Replies to post #18141 on Biotech Values

[terry hallinan]

DewDiligence,

Crock or not, Denosumab could become a $3B drug by the end of the decade if not sooner.

I wouldn't argue that for a second. Not my point at all. I was not proposing anything remotely resembling an expert opinion but little more than a raw prejudice. I have no wish to inflame but rather to propose a caution about snake oil.

Denosumab appears likely to be a very useful drug but...

With the leading edge of the baby boom turning 60 next year, a convenient, safe, and efficacious drug for osteoporosis is going to have a heck of a tail wind.

Some of this has the look and feel to me of the proposition that Macugen will not only cure your eyesight but prevent cancer.

Maybe both propositions are true but considering the decades of use and large studies that would be required to provide reasonable evidence for the claim, I submit it might not be terribly wrong to have some doubts.

Should be a multitude of cures for Bill Gates' autism. All will most certainly work because Gates was never autistic.

Using Google, I found numerous experts discussing the known fact of Bill Gates' autism when I was surprised by the claim.

Pinned down, I think the more knowledgeable and reasonable of the fine folk declaring Bill Gates is autistic (including Bill Gates' own purported confession) would admit rather that Gates might have Asperger's Syndrome.

Well yeah, they murmur, but Asperger's is in the autism spectra.

Whatever that means.

It is something like putting all lung diseases, from cancer to pneumonia, into some kind respiratory spectra IMHO.

Hope you get my drift.

Or forgive an impossibly mule-headed doubter. I am after all from Missouri. :-)

Best, Terry

[Praveen]

NPSP
Hi Dew n Board,

Do you think NPSP can take a pie of the Baby boomers osteoporosis market?

Praveen

[Biowatch]

AMGN >>Investigational Therapy Denosumab Increased Bone Mineral Density with Twice-Yearly Dosing; One Year Data Published in New England Journal of Medicine

THOUSAND OAKS, Calif., Feb 22, 2006 (BUSINESS WIRE) -- Amgen (NASDAQ: AMGN), the world's largest biotechnology company, announced today the publication of Phase 2 data demonstrating twice-yearly injections of denosumab (previously referred to as AMG 162), a RANK Ligand inhibitor, significantly increased bone mineral density (BMD) in the total hip, lumbar spine, distal 1/3 radius and total body compared to placebo. The results of this one-year study appeared in the Feb. 23, 2006 issue of the New England Journal of Medicine. Data results also included an open-label FOSAMAX(R) (alendronate)(a) arm of the same clinical trial.

Researchers reported that subcutaneous injections of denosumab significantly increased BMD at the total hip from 1.9 to 3.6 percent in women who were administered the therapy twice yearly as compared with a decrease of 0.6 percent in the placebo group (p less than 0.001) at one year. The open label FOSAMAX(R) group receiving 70 mg weekly had an increase of 2.1 percent during the same time frame. Results also indicated that denosumab had a rapid onset of action. A significant decrease in serum levels of C-telopeptide, a biomarker of bone resorption, was achieved within 72 hours after dosing.

"These exciting data suggest that denosumab, when administered in twice-yearly injections, may show promise in the treatment of osteoporosis," said Michael McClung, MD, FACP, principal investigator of the denosumab study, Providence Portland Medical Center, and director of the Oregon Osteoporosis Center, Portland, Ore. "Continued research will further our understanding of the potential of denosumab in bone loss management."

Denosumab targets RANK Ligand, a protein that acts as the primary mediator of osteoclast (cells that break down bone) activity. This investigational therapy is the first RANK Ligand inhibitor in late stage development.

Amgen is studying denosumab for its potential in a broad range of conditions associated with bone destruction including osteoporosis, treatment-induced bone loss, bone metastases, multiple myeloma and rheumatoid arthritis. Data recently presented at the American College of Rheumatology 2005 Annual Scientific Meeting show further increase in bone mineral density in postmenopausal women with osteoporosis after two years of treatment.

"These data reinforce the essential role that RANK Ligand inhibition plays in decreasing bone loss," said Willard Dere, MD, senior vice president of global development and chief medical officer, Amgen. "We are committed to expanding our data on denosumab with an extensive Phase 3 clinical program to evaluate the effect of denosumab on preventing fractures in men and women."

In the one-year trial results, researchers also reported twice-yearly subcutaneous injections of denosumab significantly increased lumbar spine BMD from 3.0 to 6.7 percent after 12 months as compared with a decrease of 0.8 percent in the placebo-treated patients (p less than 0.001). Across all doses and dosing intervals, distal 1/3 radius BMD increased from 0.4 to 1.3 percent as compared with a decrease of 2.0 percent in those taking placebo (p less than 0.001), and total body BMD increased from 0.6 to 2.8 percent as compared with a decrease of 0.2 percent in the placebo group (p less than 0.01).

The incidence of adverse events was similar among the denosumab, placebo, and FOSAMAX(R) groups, with the exception of dyspepsia. Dyspepsia occurred in 7 percent of placebo patients, 6-15 percent of denosumab patients and 26 percent of open-label FOSAMAX(R) patients. The most common adverse events among all groups included upper respiratory infection (common cold), arthralgia (joint pain), nasopharyngitis (sore throat), back pain and headache. No neutralizing antibodies to denosumab were observed.

Denosumab Study Design

This is an ongoing, multi-center dose-ranging trial. Investigators randomized 412 healthy postmenopausal women, average age 63, with low BMD to receive denosumab, placebo or FOSAMAX(R). The purpose of the study was to determine the safety and efficacy of denosumab on lumbar spine BMD compared with placebo at 12 months. The doses of denosumab evaluated included 6, 14 or 30 mg every three months or 14, 60, 100 or 210 mg every six months. The researchers administered all doses of denosumab via subcutaneous injection. Patients receiving FOSAMAX(R) followed the approved indication and oral dosing instructions of 70 mg once weekly.

At entry, the average lumbar spine T score ranged from -2.0 to -2.2 across dose groups, consistent with a diagnosis of osteopenia (thinning bone). Approximately a quarter of the patients had osteoporosis as defined by a T score equal to or below -2.5 at the lumbar spine.

About RANK Ligand

Bone is constantly formed and removed through a natural process of remodeling. Bone resorption is dependent on RANK Ligand, the protein that acts as the primary mediator of osteoclast formation, function and survival. Osteoclasts are cells responsible for bone removal.

Preclinical models have demonstrated that inhibiting RANK Ligand significantly improves cortical and trabecular bone density, volume and strength. Cortical bone is the protective outer shell around every bone in the body. Trabecular bone is known as spongy bone and is surrounded by the harder cortical layer.

The Need for Bone Loss Treatments

Osteoporosis

Bone loss represents a significant clinical and economic burden. Osteoporosis is a major public health threat for an estimated 44 million Americans, or 55 percent of the population 50 years of age and older. In the U.S. today, 10 million individuals are estimated to already have the disease and almost 34 million more are estimated to have low bone mass, placing them at increased risk for osteoporosis.

Of the 10 million Americans estimated to have osteoporosis, eight million are women and two million are men. In addition, one in two women and one in four men over age 50 will have an osteoporosis-related fracture in their remaining lifetime.

In Europe, recent estimates have stated that approximately 3.8 million people have experienced bone fractures related to osteoporosis.<<

http://wwwext.amgen.com//media/media_pr_detail.jsp?year=2006&releaseID=820731