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DBL%20Hendrix%20small.png College chemistry, 1983

Derek Lowe The 2002 Model

Dbl%20new%20portrait%20B%26W.png After 10 years of blogging. . .

Derek Lowe, an Arkansan by birth, got his BA from Hendrix College and his PhD in organic chemistry from Duke before spending time in Germany on a Humboldt Fellowship on his post-doc. He's worked for several major pharmaceutical companies since 1989 on drug discovery projects against schizophrenia, Alzheimer's, diabetes, osteoporosis and other diseases. To contact Derek email him directly: derekb.lowe@gmail.com Twitter: Dereklowe

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October 9, 2012

Lilly's Solanezumab: Did It Actually Work?

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Posted by Derek

"Hope Rises For Alzheimer's Treatment, Scientists Say". Not this scientist. That's a composite of headlines, but it captures the unfortunate tone.

We're talking about solanezumab, Eli Lilly's antibody therapy. The company presented analysis of their trial data yesterday, and put a very optimistic face on things. But wait, you say, didn't Lilly already report on this? And didn't the drug miss all its endpoints? Yes, indeed it did. But this is a secondary analysis by the Alzheimer's Disease Cooperative Study, a third-party look at the data. It's hard for me to imagine an optimistic take on the numbers that Lilly itself didn't find, to be honest, but here we have it:

But after a secondary analysis of the first study showed that there was a 42% reduction in the rate of cognitive decline among a subpopulation of patients in the solanezumab arm with only a mild form of the disease, investigators decided to hunt for confirmation of that endpoint in a second Phase III. They didn't find it, seeing the numbers fall short of statistical significance after switching from one measure (ADAS- Cog11) to another (ADAS-Cog14). But by "pooling" the data they came up with a 34% reduction in cognitive decline in that particular group. None of the data indicated a significant reduction in the rate of functional decline.

This looks to me like grasping at straws. I understand that people want to see any tiny edge of possible efficacy as an avenue for further research, but I can't help but think that the path to an effective Alzheimer's therapy would announce itself a bit more clearly than this. Anything should. Chasing after these sorts of results looks like the path to another Phase III trial that might just manage to miss its endpoints by an even narrower margin. The best one could hope for would be a therapy that might, possibly, help a few patients in the early stage of the disease a bit, for a while. Maybe.

The problem is that the pent-up need for anything effective in Alzheimer's is so great that vast hordes of people will likely rush to take anything - or put their aging relatives on anything - that might offer any shred of hope. And I know just where those people are coming from, and I sympathize greatly. Eli Lilly, for its part, is strongly motivated to have something in its large and expensive Alzheimer's portfolio actually work - the company is facing a very, very rough time with its patent expirations, and something like this is about the only thing that could pull them back from the cliff. On all sides, this is not a situation that encourages sound decision-making.

Comments (21) + TrackBacks (0) | Category: Alzheimer's Disease | Clinical Trials


COMMENTS

1. anchor on October 9, 2012 7:09 AM writes...

Derek: The operative word is "statistical significance." I am very wary of these results...and I see lot of trepidation on the part of researchers while disclosing the significance. I heard that the results as is will not get a positive nod from the FDA!

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2. needabetaguess on October 9, 2012 7:37 AM writes...

Grasping at straws? More like jabbing investors in the eyes with straws and telling them it's a new form of Lasik surgery.

Take a look at the last time a Lilly (or WashU) neuroscientist touted the peripheral sink hypothesis. When was that, five years ago? Seven?

When does willful suspension of disbelief cross the line to unethical conduct? I'd say the day the next patient gets a dose of this snake oil.

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3. SteveM on October 9, 2012 7:53 AM writes...

Of course the economic implications associated with the marginal benefit/cost ratio of Solanezumab are huge.

I'm not an expert on the drug regulatory environment, but Lilly is a known Criminal Enterprise related to drug marketing. It seems that they would attempt an Avastin type marketing blitz with Solanezumab charging thousands of dollars a year for a drug therapy that does next to nothing. Lilly will again use the "statistically significant" term to confuse doctors and its target customers about the limited/no clinical value of its drug.

Lilly is no doubt already scheming to get in, get registered and clean up as much as possible before FDA may release an Avastin type recommendation to the public indicating that paying big bucks for Solanezumab scripts is mostly flushing money down the toilet.

And so it goes...

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4. luysii on October 9, 2012 8:49 AM writes...

We certainly need something for it.

My college classmate was the head of his medical society at a state capital. I sent his wife a link to a post about a totally new angle on diabetes (he was an endocrinologist). https://luysii.wordpress.com/2012/09/30/an-incredible-paper-which-may-turn-diabetes-treatment-on-its-head/.

Not that it has much to do with Alzheimer's disease, but because it opens a whole new way of looking at the disorder with a promise of a different type of therapy. This, after nearly a century of study of insulin etc. etc. It was to give her some hope that there might be a similar new approach to Alzheimer's that we've not been smart enough to come up with.

She wrote back to say he no longer can read.

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5. newnickname on October 9, 2012 9:05 AM writes...

@2: "When does willful suspension of disbelief cross the line to unethical conduct?"

Forward looking statements are LEGAL, even if they do amount to lies. "Statements contained in this Report may constitute “forward-looking statements” within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. For this purpose, any statements herein that are not statements of historical fact may be deemed to be forward-looking statements. For example, the words “believes”, “anticipates”, and similar expressions are intended to identify forward-looking statements. [...]"

@3: "I'm not an expert on the drug regulatory environment, but Lilly is a known Criminal Enterprise related to drug marketing." There was a Congressional investigation and there were something like 24 criminal indictments against "Eli Lilly, The Ethical Drug Company" over the Oraflex fiasco. Lilly pleaded guilty to criminal charges and paid a fine of $25,000 (25 thousand, not million, dollars). Hay! It was 1982! The cost of getting caught was cheaper back then!

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6. Matthew Herper on October 9, 2012 9:44 AM writes...

The glimmer of hope is that maybe a beta-amyloid antibody would work if you tried it early enough. But how early? How early do we have to identify these patients?

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7. Lane Simonian on October 9, 2012 10:08 AM writes...

Well-said. It is time to pour a lot of water on the fire that Eli Lilly is so desperately trying to set.

There are numerous problems with the immunotherapy approach to Alzheimer's disease targeting amyloid plaques. First and most importantly, amyloid plaques are not the cause of the disease itself, peroxynitrites are. Four lines of evidence support this assertion: all the risk factors for Alzheimer's disease increase peroxynitrites, all the measures which prevent the formation of peroxynitrites appear to delay the onset of Alzheimer's disease, peroxynitrites dircetly, indirectly, or in conjunction with other factors can explain all aspects of Alzheimer's disease, and every peroxynitrite scavenger tested has ameliorated Alzheimer's disease in vitro, in animals, or in human beings. Yes, the plaques contribute to the formation of peroxynitrites, but remove all the plaques (and these "zumab" drugs only remove a small portion of them) and the damage done by peroxynitrites remain. So with an ideal immunotherapy drug with few or no side effects, the best you could ever do would be to stop the progression of the disease. And these drugs are far from ideal.

Secondly, giving it earlier may not produce much better results. At the early stages of Alzheimer's disease there is a rapid deposition of amyloid plaques. If this rate of deposition greatly excedes the ability of the drug to remove a few of those plaques, then it will do little to no good.

The key to preventing or delaying the onset of Alzheimer's disease is to stop the formation of peroxynitrites (and secondarily amyloid plaques). Protein kinase C activation leads to the formation of peroxynitrites. Protein kinase C activation plus intracellular calcium release leads to the formation of amyloid plaques. The first happens more rapidly so some peroxynitrite damage occurs even before the formation of the plaques. The enzymes that stimulate protein kinase C are phospholipase C gamma and phospholipase C beta. Phenolic compounds in various fruits, vegetables, spices, teas, and essential oils inhibit the phosphorylation and activation of phospholipase C gamma by taking a phenol away from tyrosine. Polyunsaturated fats such as fish oil inhibit the hydrolysis of phosphatidylinositol 4,5 biphosphate by phospholipase C gamma and beta thus limiting the production of inositol 1,4,5 triphosphate. The latter activates protein kinase C and causes intracellular calcium release and triggers Alzheimer's disease. A Mediterranean diet high in phenols and polyunsaturated fats thus may at least delay the onset of Alzheimer's disease.

Protein kinase C leads to the production of superoxide anions and Nuclear Factor kappa b which combine to form peroxynitrites. Again by taking phenols from other compounds, phenolic compounds inhibit the formation of both superoxide anions and inducible nitric oxide and thus the formation of peroxynitrites.

Specific phenolic compounds: methoxyphenols--a type of phenolic acid--are particularly good peroxynitrite scavengers. The reason for this is that the methyoxy group donates two electrons and the phenol groups (or the phenol and allyl group in the case of eugenol) donate two hdyrogen atoms converting peroxynitrites into water and a nitrite anion: ONOO- + 2H+ + 2e-= H20 + NO2-. Not only this the methoxy group increases the hydrogen donating capacity of the phenol so that it increases the ability of the phenol group to reverse the oxidation of critical transport systems, enzymes, and receptors by peroxynitrites including those involved in short-term memory.

Some methoxyphenols are not very water soluble and do not enter the bloodstream well. Curcumin is an example. But when you add piperine (in black pepper) to curcumin it becomes more easily absorbed into the bloodstream. The high consumption of curry along with other spices and herbs by people in India likely explains why it has among the lowest incidences of Alzheimer's disease in the world.

Finally, the methoxyphenols that do reach the brain in high enough concentrations have partially reversed Alzheimer's disease in patients with moderate to moderately severe Alzheimer's disease (indeed it is never too late to reverse part of the damage done by peroxynitrites). I will just post the results of the studies here. The first is by Jimbo and colleagues who used rosemary essential oil (eugenol) and lemon essential oil (geraniol) for cognition and lavender and sweet orange for calmness.

Results: All patients showed significant improvement in personal orientation related to cognitive function on both the GBSS-J and TDAS after therapy. In particular, patients with AD showed significant improvement in total TDAS scores. Result of routine laboratory tests showed no significant changes, suggesting that there were no side-effects associated with the use of aromatherapy. Results from Zarit's score showed no significant changes, suggesting that caregivers had no effect on the improved patient scores seen in the other tests.

Conclusions: In conclusion, we found aromatherapy an efficacious non-pharmacological therapy for dementia. Aromatherapy may have some potential for improving cognitive function, especially in AD patients.

The second by Heo, et al., used heat-processed ginseng which contains the following methoxyphenols: vanillic acid, p-coumaric acid, syringic acid, and ferulic acid.

OBJECTIVES: Ginseng has been reported to improve cognitive function in animals and in healthy and cognitively impaired individuals. In this study, we investigated the efficacy of a heat-processed form of ginseng that contains more potent ginsenosides than raw ginseng in the treatment of cognitive impairment in patients with moderately severe Alzheimer's disease (AD).

METHODS: Forty patients with AD were randomized into one of three different dose groups or the control group as follows: 1.5 g/day (n = 10), 3 g/day (n = 10), and 4.5 g/day (n = 10) groups, or control (n = 10). The Alzheimer's Disease Assessment Scale (ADAS) and Mini-Mental State Examination (MMSE) were used to assess cognitive function for 24 weeks.

RESULTS: The treatment groups showed significant improvement on the MMSE and ADAS. Patients with higher dose group (4.5 g/day) showed improvements in ADAS cognitive, ADAS non-cognitive, and MMSE score as early as at 12 weeks, which sustained for 24-week follow-up.

DISCUSSION: These results demonstrate the potential efficacy of a heat-processed form of ginseng on cognitive function and behavioral symptoms in patients with moderately severe AD.

Compare now to the "zumab" trials. The aromatherapy and the heat-processed ginseng did not simple slightly slow down the progression of the disease, they led to significant improvments in cognitive function even in people with moderately severe Alzheimer's disease. This is because these compounds target the cause of Alzheimer's disease: peroxynitrites and not just an intermediate stage (amyloid plaques).

Permalink to Comment

8. Hap on October 9, 2012 11:26 AM writes...

In theory, aren't Lilly's stockholders supposed to have a say? Since the results don't seem good, no matter how long someone tortures them, the likelihood of a P3 trial turning up roses (as opposed to pushing up daisies) seems pretty small. It doesn't seem like buying a billion-dollar lottery ticket (Now with even worse odds!) with investors' money is likely to make investors happy.

In addition, isn't this the kind of trial that pharma is supposed to avoid? If one of the problems that makes drug development unsustainably costly is running expensive trials with underwhelming indicators, why does being desperate make it a good idea? This can't be Lilly's only choice.

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9. barry on October 9, 2012 11:34 AM writes...

I'm puzzled that a project that requires mAbs to cross the Blood/Brain barrier ever got serious consideration. Perhaps the mAb was raised with the intention of conjugating it to a smuggling system (transferritin?) but that part of the project failed? The brain's status as an immuno-privileged organ may no longer be dogma, but it certainly points to a problem for mAb transport.

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10. Jumbo on October 9, 2012 11:55 AM writes...

Just an observation: A lot of piling on Lilly for trying to see a glass as not empty (much less half full). But remember, Roche has not been criticized for happily pouring millions in testing even earlier administration of a related anti-aBeta mAb. My point is Lilly is not alone in remaining positive about this hypothesis. Regrettably, I think they (and Roche) will be disappointed. But thinking is a poor substitute for clinical data. If more clinical work is necessary to stick a fork (or straw) in this hypothesis, perhaps it will be worth it.

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11. bhip on October 9, 2012 11:56 AM writes...

Ed-Please block Lane Simonian from posting. Other than the amusement factor, I'm not sure his offerings/soliloquies bring a lot to the table...

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12. MLH on October 9, 2012 1:15 PM writes...

Agree that the clinical and statistical significance needs to be critically reviewed, however, the patients', and their caregivers', needs require serious consideration as well
@4: "She wrote back to say he no longer can read."

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13. entropygain on October 9, 2012 1:46 PM writes...

Isn't this emblematic of the key problem in the industry-- a focus on Net Present Value(NPV) in decision making? The NPV calculation says that this could be a huge seller in the very near future, even though the odds of it working are very small and the odds of it making a meaningful difference to patients is probably nil. Therefore, the financial analysis says keep investing.

On the other hand discovery projects have so many layers of risk for failure, that they never have a positive NPV and the financial analysis says one should never invest in it. So even though something might have remarkable preclinical efficacy, a real drug like structure, the time horizon is far, execution risks are high, NPV is negative, so no money.

In Alzheimers, the data that struck me the most recently was bexarotene clearing plaques in mice 50% in 72 hrs. http://www.ncbi.nlm.nih.gov/pubmed/22323736. Another non-reproducible science paper? On the surface, seems a lot more exciting than these antibody based approaches...

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14. Lane Simonian on October 9, 2012 1:59 PM writes...

I don't mind being blocked, but I am not a big fan of censorship either. The pathways that I am giving you are not my own, they are based on the work of reputable scientist. For instance:

Proc Natl Acad Sci U S A. 1994 May 10; 91(10): 4489–4493. PMCID: PMC43811
Calcium regulates processing of the Alzheimer amyloid protein precursor in a protein kinase C-independent manner.
J D Buxbaum, A A Ruefli, C A Parker, A M Cypess, and P Greengard

Abstract
Various first messengers linked to phospholipase C, including acetylcholine and interleukin 1, regulate the production both of the secreted form of the amyloid protein precursor (APP) and of amyloid beta-protein. We have now identified intracellular signals which are responsible for mediating these effects. We show that activation of phospholipase C may affect APP processing by either of two pathways, one involving an increase in protein kinase C and the other an increase in cytoplasmic calcium levels. The effects of calcium on APP processing appear to be independent of protein kinase C activation. The observed effects of calcium on APP processing may be of therapeutic utility.

Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease
Mark A. Smith1, Peggy L. Richey Harris1, Lawrence M. Sayre2, Joseph S. Beckman3, and George Perry1
+ Author Affiliations

1 Institute of Pathology and
2 Department of Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, and
3 Department of Anesthesiology, School of Medicine, University of Alabama, Birmingham, Alabama 35233
Next SectionAbstract
Increasing evidence suggests that oxidative damage to proteins and other macromolecules is a salient feature of the pathology of Alzheimer’s disease. Establishing the source of oxidants is key to understanding what role they play in the pathogenesis of Alzheimer’s disease, and one way to examine this issue is to determine which oxidants are involved in damage.

In this study, we examine whether peroxynitrite, a powerful oxidant produced from the reaction of superoxide with nitric oxide, is involved in Alzheimer’s disease. Peroxynitrite is a source of hydroxyl radical-like reactivity, and it directly oxidizes proteins and other macromolecules with resultant carbonyl formation from side-chain and peptide-bond cleavage. Although carbonyl formation is a major oxidative modification induced by peroxynitrite, nitration of tyrosine residues is an indicator of peroxynitrite involvement. In brain tissue from cases of Alzheimer’s disease, we found increased protein nitration in neurons, including but certainly not restricted to those containing neurofibrillary tangles (NFTs). Conversely, nitrotyrosine was undetectable in the cerebral cortex of age-matched control brains. This distribution is essentially identical to that of free carbonyls.

Now if you know the beginning point and the endpoint of a disease would that not make it easier to prevent and treat it?

I will quote from the late Mark Smith: "I have received a lot of stick for my scientific talks where for over a decade I have challenged the amyloid hypothesis. I typically tell the audience that my views are controversial and that I would really appreciate someone pointing out the flaw in my logic or presenting evidence that shows that I am wrong. Neither has ever happened."

So if someone can show me evidence that the peroxynitrite hypothesis for Alzheimer's disease is wrong or that the pathways that I have pointed out leading to peroxynitrites are wrong (other than well it could be just another pathway or I don't like the studies)than speak up. Give it your best shot, but make it good.

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15. vasili on October 9, 2012 2:49 PM writes...

Lane Simonian, our dear history teacher with only 3 keys in his keyboard Ctrl, C and V.

Permalink to Comment

16. Lane Simonian on October 9, 2012 8:23 PM writes...

This is a really funny group. Maybe some chemists don't have the same respect for research as most historians do. Maybe that's the problem. The ego of some scientists prevents them from valuing the work of their counterparts. Not historians. We cannot invent the past; we have to gather information to understand it. We see how things go from point A to point B. If this disease had been treated in a similar manner, we would not have been spinning our wheels for the past twenty years. Basically all the answers were there twenty years ago. That's the real tragedy of Alzheimer's disease research--not that the disease was so complicated that it could never be understood, but that the people who understood it many years ago were ignored. Continue down the amyloid path and there will not be an effective treatment (partial reversal) of this disease ever.

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17. anon on October 9, 2012 10:22 PM writes...

When do they usually consider more speculative interpretations of phase 3 results? I would be very interested in any datamining that could show larger treatment effects. Perhaps in APOE negatives, in a specific demographic, or in the mildest subgroup of the mild. With such a large data set, there could be a subgroup that did quite well. There would be considerable interest in such a result

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18. BrikABrakk on October 10, 2012 7:54 AM writes...

Lane, I don't want to get into a huge debate, but I'll make a comment. The negative reaction to your post was due to your overly assured assertion that the cause of AD is known, and it's peroxynitrites. The problem is that there are multiple such "causes" that can be identified in the literature. Make a case for your favorite hypothesis, sure, but be humble and realize that it is only that.

Permalink to Comment

19. bmartinmd on October 10, 2012 9:04 AM writes...

These data must really be examined in peer-reviewed form before making any assumptions or fueling false hopes about Lilly's compound. I'd really like to know the reason for the selection of the ADAS-cog14 (as opposed to the more-often used and more objective ADAS-cog10 or ADAS-cog11). Also there has to be some perspective here on the absolute ADAS-cog differences between the treatment groups. How many times will people fall for a statistically significant, gee-whiz risk reduction (eg, 34%), only to find that the absolute treatment-related difference was 1 or 2 points?

Permalink to Comment

20. Lane Simonian on October 12, 2012 8:09 PM writes...

At the risk of upsetting a few more people, I am going to post the critical information regarding the methoxyphenol curcumin in the treatment of Alzheimer's disease:

1). Numerous pieces of evidence suggest that curcumin may be a promising therapy for AD because it has different neuroprotective activities, including antioxidant [9], anti-inflammatory [10] and antiamyloidogenic properties [11]. Curcumin has been demonstrated to have a strong antioxidant neuroprotective effects, scavenging ROS [12] and neutralizing nitric-oxide-(NO-) based free radicals [13]. However, one of the issues of curcumin as a therapeutic agent in the treatment of AD is its poor water solubility [14], which is one reason for its low bioavailability following oral administration or through parenteral route [15]. The poor bioavailability is one of the causes of its failure in randomized control trials for AD.

The structural features of curcumin that can contribute to the antioxidant activity are the phenolic and the methoxy group on the phenyl ring and the 1,3-diketone system. Moreover, the antioxidant activity of curcumin increases when the phenolic group with a methoxy group is at the ortho position [16, 17]. The orthomethoxy group can form an intramolecular hydrogen bond with the phenolic hydrogen, making the H-atom abstraction from the orthomethoxyphenols surprisingly easy [18]. The H abstraction from these groups is responsible for the remarkable antioxidant activity of curcumin.

Taking into account that in vivo evidence showed that peroxynitrite induces Alzheimer-like tau hyperphosphorylation, nitration, and accumulation [26], it was reported that curcumin mediates the direct detoxification of reactive nitrogen species such as peroxynitrite, thus exerting an antioxidant activity [27].

Davinelli, Pleitropic Protective Effects of Phytochemicals in Alzheimer's Disease (2012).

My only point is this if during the mid-1990s, a series of scientist found that peroxynitrite-mediated damage was widespread in Alzheimer's disease, would it not have made sense to at least see if inhibiting peroxynitrite formation, scavenging peroxynitrites, and partially repairing this damage might have some effect on cognitive function in Alzheimer's patients. Indeed, the evidence from small-sacle clinical trials using methoxyphenols that effectively reach the brain i.e. eugenol in rosemary essential oil via aromatherapy and several methoxyphenols (especially vanillic acid) in heat-processed ginseng suggests that the answer is yes. It's not my hypothesis; I have no financial stake in it nor any pride of ownership. I am just suggesting if your main interest is in treating this disease effectively this might be a good place to look.

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21. Hakan Rombe on April 26, 2014 4:40 AM writes...

My wife has tested this treatment för almost 4 years. She was in the early beginning of the Alz. desease. After these 4 years I can confirm that my wife still have most of her abilities left. The test results are almost the same after 4 years. In an average figure of the treatments success I guess there are a rather big variation. For us it´s like a wonder!

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