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    You are here : Home » MS Research News » Drugs » Lisinopril

    Lisinopril

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    Stanford University grants rights for exclusive use of Lisinopril in Multiple Sclerosis

    LisinoprilTransparency Life Sciences, LLC (TLS) the world's first drug development company based on open innovation and crowdsourcing, today announced that it has concluded an agreement with Stanford University giving the company an exclusive option to license intellectual property covering the use of lisinopril as a treatment for multiple sclerosis (MS).

    Separately, TLS announced that MS expert Dr. Lawrence Steinman, the George A. Zimmermann Professor of Neurology and Neurological Sciences & Pediatrics at the Stanford School of Medicine and Chair of the TLS Scientific Advisory Board, presented preclinical data on the potential of lisinopril in MS at a recent Gordon Conference.

    "This is an exciting development for those of us who have been exploring the potential of lisinopril as a treatment for MS," noted Professor Steinman. "We have assembled a substantial body of preclinical data that confirms the role of the angiotensin system in the pathology of MS, along with evidence that the widely used ACE inhibitor lisinopril can modulate those effects in target-specific ways. We are delighted that drug development game-changer Transparency Life Sciences has chosen lisinopril as its first development candidate, enabling us to test whether these provocative preclinical findings can translate into a safe and affordable new therapeutic option for MS patients."

    Interested individuals are invited to contribute to the design of the protocol for the Phase II trial of lisinopril in multiple sclerosis. The protocol template is currently available on a prototype of the company's crowdsourced web platform that allows patients, physicians, researchers and others to participate in the design of clinical studies for compounds that TLS has in-licensed for development.

    Tomasz Sablinski, M.D., Ph.D., founding CEO of TLS, noted, "Lisinopril is an inexpensive and effective drug that has been used safely by millions of people around the world to control their high blood pressure. A growing body of evidence suggests that it could also play an important role in helping to control the complex immunological and inflammatory processes associated with MS. Lisinopril is an ideal candidate for our strategy of radically redesigning the clinical trial process to assess the potential of drugs that might otherwise never be tested. We invite anyone with an interest in helping to advance MS therapy to visit our website and contribute to the design process."

    The work of Dr. Steinman and others has demonstrated that both angiotensin receptors and an angiotensin-producing enzyme are abundant at sites of disease and inflammation in brains affected by multiple sclerosis. In animal models of MS, studies have shown that blockade of these receptors with the angiotensin inhibitor lisinopril reduces the areas affected by pathology and provides significant clinical benefits, including reduction in paralysis and improved mobility. In these studies, lisinopril reduced molecular measures of inflammation that accompany MS, yet it did not inhibit overall immune function. In addition, lisinopril triggered proliferation of regulatory T cells, which are known to help moderate or prevent autoimmune disease.

    Transparency's game-changing approach is based on three principles. First, crowdsourcing is being employed to design clinical protocols with the participation of patients, medical experts, front-line physicians and others, which is expected to result in protocols focused on those parameters most relevant to actual clinical practice. Second, Transparency is leveraging telemedicine and related technologies to reduce burdens on clinical trial subjects, enhance data quality and reduce costs. Third, TLS is committed to demonstrating how data transparency can accelerate and improve the drug development process.

    Professor Steinman's talk, "New Targets for Old Arrows: Potential for Angiotensin Blockade in Multiple Sclerosis", was presented at the Gordon Conference Angiotensin: Emerging and Evolving Paradigms In the Renin-Angiotensin Systemin Ventura, CA on March 1, 2012.

    About Transparency Life Sciences

    Transparency Life Sciences (TLS) is the world's first drug development company based on open innovation. TLS acquires promising drug compounds for significant unmet medical needs and tests them in clinical trials that leverage crowdsourcing methods, advances in telemedicine and data transparency. The company expects to realize significantly reduced costs and clinical timelines.

    To learn more about TLS, visit the company's prototype crowdsourced web platform at http://transparencyls.com

    Source: Market Watch Copyright © 2012 MarketWatch, Inc (06/03/12)

    Could an inexpensive hypertension drug be a new multiple sclerosis treatment?

    LisinoprilTurning serendipity into science, researchers at the Stanford University School of Medicine have found a link, in mice and in human brain tissue, between high blood pressure and multiple sclerosis. Their findings suggest that a safe, inexpensive drug already in wide use for high blood pressure may have therapeutic value in multiple sclerosis, as well.

    While neurology professor Lawrence Steinman, MD, senior author of the new study, cautioned that extensive clinical trial work is needed to determine if the drug, known as lisinopril, can do in humans what it does in mice, he is excited that "we were able to show that all the targets for lisinopril are there and ready for therapeutic manipulation in the multiple-sclerosis lesions of human patients. Without that, this would be just another intriguing paper about what's possible in the mouse."

    The paper was published online on Aug. 17 by the Proceedings of the National Academy of Sciences.

    The genesis for the paper can be traced to about seven years ago, when Steinman learned he had high blood pressure. His doctor put him on lisinopril, which is used by millions of people all over the world and has an excellent safety profile. Chagrined, Steinman went home and, researcher that he is, immediately did a Google search on the drug. (Steinman is a renowned multiple sclerosis investigator whose earlier work on the inflammatory features of the disease spurred development of a blockbuster class of anti-inflammatory multiple-sclerosis therapeutics. The drug natalizumab, marketed under the trade name Tysabri, is one.)

    Long ago, a glitch crept into Steinman's home computer: No matter what keywords he types into the search field, the computer automatically inserts the additional term, "multiple sclerosis." Thus, to his surprise, a list of medical literature popped up offering tantalizing, if vague, hints of a possible connection between multiple sclerosis and a fast-acting hormone, angiotensin, whose receptors abound on blood-vessel walls throughout the body.

    In response to, say, a change in posture, angiotensin immediately causes blood vessels to constrict. "That raises your blood pressure so when you stand up to get out of a chair, you don't fall down and faint," said Steinman, who is also the George A. Zimmerman Professor in the medical school. But angiotensin overactivity causes chronic hypertension. Lisinopril controls blood pressure by blocking an enzyme that converts angiotensin's precursor into the active hormone. The drug also appears to have certain anti-inflammatory properties.

    Multiple sclerosis is a chronic and occasionally lethal autoimmune disease in which the body's immune system mounts recurring assaults on the myelin sheathing of nerve cells in the brain. This causes nerves to malfunction and can lead to blindness and paralysis. Both multiple sclerosis and atherosclerosis involve inflammatory processes.

    Eventually, Steinman and his colleagues decided to test the angiotensin/multiple-sclerosis relationship using modern scientific techniques. First, they examined the multiple-sclerosis lesions of brain samples from autopsied patients. In those lesions, well-established molecular-detection methods turned up significantly elevated levels of both the angiotensin receptor and the angiotensin-producing enzyme blocked by lisinopril.

    Next, the investigators turned to an equally well-established animal model: a laboratory-bred strain of mouse that, after being immunized with a particular chemical, develops brain lesions very similar to those observed in multiple sclerosis. When, before immunization with the disease-triggering chemical, mice got lisinopril dosages equivalent to those prescribed for humans with high blood pressure, they didn't develop the paralysis characteristic of disease progression. Strikingly, if it was given after the mice developed full-blown symptoms, lisinopril reversed their paralysis.

    The team also found that lisonopril administration reduced numerous molecular measures of inflammation that accompany multiple sclerosis in humans and its analog in the animal model. But, importantly, the drug didn't inhibit the mice's overall immune competence.

    An additional observation was that lisinopril administration triggered proliferation of an important class of immune cells, called regulatory T cells, that prevent autoimmune diseases by dialing down the activity of other immune cells erroneously targeting cells and tissues that should be left alone. It's likely, Steinman said, that this proliferation was a key component in the protection provided by the drug, as an infusion of regulatory T cells from mice that had been given lisinopril was sufficient to prevent or reverse the disease process in mice that had been given none.

    Steinman's results have major public-health implications, said Marc Feldmann, an Imperial College London immunologist who is familiar with the study but did not participate in it. He noted that the current therapies for multiple sclerosis (including Tysabri) are pricey monoclonal antibodies, costing tens of thousands of dollars annually for each patient treated. "If multiple-sclerosis patients can be treated with lisinopril at something like 1 percent of the price of treatment with Tysabri, then far more patients will receive adequate therapy, at a substantially lower cost to those paying for it," Feldmann said.

    Commenting on the study, Helen Yates, Multiple Sclerosis Resource Centre Chief Executive said, “This new piece of research could be very exciting news indeed. If the researchers can progress this work into a human model with similar results to those shown in mice, it could prove to be a very cost effective treatment for MS. The possibility that lisinopril could prevent lesion development is, of course, an even more exciting prospect. Let’s hope that the researchers can take this work to the next level soon”

    Source: Stanford University Medical Center (18/08/09)

    © Multiple Sclerosis Resource Centre (MSRC)

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