Considering Eli Lilly & Co. (NYSE:LLY) as well as a co-development project between Johnson & Johnson (NYSE:JNJ) and Pfizer Inc. (NYSE:PFE) both failed in semi-recent effort to develop a similar-functioning Alzheimer's drug, it would be easy to assume that particular route towards an Alzheimer's might be the wrong path to take. Sometimes though, a small tweak or a seemingly-minor nuance with the underlying problem can make all the difference. Enter Prana Biotechnology Limited (NASDAQ:PRAN). Though the company acknowledges its focal point on the development of an Alzheimer's therapy is the same broad premise that ultimately led LLY, PFE, and JNJ to failure, PRAN may have found the proverbial missing link.
It's no real secret that a buildup of beta amyloid plaque in the brain has been named as the culprit for Alzheimer's. That's been a widely-held assumption for a couple of decades now. Though it's still not exactly clear how or why it forms and what the actual impact of this plaque is, it wasn't unreasonable to assume that preventing its formation or cleaning it out would be the first best approach to take en route to a designing a successful Alzheimer's treatment. That was the intent of bapineuzumab, from Pfizer and Johnson & Johnson, and it was the intent of solanezumab, from Eli Lilly. Both drugs were deemed failures before either company bothered to request the FDA's blessing, however, and though LLY is going to redefine the ideal AD sufferer for another trial of solanezumab, even the company doesn't appear to be hopeful.
Thing is, the drugs basically worked to control or contain the production or existence of beta amyloid plaque in the brain. They just didn't do much to quell the typical symptoms or severity of Alzheimer's disease.
Truth be told, the weak results shouldn't have come as s surprise to Pfizer, Johnson & Johnson, or Eli Lilly & Co. A trial of a similar plaque-clearing drug from Elan in 2008 also failed, not because it didn't eliminate the amyloid protein (it did that pretty well, actually). The drug was a failure because even though it reduced the existence of beta-amyloid, it didn't actually prevent or undo neurodegeneration.
It's still not end-all, be-all proof that the amyloid plaque theory is off-base. It's possible that the plaque itself does damage to the brain's neurons that can't be undone, even if the amyloid protein is removed. Still, it's a long shot for big pharma to continue barking up this particular tree... unless that pharmaceutical company is Prana Biotechnology Limited, which has noticed - and actually acted upon - an important detail regarding the brain's makeup.
What if it was the existence of metals like iron and aluminum or copper that sparked the formation of these amyloid plaque proteins? More than that, what if these very same metals that prodded the formation of plaque were extracted from the very same nerves that were being damaged by these beta amyloid proteins? Indeed, what if it was the removal of metals from the brain's neurons that was the reason Alzheimer's symptoms formed in the first place.
Not only is not it a far-fetched idea, the scientists working on an AD drug at Prana Biotechnology Limited believe it's possible. They're not alone in the idea either.
See, the metals already exist in the brain. They're necessary, in fact, for a neuron to properly transmit messages to and from the brain and to and from the body. Iron is the most commonly-found transition metal acting as a conductor in a body's nervous system, and an excessive iron presence has been observed in some Alzheimer's patients' brains. And, it's makes sense. Iron has been shown to act as the core of an amyloid plaque oligimer that's toxic to brain synapses. The approach PRAN is taking simply to return those metals to the brain's nerves before they have a chance to form dangerous plaque-forming oligimers.
There's still a need to catch Alzheimer's symptoms early, ideally, but it's conceivable that the Prana Biotechnology aim of returning needed metals to the brain's network could at least undo some of the damage that has thus far been unfixable by other beta amyloid plaque reducing drugs.
A marketable drug from PRAN is still years away. Currently just called PBT2, the Alzheimer's therapy is only in Phase 2 trials right now. If there was ever a company or a drug that looked poised to do what Eli Lilly & Co., Johnson & Johnson, and Pfizer couldn't do on the amyloid plaque front, however, it's Prana Biotechnology. Investors looking for a good, long-term speculation may want to take a closer look.
For more trading ideas and insights like these, be sure to sign up for the free SmallCap Network newsletter.
No comments:
Post a Comment