The research report Immunology Market Global Industry Analysis 2019 2025 offers precise analytical information about the Immunology market. The report identifies top players in the global market and divides the market into several parameters such as major drivers market strategies and imposing growth of the key players. Worldwide Immunology Industry also offers a granular study of the market dynamics, segmentation, revenue, share forecasts and allows you to make superior business decisions. The report serves imperative statistics on the market stature of the prominent manufacturers and is an important source of guidance and advice for companies and individuals involved in the Immunology industry.

This Immunology market report bestows with the plentiful insights and business solutions that will support our clients to stay ahead of the competition. This market report contains categorization by companies, region, type, and application/end-use industry. The competitive analysis covered here also puts light on the various strategies used by major players of the market which range from new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and many others that leads to increase their footprints in this market. The transparent research method carried out with the right tools and methods makes this Immunology market research report top-notch.

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Competitive Landscape

Global Immunology market is highly split and the major players have used numerous tactics such as new product launches, acquisitions, innovation in products, expansions, agreements, joint ventures, partnerships, and others to increase their footprints in this market.

Key players profiled in the report include: AbbVie, Amgen, F. Hoffmann-La Roche, Johnson & Johnson, Bionor Pharma, Celgene, Cellectar Biosciences, eFFECTOR Therapeutics

Market Segmentation

Immunology Market report segmentation on Major Product Type:Immuno Boosters, Immunosuppressants

Market by Application: Here, various application segments of the global Immunology market are taken into account for the research study.

Autoimmune Diseases, Oncology, Organ Transplantation, Others

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Regional Analysis

The Immunology market report keenly emphasizes on industrial affairs and developments, approaching policy alterations and opportunities within the market. The regional development methods and its predictions are explained in every key point that specifies the general performance and issues in key regions such as North America, Europe, Asia Pacific, Middle East, South America, and Middle East & Africa (MEA). Various aspects such as production capability, demand, product value, material parameters and specifications, distribution chain and provision, profit and loss, are explained comprehensively in the market report.

Key Questions Answered in Global Immunology Market Report:-

What will the market growth rate, overview, and analysis by type of global Immunology Market in 2026?

What are the key factors driving, analysis by applications and countries Global Immunology Market?

What are dynamics, this summary includes analysis of the scope and price analysis of top players profiles of Global Immunology Market?

Who are the opportunities, risk and driving forces of the global Immunology Market?

Who are the opportunities and threats faced by the vendors in the Global Immunology Market?

What are the Global Immunology market opportunities, market risk and market overview of the Market?

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Global Immunology Market 2019 by Manufacturers, Countries, Type and Application, Forecast to 2025 - E-Industry News

Wonder Drake of Vanderbilt University in Nashvillein her lab with some of the students she supports through the National Institutes of Healths diversity supplements

By Jeffrey MervisDec. 13, 2019 , 4:10 PM

Wonder Drake knows how being poor can hinder someones dream of becoming a biomedical researcher.

Raised in rural Alabama by a single mother who never graduated from high school, Drake overcame those obstacles by finding mentors willing to take her under their wing. Now a professor of medicine at Vanderbilt University in Nashville, Drake has repeatedly returned that favor by participating in a National Institutes of Health (NIH) program aimed at improving the diversity of the biomedical workforce.

Under the program, NIH grantees such as Drake can win additional funding, called diversity supplements, to aid students from one of several groups underrepresented in biomedical research. Some 90% of the awards made in 2018 serve students who are Hispanic or African American, whereasfewer than 1% of investigators cite the category of economically disadvantaged when applying for a diversity supplement.

NIH officials think that tiny slice should be bigger. So last month, the agency tweaked its definition of the word disadvantaged in hopes that the diversity supplements would serve a broader swath of that population.

Diversity supplements can be used to support students from high school through postdoctoral training. NIHs previous definition of disadvantaged referred to students whose pursuit of a research career was hampered by living in an educational environment such as those found in certain rural or inner-city environments. But that language may have confused people, says Michael Lauer, who leads NIHs office of extramural research. What does [that] mean? Lauer asked in a 26 November blog announcing the change, adding that the phrase is nearly impossible to evaluate.

NIHs new definition of disadvantagedwhich applies to all of the agencys programs meant to foster diversityhas seven components. A person is eligible if they have been homeless, or qualified for a free or reduced-priced lunch in elementary or high school, or if they meet the income level requirements to receive a federal Pell grant to help finance their college education. NIH also invites in those who were in foster care, whose parents never graduated from college, or who grew up in a rural area or a region with a shortage of health professionals.

We wanted to make it easy for students to self-identify while not being overly redundant, says Jon Lorsch, director of the National Institute of General Medical Sciences in Bethesda, Maryland, the hub of NIHs diversity activities. The goal of the supplements remains the same, he says: helping students overcome barriers caused by their low economic status.

Drake, for one, applauds NIHs move. The new definition may attract more students who are immigrants, or poor Caucasians, she speculates. Just think how useful their input would be in finding solutions to the opioid crisis, which is ravaging so many low-income communities.

Drake notes that she would have met several of the new eligibility criteria when she was a student. I certainly grew up disadvantaged, she says. She is also African American, so she would have qualified in that category as well.

Drake, who has received many diversity supplements, typically chooses students from a racial or ethnic minority because its obvious. Students of color at Vanderbilt who want a research experience tend to seek her out, Drake adds.

But she also contacts nearby institutions that educate large numbers of students who fit NIHs definition of diversity. I call up the chair of the basic science department and I tell them, I need your best student, she says. Then I give them the chance to see what its like to be a scientist. The goal is to have them complete a research project over the summer, she says, and then present a poster session at a scientific conference.

The new definition of disadvantaged could help more students tap into such experiences. And Drake says, Based on my experience, the economically disadvantaged students are sometimes the most talented because they have had to overcome so much adversity.

A National Institutes of Health diversity program helped Matthew Bruce begin to trainfor a career as a biomedical researcher after he spent 4 years in prison for armed robbery.

Some diversity experts fear eligible students could shy away from identifying themselves as economically disadvantaged because of the stigma associated with the term. I was a single mother on Medicaid and food stamps during part of my student years, and also the first in my family to go to college, but I never thought of it as being a disadvantage, says a researcher who has led diversity efforts at her institution. I am also averse to playing the hardship card.

But others arent too worried. I think that students with the potential to succeed in graduate school would not be dissuaded, says Jacqueline Tanaka, a professor emeritus of biology at Temple University in Philadelphia, Pennsylvania, and former director of its Minority Access to Research Careers (MARC) program, one of NIHs longest running diversity initiatives. They are probably already carrying a lot of student debt, and this is an opportunity to get the type of research experience they need to move ahead.

In fact, Tanaka would like to see NIH broaden the definition even more to include students with backgrounds like that of Matthew Bruce, now a third-year graduate student in immunology at the University of California, Davis. In 2008, Bruce used a gun to rob a convenience store for money to support his drug habit. A few months, later he turned himself in, pleaded guilty, and served 4 years in a Pennsylvania state prison.

After his release, Bruce juggled work and a full load of courses at a local community college before transferring to Temple. There, Tanaka recruited him to the MARC program, which offers high-achieving, upper-level undergraduate students the type of research experiences they need to get into a good graduate program, the first rung on an academic career.

It may sound corny, Bruce says, but being in the MARC program was everything to me. I was feeling the imposter syndrome times 100, he says about the well-documented phenomenon of students from disadvantaged backgrounds underestimating their ability to make it in science.

I didnt come from the same background as my peers, and I hadnt really paid much attention in school [because of his drug dependency], Bruce continues. When Dr. Tanaka told me that, as a scientist, I would essentially get paid to solve problems, I said, That sounds phenomenal. Sign me up. In 2017 he graduated from Temple with a near-perfect academic record.

Bruce grew up in rural Pennsylvania, was the first in his family to attend college, and received a Pell grant, so he would likely qualify as disadvantaged under NIHs new definition. But what really sold Tanaka on Bruce was how he had overcome a huge obstacleincarcerationthat is not included in the definition.

Lorsch saysNIH is open to further revisions of the criteria for disadvantaged. Our goal is to give students as many on-ramps as possible, he says.

And money is not an impediment. Lorsch estimates that NIH could, without straining its budget, accommodate a 10-fold increase in the number of supplement applications that cite the disadvantaged category; in 2018 there were fewer than 11 such applications.

Given that NIH funds nearly two-thirds of the proposals it receives for diversity supplements, Drake doesnt understand why more of her colleagues dont apply. I think [the diversity supplements] are one of the best-kept secrets at NIH, she says. And were doing everything we can at [Vanderbilt] to spread the word.

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NIH clarifies meaning of 'disadvantaged' in bid to boost diversity in science - Science Magazine

On 9 December, 1979, health officials declared smallpox as the first and only human disease to be eradicated in what is considered the greatest achievement of modern medicine. Four decades on, the U.S. and Russia still maintain samples of the potentially deadly virus, and the debate on whether they should be kept or destroyed rages on.

We don't know where smallpox came from. But the infectionwhich is caused by two related variola virusesis thought to date back to the Egyptian Empire in the 3rd Century BCE, with its pustules found on the head of the Egyptian Pharaoh Ramses V. Trade and the expansion of civilizations helped the disease, found only in humans, spread. Characterized by symptoms including a fever, a widespread rash of fluid-filled blisters, vomiting and diarrhea, smallpox is estimated to have killed as many as 300 million people in the 20th century alone.

Following a failed attempt to wipe out the disease in 1959, efforts were renewed in 1967. Thanks to a worldwide vaccination program, the last person to ever be naturally infected by smallpox fell ill in Somalia, on October 12, 1977. By 9 December, 1979, the WHO had concluded the virus had been eradicated worldwide. And on May 8, 1980, the 33rd World Health Assemblythrough which the World Health Organization is governed by its member statesdeclared the world free of smallpox. Amid the Cold War, the body decided it would be wise to have two smallpox repositories in the West and one in the Soviet Bloc, in the interests of political neutrality.

To this day, only two remaining stocks of the variola virus are known to exist. They are kept under high-security conditions at a U.S. Centers for Disease Control and Prevention laboratory in Atlanta, and at Russia's State Research Centre of Virology and Biotechnology (Vector) in the Siberian city of Novosibirsk. Everything known about their location is in the public domain except for the exact rooms and freezers where the samples are kept, David Relman, professor of microbiology and immunology at Stanford University, told Newsweek.

Experts agreed on keeping the virus in case the disease reappears, and in order to help to improve vaccines, create treatments, antivirals and improve diagnostics methods. Any work on variola must be pre-approved by the World Health Organization, which takes inventories on samples every year, and inspects the labs biennially.

Until these objectives are met, the World Health Organization agrees the stocks should not be destroyed. Professor Grant McFadden, director of the Biodesign Center for Immunotherapy, Vaccines, and Virotherapy at Arizona State University, told Newsweek: "There remains debate about how close each of these goals is to completion."

So far, the decision to retain the samples has been somewhat fruitful. In 2018, for instance, the FDA approved the first drug that it believes could treat smallpox. Following a meeting in September 2018, members of the WHO's Advisory Committee on Variola Virus Research were divided, but once again concluded the repositories are still needed to develop an antiviral drug different from the one approved by the FDA.

While some argue the aims of the research agenda have been essentially achieved, McFadden said, others point to the fact only one new drug is now available, the animal models to test the new vaccines are currently inadequate, and the new generation of diagnostics remain unproven, he said.

The virus is needed to test the efficacy of new vaccines and drugs, David Relman, professor of microbiology and immunology at Stanford University, told Newsweek. "And chemical synthesis of the virus, in the event of destruction and then unexpected re-emergence and the need for new testing with the virus, would take too long," he said.

But what ifothers arguethe virus was released by accident, or on purpose? As people are no longer vaccinated against smallpox, this could potentially spark a large and deadly epidemic or pandemic, Amesh A. Adalja, a senior scholar at Johns Hopkins Center for Health Security, told Newsweek. Its potential as a tool of bioterrorism adds another layer to the controversial question of smallpox stock retention.

Concerning incidents have reignited the debate over the years. Previously unknown smallpox vials were found in an FDA building at the NIH Bethesda campus back in 2014. Last year, biosecurity experts feared the publication of a study that detailed the replication of the horsepox virus could provide terrorists with a recipe for making a pathogen that causes smallpox. And in September of this year, an explosion occurred at the Vector lab, (during which the smallpox samples were unscathed).

Relman told Newsweek that while he believes it is safe, but "not foolproof," to keep the repositories, he is "much more worried about the re-synthesis of smallpox from chemicals in the library and re-booting the virus with methods that have now been published."

McFadden is also concerned by that prospect, as well as the potential existence of any undeclared stocks.

For Adalja, the time has come to get rid of smallpox once and for all. "The virus should be destroyed," he said. "As time passes, the initial reason for keeping viable virus has less support."

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"In 2019, we now have achieved most of those milestones so it has become increasingly unnecessary to keep viable virus, especially since its genetic sequence is known and the virus could be recreated if needed," he argued.

"Keeping the viable stocks and working with them could lead to laboratory accidents with resultant infection and spread. The stocks could also be misused or fall into the wrong hands and be used nefariously," Adalja said.

Relman countered that in his view, the arguments for retention are stronger than the arguments for destruction. Not until re-synthesis can happen overnight and is reliable "will the balance of the arguments shift, and by then, by definition, we're back to the same or greater danger despite destruction," he said.

McFadden, meanwhile, said remains agnostic on the issue. "A great deal has been achieved on the original research goals, but the argument that more remains to be done is hard to refute," he said.

"I believe that a fully unanimous opinion of the research community and public health experts familiar with variola virus will be hard to achieve in the near future, and so the destruction decision will need to be political," he said. "It is important to have these debates about whether mankind should deliberately eliminate feared pathogens, or study them."

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Smallpox Was Eradicated 40 Years Ago, So Why Are the U.S. and Russia Still Holding Stocks of the Virus? - Newsweek

Viral and bacterial infections are not the only causes of inflammation of body tissue. It has been known for some time that certain fat molecules in our bloodstream can also trigger an inflammatory response. Patients with higher levels of these fats in their blood have a significantly greater chance of dying early from kidney damage or vascular disease. This causal link has now been clearly demonstrated by an international team of researchers led by Dr. Timo Speer of Saarland University.

The research team was able to show how these fat molecules interact with body cells and how they can mobilize the body's own immune system to damaging effect. The study's findings have now been published in the highly respected medical journal 'Nature Immunology'.

Doctors interested in ways to minimize the risk of cardiovascular disease have long had blood cholesterol levels in their sights. But other types of blood fats (also known as 'lipids') can also be damaging to health.

Our work has involved studying a special group of lipids, the triglycerides. We've been able to show that when these naturally occurring fats are present at elevated concentrations they can alter our defense cells in such a way that the body reacts as if responding to a bacterial infection. This leads to inflammation, which, if it becomes chronic, can damage the kidneys or cause atherosclerosis - the narrowing of arteries due to a build up of deposits on the inner arterial wall. And atherosclerosis is one of the main causes of heart attacks and strokes."

Timo Speer, Saarland University

Speer, who has doctorates in medicine as well as biology, is the lead author of the work just published in Nature Immunology.

The large-scale study was able to demonstrate that patients with elevated levels of triglycerides in their blood had a significantly higher mortality rate than comparison groups with a similar health history. 'Put another way, we can now say that adopting a low-fat diet can significantly extend the life expectancy of high-risk patients, such as those with diabetes or those whose blood pressure is too high,' says Timo Speer. Blood triglyceride levels rise substantially in people who eat a high-fat diet. 'As a result of biochemical changes, the triglycerides develop toxic properties that activate the body's innate immune system. This initiates a series of self-destructive processes including those in which the walls of the arteries are attacked and the blood vessels become occluded, reducing blood flow,' explains Speer. The study has established a definitive link between the chronic inflammation triggered by an elevated triglyceride concentration in the blood and secondary diseases such as kidney failure or heart attack. 'We hope that our results will help in developing new strategies for treating and preventing these life-threatening diseases,' says Timo Speer.

The publication in Nature Immunology is one of the results of the diverse range of scientific investigations being carried out as part of a Transregional Collaborative Research Centre between Saarland University and RWTH Aachen University. The focus of the work performed within the Collaborative Research Centre is to discover which cardiac and vascular diseases can be caused by chronic kidney disease. The German Research Foundation (DFG) is funding this major research programme with ten million euros over a three-year period. Timo Speer is the lead researcher for one the research projects. He is also a senior physician at Saarland University Hospital and laboratory director for experimental and translational nephrology.

Source:

Journal reference:

Zewinger, S., et al. (2019) Apolipoprotein C3 induces inflammation and organ damage by alternative inflammasome activation. Nature Immunology. doi.org/10.1038/s41590-019-0548-1.

Posted in: Medical Science News | Medical Research News | Medical Condition News

Tags: Apolipoprotein, Atherosclerosis, Blood, Blood Pressure, Blood Vessels, Cardiovascular Disease, Cholesterol, Chronic Kidney Disease, Diabetes, Diet, Heart, Heart Attack, Hospital, Immune System, Immunology, Inflammasome, Inflammation, Kidney, Kidney Disease, Kidney Failure, Laboratory, Life Expectancy, Lipids, Medicine, Mortality, Nephrology, Research, Triglyceride, Vascular

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Research shows how high levels of blood fat induce inflammation and organ damage - News-Medical.net

La Jolla, California-based immunology specialist Equillium has inked a deal with Biocon, expanding an existing collaboration and license agreement.

The deal builds on the firms research into Biocons novel biologic itolizumab, granting Equillium exclusive rights for developing and commercializing the candidate in Australia and New Zealand. The firm secured rights to the US and Canadian markets in May 2017.

Itolizumab is a novel first-in-class humanized anti-CD6 monoclonal antibody, which Biocon developed and launched in India under the brand name Alzumab, to treat moderate to severe plaque psoriasis in 2013.

The firms are working to develop the candidate for a wide range of autoimmune disorders.

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BRIEFEquillium and Biocon expand itolizumab deal - The Pharma Letter

Illinois-based AbbVie and La Jolla, California-based The Scripps Research Institute entered into a broad research collaboration in oncology, immunology, neurology and fibrosis.

Based on our strong switchable CAR-T alliance launched in 2018, we feel the expanded relationship with AbbVie represents a robust path forward for some of our programs, complementing a diverse ecosystem of innovation weve created over the past several years at Scripps to advance life-changing therapies, said Peter Schultz, chief executive officer of Scripps Research and Calibr, its drug discovery division.

Under the terms of the 2018 agreement, AbbVie paid Calibr an upfront license fee and picked up exclusive access to Calibrs switchable CAR-T platform for up to four years. The plan was to develop T-cell therapies against solid tumor targets chosen by AbbVie. AbbVie had the option to develop more cell therapies toward its targets and license existing Calibr cell therapy programs in hematological and solid cancers, including Calibrs lead programs.

In the new collaboration, in addition to the initial programs, Scripps will offer AbbVie a certain number of preclinical programs each year to be included in the partnership. They will work together in parallel to advance CD3 bispecifics against cancer targets picked by AbbVie

Under the terms of the deal, Scripps will run preclinical R&D, and in some cases, Phase I clinical trials. AbbVie will have an exclusive option to continue development and possible commercialization activities.

Once AbbVie chooses to exercise its option on any given program, it will pay Scripps additional payments that include option exercise fees, success-based development and commercial milestone payments, and tiered royalties. At hitting a milestone, AbbVie will make an undisclosed upfront payment as well as near-term milestone payments.

The best way to develop transformational medicines is through collaborations that bring together the brightest minds, said Mohit Trikha, vice president and head of oncology early development at AbbVie. This partnership with Scripps Research will collaboratively advance next generation programs, build stronger relationships with proven and emerging scientific leaders, and most importantly help us advance novel medicines for patients.

Trikha added, We are eager to partner with Scripps on these assets as they enter the clinic over the next few years as Scripps has one of the strongest track records of any academic institution when it comes to advancing novel medicines for patients.

Although neither organization released financial terms, they did say the partnership requires antitrust review. Under the law, reports The San Diego Union-Tribune, antitrust review has to be conducted for deals exceeding $84.4 million.

The Tribune notes, A deal of that size will bolster the La Jolla biomedical science institutes troubled finances for several years, and perhaps much longer. And if approved cancer therapies result, the payout could be gigantic.

The early work will be on an immuno-oncology treatment for lymphoma, which Calibr plans to launch in the clinic in 2020.

What were developing is a fully controllable, universal switchable CAR-T cell platform that allows a physician fine control over the activation and specificity of the CAR-T cells, Travis Young, director of protein sciences at Calibr told The Tribune.

At the moment, there are two CAR-T products approved, Novartis Kymriah and Gilead Sciences Yescarta. Both are quite effective in certain patient populations, but the process is expensive and time-consuming, requiring immune cells be collected from the patient, engineered to focus on the patients specific cancer, then be infused back into the patient. A number of companies are working on off-the-shelf CAR-T, that would not require the specific engineering catered to each patient.

CAR-T and other immunotherapy approaches also have high risks of immune reactions, although Novartis and Gilead have both developed protocols for minimizing or dealing with them. Scripps argues that their type of CAR-T improves over these, particularly in terms of safety, convenience and versatility.

These antibody-based switches bridge the CAR-T cells to the target cell. And so, by forming that bridge, they develop an immunological synapse, which redirects the CARs very specifically towards the target cells, said Young.

They also claim they can control the intensity of the response by varying the number of antibodies infused, would should minimize the adverse immune reactions.

The Tribune notes that in recent years Scripps has reported annual deficits that have hit as high as $20 million. The company currently has a drug in early clinical trials for osteoarthritis and is prepping another for prostate cancer, which it is hoping to partner with a company for commercialization.

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AbbVie and Scripps Research Enter Research Partnership in Cancer, Immunology, Neurology and Fibrosis - BioSpace

Chase Burton, Mee Y Bartee, Eric Bartee

Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA

Correspondence: Eric BarteeDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, USAEmail bartee@musc.edu

Introduction: Cancer has become one of the most critical health issues of modern times. To overcome the ineffectiveness of current treatment options, research is being done to explore new therapeutic modalities. One such novel treatment is oncolytic virotherapy (OV) which uses tumor tropic viruses to specifically target and kill malignant cells. While OV has shown significant promise in recent clinical trials, the therapeutic use of viruses poses a number of unique challenges. In particular, obtaining effective viral spread throughout the tumor microenvironment remains problematic. Previous work has suggested this can be overcome by forcing oncolytic viruses to induce syncytia formation.Methods: In the current work, we generated a series of recombinant myxoma viruses expressing exogenous fusion proteins from other viral genomes and examined their therapeutic potential in vitro and in vivo.Results: Similar to previous studies, we observed that the expression of these fusion proteins during myxoma infection induced the formation of multinucleated syncytia which increased viral spread and lytic potential compared to non-fusogenic controls. Contrary to expectations, however, the treatment of established tumors with these viruses resulted in decreased therapeutic efficacy which corresponded with reduced viral persistence.Discussion: These findings indicate that enhanced viral spread caused by syncytia formation can actually reduce the efficacy of OV and supports a number of previous works suggesting that the in vitro properties of viruses frequently fail to predict their in vivo efficacy.

Keywords: myxoma virus, syncytia, fusogenic, oncolytic virotherapy, lung cancer

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Impact of Induced Syncytia Formation on the Oncolytic Potential of Myx | OV - Dove Medical Press

CHICAGO, Dec. 9, 2019 /PRNewswire/ -- Advaite Inc., a Chicago, IL based oncology-focused biotech company developing novel therapeutics and diagnostics to help patients suffering from debilitating diseases, has announced that it has entered into an exclusive license option agreement with the George Washington University with respect to the intellectual property of a novel AMES Negative HDAC6 inhibitor. Histone Deacetylases modulate a multitude of cellular processes and are part of the regulation of cellular pathways involved in anti-tumor immunologic responses. Selective inhibition of HDAC6 slows tumor growth in various cancer models. Under terms of this agreement, Advaite has the option to exclusively license intellectual property covering methods of use and pharmaceutical compositions.

"We look forward to future success by advancing the development of this novel HDAC6 inhibitor to treat a multitude of cancers, to ease suffering and extend life. This epigenetic regulator can have a potentially enormous therapeutic effect on patients who continue to suffer from debilitating cancer, as there is a great need for therapies that deliver an effective response, and specifically ones which are not limited by their toxicity profile. George Washington University's expertise with HDACs provide a perfect relationship for Advaite to advance truly viable, state of the art, impactful technology," said Karthik Musunuri, CEO & Co-Founder of Advaite.

"The quest for newer and more effective ways of treating cancer has now led to an extensive focus on the involvement of the immune system and its capacity to recognize and engage tumor cells. Recent findings from several research groups have demonstrated that ultra-selective HDAC6 inhibitors have the unique capacity of remodeling of the cellular composition of tumors, favoring the recognition and killing of cancer cells by the immune system. Our novel HDAC6 inhibitor has shown to have reduced toxic effects, thus clearly differentiating from previous HDAC inhibitors used in the clinic," said Alejandro Villagra, Ph.D., Member of the Immunology and Microbial Oncology Research Program at the GW Cancer Center and Assistant Professor of Biochemistry and Molecular Medicine at the GW School of Medicine and Health Sciences.

About Advaite

Advaite Inc. is a biotech company focused on developing novel therapeutics and diagnostics to help patients suffering from a variety of debilitating diseases, primarily within the oncology space. Advaite strives to maintain a patient centric approach in developing healthcare innovations. For more information, please visit http://www.advaite.com.

Forward Looking Statement

This press release includes statements that are "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. While Advaite has based any forward looking statements contained herein on its current expectations, the information on which such expectations were based may change. These forward-looking statements rely on a number of assumptions concerning future events and are subject to a number of risks, uncertainties, and other factors, many of which are outside ofAdvaite's control.

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SOURCE Advaite Inc.

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Advaite Inc. Enters into Exclusive License Option Agreement with the George Washington University for Novel AMES Negative HDAC6 Inhibitor Technology -...

LAWRENCE The University of Kansas has lost a longtime faculty member to a battle with cancer. Stephen Benedict, professor of microbiology, died Dec. 2 in Lawrence. He was 72.

Professor Benedict was a dedicated researcher and an inspirational and award-winning teacher to his many hundreds of students during his long career at KU, said Chancellor Douglas A. Girod. On behalf of the entire university, I offer my sincere condolences to his family, his friends and all who knew him throughout his time at KU.

Benedict came to KU in 1990 as an assistant professor of pharmacology & toxicology and later moved to the Department of Molecular Biosciences. Benedict was named full professor in 2008, a position he held until his death.

He touched the lives of many hundreds of KU undergraduates, said Susan Egan, professor and chair of the Department of Molecular Biosciences. Among Benedicts career honors were numerous awards recognizing his influence on students. Those honors included the Kemper Teaching Award, the Robert Weaver Graduate Mentoring Award, the J. Michael Young Academic Advisor Award, the Chancellors Club Teaching Professorship and the Mortar Board Outstanding Educator Award.

Moreover, Benedict was voted Favorite Biology Professor from among nearly 50 biology faculty members five times over the past 15 years, Egan said.

Benedicts research interests centered on immune-related disorders specifically related to T-cells. He published nearly 90 academic papers, received six U.S. patents and made numerous service contributions to the field, from serving on grant review panels for the National Institutes of Health to serving as associate editor of the Journal of Immunology.

Steves loss will be felt widely among the KU community and far beyond, Egan said. He will be remembered for the deep caring he showed for his students, his positivity and his tremendous sense of humor.

A celebration of life service is planned for Jan. 18, 2020, in Lawrence.

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University community mourns the death of Stephen Benedict, professor of microbiology - KU Today

New research by scientists at Harvard Medical School has found that nerves in the guts of mice do not merely sense the presence ofSalmonellabut actively protect against infection by this dangerous bacterium by deploying two lines of defense.

The study,published Dec. 5 inCell, casts in a new light the classic view of the nervous system as a mere watchdog that spots danger and alerts the body to its presence. The results show that by directly interfering withSalmonellas ability to infect the intestines, the nervous system is both a detector of danger and a defender against it.

Our results show the nervous system is not just a simple sensor-and-alert system, said neuro-immunologistIsaac Chiu, the studys lead investigator and assistant professor of immunology in the Blavatnik Institute at Harvard Medical School. We have found that nerve cells in the gut go above and beyond. They regulate gut immunity, maintain gut homeostasis and provide active protection against infection.

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Specifically, the experiments reveal that pain-sensing neurons embedded in the small intestine and beneath cells called Peyers patches are activated by the presence ofSalmonella, a foodborne bacterium responsible for a quarter of all bacterial diarrheal disease worldwide.

Once activated, the nerves use two defensive tactics to prevent the bug from infecting the intestine and spreading throughout the rest of the body. First, they regulate the cellular gates that allow microorganisms and various substances to go in and out of the small intestine. Second, they boost the number of protective gut microbes called SFB (segmented filamentous bacteria), which are part of the microbiome in the small intestine.

Bacteria get on our nerves

Under normal conditions, Peyers patchesclusters of lymphatic and immune tissue found exclusively on the wall of the small intestinescan the environment, sample substances and determine what can go into the intestine. To perform this function, Peyers patches are studded with microfold cells, or M cells, which are cellular channels that open and close to regulate influx of substances and microorganisms into the intestine. M cells are the major entry points thatSalmonellaand other dangerous bacteria exploit to invade the small intestine. To do so, theSalmonellabacterium injects into the gut transcription factors that stimulate intestinal cells to become M cells. Next, Salmonella latches onto sugars sitting atop the M cellsthe cellular gatesand uses its tentacles to prop the gates open. The bacterium then wiggles its way into the intestine.

To understand the role of pain-sensing gut neurons in infection protection, researchers compared how mice with and without them responded toSalmonella. One group of mice had intact gut neurons, another group had these neurons genetically disabled or deleted, and yet another cohort had them chemically disabled.

Experiments showed that in the presence ofSalmonella, gut neurons fire back by releasing a neurochemical called CGRP, which slows down M cell differentiation, thereby reducing the number of entry points that Salmonella can use. Additionally, the experiments show, gut neurons launch another form of defense. By releasing CGRP, they boost the presence of SFB microbesmicroorganisms that, among performing other beneficial functions, also guard againstSalmonellainvasion. Precisely how they do so remains unclear, but Chiu and colleagues say one plausible mechanism may be that SFB uses its tiny little hooks to attach itself to the intestinal wall and form a repellent coating that shields against the disease-causing bacteria.

Both defense mechanisms functioned reliably in mice with intact gut neurons. Not so, however, in animals that lacked these gut neurons. Indeed, intestinal biopsies from mice with inactivated neurons showed their Peyers patches more densely infiltrated by Salmonella at a greater rate than animals with intact neurons. The neuron-deficient animals also had fewer protective SFB microbes in their guts. Not surprisingly, these mice got sick fromSalmonellaat a greater rate and had more widespread disease than mice with intact nerve fibers.

It is becoming increasingly clear that the nervous system interacts directly with infectious organisms in various ways to affect immunity, Chiu said. Bacteria literally do get on our nerves.

The findings are in line with past research by Chius group showing a powerful three-way interplay between infection and the nervous and the immune systems. But in contrast to the new findings, the previous work showed that the nervous system can, at times, be exploited by infectious organisms to their advantage. For example, Chius previousresearchfound that nerves in the lungs can alter immune response in serious lung infections with the bacteriumStaphylococcus aureus, commonly known as staph. In anotherstudy, Chius team discovered that the bacterium that can cause flesh-eating disease hijacks nerves as a way to dampen immune defenses and weaken the bodys defenses.

A diverse repertoire

The new findings add to a growing body of knowledge showing that the nervous system has a repertoire far broader than signaling to and from the brain.

Our findings illustrate an important cross talk between the nervous system and the immune system, said study first author Nicole Lai, research fellow in immunology in the Chiu lab. It is clearly a bidirectional highway with both systems sending messages and influencing each other to regulate protective responses during infection.

Indeed, the gut contains so many nerves that it has often been called the second brain. As an alert system designed to warn the body of looming threats, the nervous system acts ultrafast. Thus, the new findings, the researchers said, suggest that evolution has taken advantage of this feature for added protection.

If you think about it, the nervous systems involvement in immunity is an evolutionarily smart way to protect the gut from infection by repurposing an existing feature, Chiu said.

The researchers say their findings could also help explain previous observations showing that the use of opioidswhich silence pain-sensing nerve fibersand other nerve-modulating drugs can make people more prone to infections.

If you dial down nerve signaling in an effort to reduce pain, you may be inadvertently also dampening their protective abilities, Chiu said. Our observations support that idea.

The interaction between gut neurons and gatekeeping M cells represents an area ripe for future research, the team said, because M cellsthe molecular gates of the small intestineare also exploited by other organisms that cause serious human disease, including the bacteriaE. coli, ShigellaandYersinia, as well as prions, self-propagating clumps of misfolded protein that can cause rare but universally fatal neurodegenerative conditions.

The results also point to a possible therapeutic pathway that involves modulating nerve signaling either for boosting gut immunity or intestinal inflammation.

The idea would be that if we could somehow stimulate these protective gut neurons or mimic their activity with a drug, we could activate the immune response and increase the bodys ability to fend off infection, Chiu said.

Other researchers included Melissa Musser, Felipe Pinho-Ribeiro, Pankaj Baral, Amanda Jacobson, Pingchuan Ma, David Potts, Zuojia Chen, Donggi Paik, Salima Soualhi, Yiqing Yan, Aditya Misra, Kaitlin Goldstein, Valentina Lagomarsino, Anja Nordstrom, Kisha Sivanathan, Antonia Wallrapp, Vijay Kuchroo, Roni Nowarski, Michael Starnbach, Hailian Shi, Neeraj Surana, Dingding An, Chuan Wu, Jun Huh, and Meenakshi Rao.

This work was supported by National Institutes of Health grants DP2AT009499 and K08 AI108690, National Institute of Allergy and Infectious Diseases grant R01AI130019, NIH grant R01 DK110559, the Chan-Zuckerberg Initiative, Harvard Digestive Disease Center, National Institute of Diabetes and Digestive and Kidney Diseases (grant K08 DK110532), National Multiple Sclerosis Society (Career Transition award TA3059-A-2), and Whitehead Scholar award and Translating Duke Health Scholar award.

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