a luteinizing hormone-releasing hormone (LHRH) agonist. Sustained levels of leuprolide decrease testosterone levels to inhibit tumor growth in patients with hormone-responsive prostate cancer. Using QLT’s own unique drug delivery mechanism, Atrigel®, Eligard is injected into the body subcutaneously as a liquid, where it solidifies and delivers a dose of leuprolide acetate at a controlled rate for the specified therapeutic period of time.

There are about 220,000 new cases of prostate cancer in the U.S. each year. The worldwide market is over $1.5 billion, of which $800 million is in the U.S.

ELIGARD - A Hormonal Therapy for Prostate Cancer

ELIGARD is a prescription medication for the palliative treatment (management of symptoms) of advanced prostate cancer. ELIGARD is an LHRH (luteinizing hormone-releasing hormone) agonist. It is designed to reduce the amount of testosterone in the body by reducing the testicles’ production of testosterone. It is not a cure for advanced prostate cancer.

ELIGARD is now available in 4 different prescription doses, giving you and your physician flexible dosing options for treating your advanced prostate cancer. The ELIGARD 45 mg shot, the newest addition to the ELIGARD family, is the first and only 6-month hormone therapy for the treatment of advanced prostate cancer. ELIGARD 45 mg gives you the benefit of a full year of hormone therapy with just 2 injections. Ask you doctor about twice-yearly ELIGARD.

How It Works on Advanced Prostate Cancer
ELIGARD is an LHRH agonist. Male hormones, such as testosterone, stimulate the growth of prostate cancer cells. The goal of hormonal therapy for advanced prostate cancer is to lower the body’s level of male hormones and thereby shrink or slow down the growth of prostate tumors. Most of the body’s testosterone is made by the testicles; ELIGARD prevents the testicles from producing testosterone.

As with other LHRH agonists, the first shot of ELIGARD will make testosterone levels rise temporarily. However, within 2 to 4 weeks, the ELIGARD shot causes testosterone levels to fall. In most cases, the level of testosterone that results from ELIGARD is the same level or lower than that achieved by surgical castration.

Visudyne® (verteporfin) was the first therapeutic treatment approved worldwide for certain forms of wet age-related macular degeneration (AMD), the leading cause of blindness in people over the age of 55.

Visudyne is commercially available in more than 75 countries for the treatment of predominantly classic subfoveal choroidal neovascularization (CNV) and in a number of countries for occult subfoveal CNV caused by AMD. Visudyne is reimbursed in the United States by the Center for Medicare and Medicaid Services for certain patients with the occult and minimally classic forms of wet AMD. It is also approved in over 60 countries, including the European Union, the U.S. and Canada, for the treatment of subfoveal CNV due to other macular diseases such as minimally classic AMD, pathologic myopia (severe near-sightedness) and ocular histoplasmosis.

Recently, alternative treatments for wet AMD with different modes of action have been approved or used. We expect that Visudyne will maintain its niche in the AMD marketplace and we believe that it will continue to be used in combination with other treatment options for certain forms of AMD.

Visudyne is developed and commercialized by QLT Inc. with Novartis Ophthalmics.

VISUDYNE PRODUCT CHARACTERISTICS, IDEAL FOR TREATING OCULAR DISEASES
* Photosensitizer that exhibits no activity until activated by light at a wavelength of 690 nanometers
* Rapid and selective uptake by the walls of the abnormal blood vessels in the eye results in a very short treatment procedure
* Short half life and fast clearance eliminates need for long photosensitivity precautions commonly associated with first-generation photosensitizers

How Visudyne works?

The objective of Visudyne® therapy is to slow or arrest the progression of wet age-related macular degeneration (AMD), pathologic myopia and presumed ocular histoplasmosis. It does not restore or improve vision in eyes that have already been significantly damaged by these diseases.

Administering Visudyne Therapy

Visudyne therapy is easy to administer and can be done in the physician’s office.

Step №1: Visudyne is injected into the patient’s arm over a period of ten minutes.     Visudyne is injected into the patient’s arm over a period of ten minutes.
Step №2: In the bloodstream, Visudyne attaches to lipoproteins which selectively carry the drug to abnormal vessels in the eye.     In the bloodstream, Visudyne attaches to lipoproteins which selectively carry the drug to abnormal vessels in the eye.
Step №3: Five minutes after the infusion, Visudyne is activated by shining a red, non-thermal laser light into the patient’s eye for 83 seconds.     Five minutes after the infusion, Visudyne is activated by shining a red, non-thermal laser light into the patient’s eye for 83 seconds.
Step №4: Once Visudyne is activated, the abnormal blood vessel cells are destroyed by the release of singlet oxygen, resulting in closure of the abnormal vessels and cessation of leakage.     Once Visudyne is activated, the abnormal blood vessel cells are destroyed by the release of singlet oxygen, resulting in closure of the abnormal vessels and cessation of leakage.

Lasers

Visudyne therapy involves the use of a specially designed diode laser that produces the low level, non-thermal (non-burning) light required to activate the drug. These lasers have been developed by two of the world’s leading laser companies, Lumenis, based in California, and Carl Zeiss, based in Germany.

A 42-year-old HIV patient with leukemia appears to have no detectable HIV in his blood and no symptoms after a stem cell transplant from a donor carrying a gene mutation that confers natural resistance to the virus that causes AIDS, according to a report published Wednesday in the New England Journal of Medicine.

“The patient is fine,” said Dr. Gero Hutter of Charite Universitatsmedizin Berlin in Germany. “Today, two years after his transplantation, he is still without any signs of HIV disease and without antiretroviral medication.”

The case was first reported in November, and the new report is the first official publication of the case in a medical journal. Hutter and a team of medical professionals performed the stem cell transplant on the patient, an American living in Germany, to treat the man’s leukemia, not the HIV itself.

However, the team deliberately chose a compatible donor who has a naturally occurring gene mutation that confers resistance to HIV. The mutation cripples a receptor known as CCR5, which is normally found on the surface of T cells, the type of immune system cells attacked by HIV.

The mutation is known as CCR5 delta32 and is found in 1 percent to 3 percent of white populations of European descent.

HIV uses the CCR5 as a co-receptor (in addition to CD4 receptors) to latch on to and ultimately destroy immune system cells. Since the virus can’t gain a foothold on cells that lack CCR5, people who have the mutation have natural protection. (There are other, less common HIV strains that use different co-receptors.)

People who inherit one copy of CCR5 delta32 take longer to get sick or develop AIDS if infected with HIV. People with two copies (one from each parent) may not become infected at all. The stem cell donor had two copies.

While promising, the treatment is unlikely to help the vast majority of people infected with HIV, said Dr. Jay Levy, a professor at the University of California San Francisco, who wrote an editorial accompanying the study. A stem cell transplant is too extreme and too dangerous to be used as a routine treatment, he said.

“About a third of the people die [during such transplants], so it’s just too much of a risk,” Levy said. To perform a stem cell transplant, doctors intentionally destroy a patient’s immune system, leaving the patient vulnerable to infection, and then reintroduce a donor’s stem cells (which are from either bone marrow or blood) in an effort to establish a new, healthy immune system.

Levy also said it’s unlikely that the transplant truly cured the patient in this study. HIV can infect many other types of cells and may be hiding out in the patient’s body to resurface at a later time, he said.

“This type of virus can infect macrophages (another type of white blood cell that expresses CCR5) and other cells, like the brain cells, and it could live a lifetime. But if it can’t spread, you never see it– but it’s there and it could do some damage,” he said. “It’s not the kind of approach that you could say, ‘I’ve cured you.’ I’ve eliminated the virus from your body.”

Before undergoing the transplant, the patient was also found to be infected with low levels of a type of HIV known as X4, which does not use the CCR5 receptor to infect cells. So it would seem that this virus would still be able to grow and damage immune cells in his body. However, following the transplant, signs of leukemia and HIV were absent.

“There is no really conclusive explanation why we didn’t observe any rebound of HIV,” Hutter said. “This finding is very surprising.”

Hutter noted that one year ago, the patient had a relapse of leukemia and a second transplant from the same donor. The patient experienced complications from the procedure, including temporary liver problems and kidney failure, but they were not unusual and may occur in HIV-negative patients, he said.

Researchers including Hutter agree that the technique should not be used to treat HIV alone. “Some people may say, ‘I want to do it,’” said Levy. A more logical — and potentially safer — approach would be to develop some type of CCR5-disabling gene therapy or treatment that could be directly injected into the body, said Levy.

Less invasive options to alter CCR5 could be on the horizon within the next five years, said Levy. “It’s definitely the wave of the future,” he said. “As we continue to follow this one patient, we will learn a lot.”

One drug that’s currently on the market that blocks CCR5 is called maraviroc (Selzentry). It was first approved in 2007 and is used in combination with other antiretroviral drugs.

In 2007, an estimated 2 million people died from AIDS, and 2.7 million people contracted HIV. More than 15 million women are infected worldwide. HIV/AIDS can be transmitted through sexual intercourse, sharing needles, pregnancy, breast-feeding, and/or blood transfusions with an infected person.

“For HIV patients, this report is an important flicker of hope that antiretroviral therapy like HAART [highly active antiretroviral therapy] is not the endpoint of medical research,” Hutter said.