Showing posts with label Promising. Show all posts
Showing posts with label Promising. Show all posts

Saturday, 21 September 2013

Zalicus Is A Promising Biotech With Echoes Of Acadia Pharmaceuticals

Imagine what investors would give to be able to turn back time to November 2012 when Acadia Pharmaceuticals (ACAD) was trading in penny-stock territory. The stock has since recovered to be one of the top biotech performers of the last year. Many biotech investors missed out and I'll explain why in a minute.

First let me delve into Acadia's history to see how it got there, then I will explain why Zalicus (ZLCS) could very well be the next ACAD.

Several years ago, clinical trials failed to show that Pimavanserin was statistically significant in a late-phase trial. The company attributed part of this failure to better-than-expected placebo results, which is entirely possible. There was one other factor at play, two different doses of the drug. In the first study, the company tested patients with both 10 mg and 40mg dose. The overall result was that Acadia failed to show a statistically significant result; however, the 40 mg dosing showed a clear benefit compared to placebo. The company realized that the product was less effective at a 10 mg dose, and then focused the entire trial around what worked, the 40 mg dose. A follow-up study showed a statistically significant improvement over placebo. Pimavanserin (ACAD's lead pipeline candidate) is a potential blockbuster with a large market for off-label usage (an approved drug can be prescribed for other conditions). Savvy investors understood this and quickly gobbled up shares. Those who bought even at $6 after doubling on positive study results have quadrupled their money in less than 10 months.

Looking back on ACAD's previous study and the results that transpired, I know many investors wish they had invested in the company but the negative perception surrounding the company after the first trial failure turned off many short-sighted investors.

Zalicus also has a checkered history with the failure of Synavive (results were positive just not as effective as existing rheumatoid arthritis treatments) that caused shares to plummet.

Zalicus is developing Z160 as a first in class, oral, state dependent, selective N-type calcium channel (Cav 2.2) blocker for the treatment of neuropathic and inflammatory pain. Investors are well aware of the 2006 partnership between Merck and Neuromed where Merck licensed the compound (originally named NMED-160) from Neuromed for $25 million upfront and potentially as much as $450 million in milestones and royalties on sales. Merck dissolved the partnership a year later after a phase 2 study showed bioavailability issues. Merck noted that no serious adverse events were seen even at the highest doses. Zalicus then spent the next 7 years correcting the bioavailability issues.

A phase 1 study released in March 2012 appears to indicate the bioavailability issues have been corrected and the drug has so far showed no significant adverse events. The only question mark that remains is efficacy.

(click to enlarge)

The above diagram from phase 1 studies shows the new formulation as compared to N-MED160 compound.

Phase 1 trials results showed that the new formulation (Z-160) has a peak plasma concentration that is 8 times higher (maximum level of drug concentration in blood plasma after administration) and a 5 fold increase in bioavailability (defined as the fraction of administered drug that reaches systemic circulation). When a medication is administered intravenously, it's bioavailability is 100% but decreases when given orally due to incomplete absorption and first-pass metabolism. Pharmacodynamics is the study of what the drug does to the body while pharmacokinetics is the study of what the body does to the drug. Pharmacokinetics was the cause of the previous bioavailability issues.

(click to enlarge)

click to enlarge)

The diagram above is from a spinal nerve ligation model (Chung) showing preclinical data suggestive of efficacy on par with ziconotide, gabapentin, and morphine. Note that this model is one of the most widely used neuropathic pain models in pre-clinical testing.

Zalicus in conducting a randomized, double-blind, placebo controlled clinical study in lumbosacral radiculopathy, evaluating Z160 compared to placebo in approximately 140 subjects. The primary efficacy endpoint for this study is the change in weekly pain scores on a numerical rating scale. Other endpoints include multiple other pain, functional and safety measures. LSR is a significant unmet medical need and attractive market opportunity.

On January 3, 2013, Zalicus initiated the second phase 2a study (Clinicaltrials.gov Identifier: NCT01757873) with Z160 in patients with post-herpetic neuralgia (PHN). Clinical trials in PHN are an industry-accepted standard condition for establishing clinical proof-of-concept in neuropathic pain. It is also a potential orphan indication because the prevalence is less than 200,000 patients in the U.S.

Z944

On Sep 9th 2013, Zalicus announced the initiation of a phase 1b single ascending dose clinical trial evaluating the pharmacokinetics and safety of Z944, a novel oral T-type calcium channel blocker with demonstrated preclinical potential for the treatment of acute and inflammatory pain in animal pain models. The phase 1 trial took place in the United Kingdom. In June 2012, management reported that the trial was a success and that a maximum tolerated dose (MTD) has been identified.

There are no approved T-Type calcium channel blockers on the market. Z944 represents a potentially new and revolutionary way to treat acute pain. T-type calcium channels have been implicated in the frequency and intensity of pain signals. During the first quarter 2012, Zalicus published preclinical data in the journal Science Translational Medicine, describing the activity of Z944 to potentially suppress seizures. This data reinforces the potential biologic activity of Z944. It is generally understood that conditions of neuronal hyper-excitability, such as epilepsy and pain, are mechanistically linked.

In February 2013, Zalicus announced it had been granted a patent by the U.S. Patent and Trademark office (USPTO) covering Z944. United States patent number 8,377,968 entitled "N-Piperidinyl Acetamide Derivatives as Calcium Channel Blockers" provides broad coverage for Z944 including compositions of matter and certain therapeutic methods of use through April 2029.

Zalicus remains significantly undervalued with shares trading at less than $1 (I don't expect that to remain much longer) with a looming catalyst for a drug that could potentially generate over $2 billion in sales. Company generated revenues of $3.9 million in the third quarter, which include collaborative payments and royalties on sales of Exalgo at partner Mallinckrodt. Not many biotechs trading under $3 generate any revenue. If Z160 is successful in clinical trials and matches gabapentin, or lyrica sales, it would easily justify a stock price over 20 times the current price. Analysts have estimated the market opportunity for Z160 to be anywhere from $500 million to $2.7 billion, comparable to peak sales for gabapentin. Z160 could see significant off label usage being that it is a non-opioid with a superior side effect profile. The FDA has made a significant effort to approve drugs with less abuse potential which favors non-opioids such as Z160.

Past failures may have turned off short-sighted investors but the fundamentals remain intact. They say what doesn't kill you makes you stronger and I believe that is true in the case of ACAD and Zalicus. I also believe management has learned from past mistakes and is less likely to repeat them. The big risk is that clinical trials are inherently risky and the majority will fail for many reasons. Investors risk losing majority of their investment if the trials happen to fail. Invest only what you can afford to lose.

Disclosure: I am long ZLCS, ACAD. I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it. I have no business relationship with any company whose stock is mentioned in this article. (More...)


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Friday, 16 August 2013

CDK6 represents a promising target for anti-cancer therapy

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 15 Aug 2013 - 0:00 PDT Current ratings for:
CDK6 represents a promising target for anti-cancer therapy
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Cell division is tightly controlled by a number of genes and because of the importance of ensuring that the process stays in check - mistakes frequently lead to cancer - mammalian cells often have several inbuilt layers of security. The two cyclin-dependent kinases CDK4 and CDK6 are widely believed to have almost identical functions, so either one of them can compensate for problems with the other. New work at the University of Veterinary Medicine, Vienna challenges this view and shows that, unlike CDK4, CDK6 also promotes the growth of blood vessels. This explains why CDK6 is so frequently misregulated in certain types of cancer. The results are published in the current issue of the prestigious international journal Cancer Cell.

Cancer in humans is frequently associated with unusually high amounts of one or more proteins responsible for controlling the rate at which cells divide. As an example, excessive amounts of the cyclin-dependent kinase CDK6 are often found in types of cancer such as lymphoma. Together with a number of collaborators within Vienna and beyond, Karoline Kollmann of the University of Veterinary Medicine, Vienna (Vetmeduni) has now shown that CDK6 is part of a multiprotein complex that stimulates the production of one of the so-called INK4 family members (confusingly termed p16INK4a), which suppresses tumour growth. In other words, the cell has an inbuilt mechanism to help it cope with excessive amounts of CDK6.

The problems really start when p16INK4a is missing, as is frequently the case in lymphomas or leukaemias. Now the high levels of CDK6 are unchecked and so can lead directly to a stimulation of cell division. Furthermore, Kollmann and her colleagues showed that another CDK6-containing complex can also promote the production of an additional factor, known as VEGF-A, that increases the growth of blood vessels and thus ensures that the cells in the growing tumours are supplied with sufficient energy and oxygen to multiply. CDK6 is the first factor to be shown to be involved in regulating tumour growth while simultaneously helping to supply tumours with blood.

As its name implies, CDK6 is a kinase, i.e. it adds phosphate groups to other proteins and thereby alters their activity. In a further twist to the tale, the Vetmeduni scientists have shown that CDK6 can still exert its effects on p16INK4a and VEGF-A when it lacks its kinase activity: a mutant form of the CDK6 protein with the kinase function inactivated retains the ability to regulate expression of the p16INK4a and VEGF-A genes.

Veronika Sexl, Head of the Vetmeduni's Institute of Pharmacology and Toxicology, where the work was performed, notes the medical importance of her group's findings. "Because it is known to be involved in so many cancers, CDK6 represents a promising target for anti-cancer therapy and lots of labs are trying to design specific inhibitors. But their efforts are focused on inhibiting CDK6's kinase function. We have shown that CDK6 has an additional, kinase-independent mode of action that is responsible for the uncontrolled cell growth and increased production of blood vessels that are a hallmark of cancer. CDK6 inhibitors will also need to block this new function if they are to be effective in treating cancer."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.

The paper - A new kinase-independent function of CDK6 links the cell cycle to tumor angiogenesis by Karoline Kollmann, Gerwin Heller, Christine Schneckenleithner, Wolfgang Warsch, Ruth Scheicher, Rene G. Ott, Markus Schäfer, Sabine Fajmann, Michaela Schlederer, Ana-Iris Schiefer, Ursula Reichart, Matthias Mayerhofer, Christoph Hoeller, Sabine Zoechbauer-Mueller, Dontscho Kerjaschki, Christoph Bock, Lukas Kenner, Gerald Hoefler, Michael Freissmuth, Anthony R. Green, Richard Moriggl, Meinrad Busslinger, Marcos Malumbres and Veronika Sexl; Cancer Cell, Volume 24, Issue 2, 167-181, 12 August 2013; 10.1016/j.ccr.2013.07.012

University of Veterinary Medicine -- Vienna

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Monday, 5 August 2013

Promising compound could offer new treatment for heart failure

Main Category: Cardiovascular / Cardiology
Article Date: 03 Aug 2013 - 0:00 PDT Current ratings for:
Promising compound could offer new treatment for heart failure
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Heart failure occurs when the heart cannot pump enough blood to meet the body's needs. It's a very common condition, affecting about six million people in the United States, but current therapies are not adequately effective at improving health and preventing deaths. A study published by Cell Press August 1st in the journal Cell reveals the key role of a family of molecules known as bromodomain and extraterminal domain (BET) proteins in activating genes that contribute to heart failure. The study also demonstrates that a BET-inhibiting drug can protect against heart failure in mice, opening up promising new avenues for the treatment of this devastating condition.

"New insights into the biology of heart failure are desperately needed to prompt new types of targeted therapeutic agents," says senior study author James Bradner of the Dana-Farber Cancer Institute and Harvard Medical School. "Our findings comprise significant progress toward fulfilling this clinical need, which is great news for heart failure patients."

Heart failure is a debilitating condition that causes fatigue, shortness of breath, organ damage, and early death. It is triggered by the activation of a large set of genes that cause the walls of the heart to thicken and develop scar tissue, impairing the organ's ability to pump blood normally. BET proteins can have a huge impact on gene activity because they belong to a class of molecules called epigenetic readers, which recognize special marks on DNA-protein complexes and attract gene-activating proteins to those spots. Bradner and his collaborators recently developed a potent BET inhibitor called JQ1, which shows promise as a potential anticancer therapy. But until now, nothing was known about the role of BET proteins in heart function.

To address this question, Bradner teamed up with study senior author Saptarsi Haldar of Case Western Reserve University School of Medicine and University Hospitals Case Medical Center. They found that BET proteins regulate the growth of heart muscle cells and activate a broad set of genes involved in heart failure. Treatment with JQ1 inhibited this abnormal pattern of gene activity and protected against heart-wall thickening, the formation of scar tissue, and pump failure in a mouse model of cardiac disease.

"Based on our findings, we are highly motivated to bring a drug-like derivative of JQ1 forward as a new type of heart failure drug for humans," Haldar says. "These compounds will shortly enter the clinic for therapeutic development in cancer, and we expect they can also be immediately developed into therapies for heart failure."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cardiovascular / cardiology section for the latest news on this subject.

Cell, Anand et al.: "BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure."

Cell Press

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Study offers promising new direction for organ regeneration and tissue repair

Main Category: Biology / Biochemistry
Also Included In: Rehabilitation / Physical Therapy
Article Date: 02 Aug 2013 - 1:00 PDT Current ratings for:
Study offers promising new direction for organ regeneration and tissue repair
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Because most human tissues do not regenerate spontaneously, advances in tissue repair and organ regeneration could benefit many patients with a wide variety of medical conditions.

Now a research team led by investigators at Beth Israel Deaconess Medical Center (BIDMC) and Dana-Farber/Boston Children's Cancer and Blood Disorders Center has identified an entirely new approach to enhance normal tissue growth, a finding that could have widespread therapeutic applications.

Their findings were published on-line in the Proceedings of the National Academy of Sciences (PNAS).

Tissue regeneration is a process that is not fully understood, but previous research has demonstrated that endothelial cells lining the insides of small blood vessels play a key role in tissue growth. It is also known that these endothelial cells generate chemical messengers called epoxyeicosatrienoic acids (EETs), which stimulate blood vessel formation in response to tissue injury.

In this new research, first author Dipak Panigrahy, MD, an investigator in BIDMC's Center for Vascular Biology Research, and his colleagues wanted to find out how EETs might participate in organ and tissue regeneration. To answer this question, they created seven different mouse models. The models focused on liver, kidney and lung regeneration; wound healing; corneal vascularization; and retinal vascularization.

"We used genetic and pharmacologic tools to manipulate EET levels in the animals to show that EETs play a critical role in accelerating tissue growth, providing the first in vivo demonstration that pharmacological modulation of EETs can affect organ regeneration," explains Panigrahy, an Instructor in Pathology at Harvard Medical School. Administering synthetic EETs spurred tissue growth in the research models; conversely, lowering EET levels - by either manipulating genes or administering drugs - delayed tissue regeneration.

The team also demonstrated that proteins called soluble epoxide hydrolase (sEH) inhibitors, known to elevate EET levels, promoted liver and lung regeneration. (sEH is the main metabolizing enzyme of EETs.)

"Our results offer a mechanistic rationale for evaluating sEH inhibitors as novel therapeutics for a number of human diseases such as hepatic insufficiency after liver damage and diseases characterized by immature lung development, such as bronchopulmonary dysplasia," says Panigrahy, adding that the use of topical sEH inhibitors on the skin might also be useful for the acceleration of wound healing.

The researchers suspected that EETs were stimulating tissue regeneration by way of blood vessel formation, specifically by producing vascular endothelial growth factor (VEGF) to promote vessel growth. As predicted, when the investigators depleted VEGF in the mice, EETs' effects on organ regeneration disappeared.

"Discovering EETs' role could be of critical importance to help control the repair of liver, lungs and kidneys," says senior author Mark Kieran, MD, PhD, of the Division of Pediatric Oncology at Dana-Farber/Boston Children's Cancer and Blood Disorders Center. "Since diseases of these organs are a major cause of morbidity and mortality in the North American population, the opportunity to modulate the regeneration of healthy tissue could have significant therapeutic implications for many patients." These findings may also apply to conditions or physical defects that lead to the loss of specialized cells in other organ systems, such as the nervous system and the immune system.

The investigators stress that it will be important to determine whether EETs affect other factors, besides VEGF, in influencing tissue repair. Additionally, they add, the beneficial effects of EETs will have to be carefully weighed against their finding that direct administration of EETs can stimulate cancer growth in animal models. Several clinical trials that are currently testing the potential of sEH inhibitors for purposes other than organ regeneration or wound repair could offer valuable insights into the safety of elevating EET levels in patients.

"Although our work suggests synthetic EETs would promote wound healing after surgery, more clinical trials are needed to assess the potential benefits and possible risks of these novel lipids," adds co-corresponding author Darryl Zeldin, MD, Scientific Director for the National Institute of Environmental Health Sciences, part of the National Institutes of Health.

In addition to laying the groundwork for future research, the investigators point out that this study highlights the benefits of experts from varying disciplines and organizations working together, noting that coauthors work in departments ranging from oncology to ophthalmology and from pharmacotherapy to transplantation. They included investigators from Boston Children's Hospital; the Institute for Systems Biology; the University of California, Davis; the National Institute of Environmental Health Science at the National Institutes of Health; the University of North Carolina at Chapel Hill; the Lahey Clinic Medical Center; the University of Texas Southwestern Medical Center; the Fred Hutchinson Cancer Research Center; and Schepens Eye Research Institute/Massachusetts Eye and Ear.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our biology / biochemistry section for the latest news on this subject.

Epoxyeicosanoids promote organ and tissue regeneration, PNAS published online before print July 29, 2013, doi: 10.1073/pnas.1311565110

In addition to Panigrahy, Kieran and Zeldin, coauthors include Bruce D. Hammock (co-corresponding author); Brian T. Kalish, Sui Huang, Diane R. Bielenberg, Hau D. Lee, Jun Yang, Matthew L. Edin, Craig R. Lee, Ofra Benny, Dayna K. Mudge, Catherine E. Butterfield, Akiko Mammoto, Tadanori Mammoto, Bora Inceoglu, Roger L. Jenkins, Mary A. Simpson, Tomoshige Akino, Fred B. Lih, Kenneth B. Tomer, Donald E. Ingber, John R. Falck, Vijaya L. Manthati, Arja Kaipainen, Patricia A. D'Amore, and Mark Puder.

This work was supported by grants from the National Cancer Institute (RO1CA148633-01A4); the Stop and Shop Pediatric Brain Tumor Fund; the C. J. Buckley Pediatric Brain Tumor Fund; the Children's Hospital Boston Surgical Foundation and the Vascular Biology Program; the Robert A. Welch Foundation (GL625910); the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01 025034 and Z01 050167); the National Institutes of Health (R01 GM088199; GM31278; R01 ES002710; R01 ES013933, and CA045548; and the NIEHS Superfund Basic Research Program (NIH Grant P42 ES004699). The work was also supported through the Joshua Ryan Rappaport Fellowship and Howard Hughes Medical Institute Research Fellowship.

Beth Israel Deaconess Medical Center

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Monday, 29 July 2013

'Promising' blood test discovered for Alzheimer's dementia

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Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience;  Mental Health;  Psychology / Psychiatry
Article Date: 29 Jul 2013 - 0:00 PDT Current ratings for:
'Promising' blood test discovered for Alzheimer's dementia
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Researchers in Germany have identified a new blood test that may in future provide much earlier diagnosis of Alzheimer's disease and other degenerative disorders.

The team, from Saarland University and Siemens Healthcare, describe their test in the open access journal Genome Biology. They found it could be used to discriminate between people with Alzheimer's from healthy people without the dementia.

Alzheimer's disease, the most common form of dementia, can currently only be diagnosed with certainty at autopsy, so there is considerable interest in finding reliable, non-invasive biomarkers for diagnosis in living people.

Andreas Keller focused on microRNAs (miRNAs), working with colleagues from Siemens Healthcare, Saarland University at Homburg, and three other German universities, as well as The Scripps Research Institute, of La Jolla, California. The small non-coding RNA molecules are known to influence the way genes are expressed, and miRNAs can be found circulating in bodily fluids, including blood. ?

The team highlighted and tested a 'signature' panel of 12 miRNAs among 48 people with Alzheimer's and 22 healthy controls and discovered different levels in the people with the dementia.

They then developed the tests in a larger cohort of 202 people, comprising not only people with Alzheimer's disease alongside healthy controls, but also patients with other neurological and neurodegenerative disorders.

Here, the new test not only reliably distinguished people with Alzheimer's from the controls with normal health but was also able to identify other conditions.

Useful biomarkers need to be accurate, sensitive (correctly identifying people with the disease) and specific (correctly filtering out people without the disease).

The new test scored highly on all three measures. It was:

93% accurate95% sensitive92% specific.

However, the authors caution that while their blood test shows obvious promise, it still needs to be validated for clinical use, and may eventually work best when combined with other standard diagnostic tools, such as imaging.

Since people with other brain disorders can sometimes show Alzheimer's-like symptoms, the team also looked for the miRNA signature in other patient groups. Interestingly, while the 12 miRNAs were chosen for their potential to separate Alzheimer's disease from controls, the same signature was more than 95% accurate in distinguishing controls from people with various psychiatric disorders, such as schizophrenia, depression and bipolar conditions.

It was less accurate (around 82%) in distinguishing patients with other neurodegenerative disorders, such as mild cognitive impairment, Parkinson's disease and multiple sclerosis, from controls.

The test was also able to discriminate between Alzheimer's patients and those with other neurodegenerative disorders, with an accuracy of around 75%.

The authors believe accuracy in distinguishing Alzheimer's disease from the wider range of neurodegenerative conditions might be improved by tweaking the miRNAs used in the test. They explained:

"Since the 12-miRNA signature has been tailored to differentiate between Alzheimer's disease and controls, other miRNAs may likely contribute to a signature that permits also a better differentiation between the other tested diseases and Alzheimer's disease."

The work at Saarland builds on previous studies highlighting the potential of miRNAs as blood-based biomarkers for many diseases, including numerous cancers. It also suggests that miRNAs could yield useful biomarkers for various brain disorders and sheds further light on the mechanisms underpinning Alzheimer's disease.

Two of the miRNAs are known to be involved in amyloid precursor protein processing, which itself is involved in the formation of plaques, a classic hallmark of Alzheimer's disease. Further, many of the miRNAs are believed to influence the growth and shape of neurons in the developing brain. ?

Written by Nick Valentine


Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our alzheimer's / dementia section for the latest news on this subject. Genome Biology 2013, 14: R78. DOI: 10.1186/gb-2013-14-7-r78. Published online 29 July 2013. Please use one of the following formats to cite this article in your essay, paper or report:

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