Israel Institute for Biological Research is an Israeli government defense research institute specializing in biology, medicinal chemistry and environmental science. The institute's work is a closely guarded secret. It is suspected of also developing biological and chemical weapons and defenses against them, as well as toxins for use by Israeli intelligence in assassinations. It is located in Ness Ziona, 20 kilometers south of Tel Aviv. IIBR has approximately 350 employees, 150 of whom are scientists. Wikipedia.
Israel Institute for Biological Research | Date: 2017-01-04
The invention provides a pharmaceutical composition comprising as an active ingredient a combination of three isolated monoclonal antibodies or any antigen-binding fragment thereof which bind ricin toxin and neutralize its toxic effects, and a pharmaceutically acceptable carrier, excipient or diluent. The invention also provides a method of prophylaxis, treatment or amelioration of ricin toxin poisoning including administering to a subject in need thereof a therapeutically effective amount of the pharmaceutical composition.
News Article | February 10, 2017
WASHINGTON — It has been used by an assassin wielding a poisoned umbrella and sent in a suspicious letter to a president. Ricin, the potent toxin and bioterrorism agent, has no antidote and can cause death within days. But a cocktail of antibodies could one day offer victims at least a slim window for treatment. A new study presented February 7 at the American Society for Microbiology’s Biothreats meeting reveals a ricin antidote that, in mice, works even days after exposure to the toxin. Another presented study offers a potential explanation for how such an antidote might work. Doctors need some way to deal with ricin poisoning, said Patrick Cherubin, a cell biologist at the University of Central Florida in Orlando. Immunologist Nicholas Mantis agreed: “There is no specific treatment or therapy whatsoever.” Though ricin has an innocuous origin (it’s found in castor beans), the poison is anything but harmless. It’s dangerous and relatively easy to spread — rated by the U.S. Centers for Disease Control and Prevention as a category B bioterrorism agent, just behind the highest-risk category A agents such as anthrax, plague and Ebola. Ricin poisoning is rare but has featured in some high-profile cases. In 1978, Bulgarian writer Georgi Markov was hit in the thigh with a ricin-poisoned pellet shot from an umbrella gun. A few days later, he was dead. In 2013, a letter addressed to President Barack Obama tested positive for granules of the deadly toxin. A Texas woman had ordered castor bean seeds and lye online, for a do-it-yourself approach to making ricin. No one was injured. Symptoms of ricin poisoning depend on how the toxin enters the body, and how much gets in. Inhaling ricin can make breathing so difficult the skin turns blue. Ingesting ricin can cause diarrhea, vomiting and seizures. Death can come as soon as 36 hours after exposure. Ricin is known as an RIP — a scary-sounding acronym that stands for ribosome-inactivating protein, said Mantis, of the New York State Department of Health in Albany. In the cell, ribosomes serve as tiny protein factories. After ricin exposure, “the whole machinery comes to a screeching halt,” Mantis said. For cells, shutting down protein factories for too long is a death sentence. Scientists have developed two vaccines for ricin, though neither is available yet for use in humans. A vaccine may be “good for soldiers going into the field,” said biochemist Ohad Mazor of the Israel Institute for Biological Research in Ness Ziona. But unvaccinated people are out of luck. Mazor and colleagues developed a new treatment that could potentially help. The treatment is a mixture of three proteins called neutralizing antibodies; they grab onto ricin and don’t easily let go. With antibodies hanging onto its back, ricin has trouble slipping into cells and wreaking its usual havoc. Even 48 hours after inhaling ricin, roughly 73 percent of mice, 22 out of 30, treated with the antibodies survived, the team reported at the meeting and in a paper published in the March 1 Toxicon. Untreated mice died within a week. Previous antibody treatments for ricin work well only if mice are treated within hours after exposure, Mazor said. For poisoned humans, that may not be long enough to diagnose the problem. Mazor doesn’t know how his antibodies might work in people, but he’d like to follow up his mouse work with studies in monkeys or pigs. Scientists haven’t figured out exactly how antibodies help animals recover, but another study presented at the meeting offers a clue. Cherubin and colleagues added ricin to monkey cells in a dish, and then tracked how much protein was manufactured by the cells. At high enough levels, ricin exposure shuttered the factories as expected. But when researchers stopped exposing cells to the toxin, protein synthesis started up again and cells recovered. “You need ongoing toxin delivery to eventually kill the cell,” Cherubin said. It’s possible that antibody treatments could cut off ricin delivery to cells, letting them bounce back from poisoning, said study coauthor Ken Teter, also a cell biologist at the University of Central Florida.
Harrus S.,Hebrew University of Jerusalem |
Waner T.,Israel Institute for Biological Research
Veterinary Journal | Year: 2011
Canine monocytotropic ehrlichiosis (CME), caused by the rickettsia Ehrlichia canis, an important canine disease with a worldwide distribution. Diagnosis of the disease can be challenging due to its different phases and multiple clinical manifestations. CME should be suspected when a compatible history (living in or traveling to an endemic region, previous tick exposure), typical clinical signs and characteristic hematological and biochemical abnormalities are present. Traditional diagnostic techniques including hematology, cytology, serology and isolation are valuable diagnostic tools for CME, however a definitive diagnosis of E. canis infection requires molecular techniques. This article reviews the current literature covering the diagnosis of infection caused by E. canis. © 2010 Elsevier Ltd.
Adiri T.,Tel Aviv University |
Marciano D.,Israel Institute for Biological Research |
Cohen Y.,Tel Aviv University
Chemical Communications | Year: 2013
We report on the first secondary and tertiary complexes of the pillararene derivative 3 with xenon in water. We show that the chemical shift of the encapsulated xenon provides information on the type of the formed complex suggesting that 3 has the potential to be used as a platform for NMR biosensors. © 2013 The Royal Society of Chemistry.
Fisher A.,Israel Institute for Biological Research
Journal of Neurochemistry | Year: 2012
The prescribed drugs for treatment of cognitive deficits in Alzheimer's disease (AD) patients are regarded as symptomatic drugs. Effective disease modifying therapies are not yet prescribed in AD patients. Three major hallmarks of AD (e.g. cholinergic hypofunction, Aβ and tau neuropathologies) are closely linked raising the expectation that restoring the cholinergic hypofunction to normal, in particular via selective activation of M1 muscarinic receptors, may alter the onset or progression of AD dementia. This review is focused mainly on modulation of amyloid precursor processing and Aβ levels in the brain via cholinergic treatment strategies based on M1 muscarinic agonists versus other cholinergic treatments (e.g. cholinesterase inhibitors prescribed for treatment of AD, M2 antagonists and nicotinic agonists). Advantages and potential drawbacks of these treatment modalities are reviewed versus the notion that due to an elusive etiology of AD, future disease modifiers should address comprehensively most of these AD hallmarks (e.g. Aβ pathology, tau and tangle pathologies, as well as the cholinergic hypofunction and cognitive impairments). This major requirement may be fulfilled with M1-selective muscarinic agonists and less with other reviewed cholinergic treatments. © 2011 International Society for Neurochemistry.
Chitlaru T.,Israel Institute for Biological Research |
Altboum Z.,Israel Institute for Biological Research |
Reuveny S.,Israel Institute for Biological Research |
Shafferman A.,Israel Institute for Biological Research
Immunological Reviews | Year: 2011
Summary: The lethal anthrax disease is caused by spores of the Gram-positive Bacillus anthracis, a member of the cereus group of bacilli. Although the disease is very rare in the Western world, development of anthrax countermeasures gains increasing attention due to the potential use of B. anthracis spores as a bio-terror weapon. Protective antigen (PA), the non-toxic subunit of the bacterial secreted exotoxin, fulfills the role of recognizing a specific receptor and mediating the entry of the toxin into the host target cells. PA elicits a protective immune response and represents the basis for all current anthrax vaccines. Anti-PA neutralizing antibodies are useful correlates for protection and for vaccine efficacy evaluation. Post exposure anti-toxemic and anti-bacteremic prophylactic treatment of anthrax requires prolonged antibiotic administration. Shorter efficient postexposure treatments may require active or passive immunization, in addition to antibiotics. Although anthrax is acknowledged as a toxinogenic disease, additional factors, other than the bacterial toxin, may be involved in the virulence of B. anthracis and may be needed for the long-lasting protection conferred by PA immunization. The search for such novel factors is the focus of several high throughput genomic and proteomic studies that are already leading to identification of novel targets for therapeutics, for vaccine candidates, as well as biomarkers for detection and diagnosis. © 2010 John Wiley & Sons A/S.
Israel Institute for Biological Research | Date: 2015-11-25
An isolated monoclonal antibody or any antigen-binding fragment thereof which binds to ricin toxin, an expression vector including the isolated nucleic acid molecule and a host cell transfected with said isolated nucleic acid molecule or with the expression vector, a pharmaceutical composition including as an active ingredient the isolated monoclonal antibody or any antigen-binding fragment thereof, the bispecific molecule or the immunoconjugate and a pharmaceutically acceptable carrier, excipient or diluent, and a method of prophylaxis, treatment or amelioration of ricin toxin poisoning including administering to a subject in need thereof a therapeutically effective amount of the isolated monoclonal antibody or any antigen-binding fragment thereof, the bispecific molecule, the immunoconjugate or the pharmaceutical composition.
Israel Institute for Biological Research | Date: 2016-04-04
Fusion polypeptides are provided including modified human Acetylcholinesterase conjugated to the Fc region of an immunoglobulin. Methods of preparing these polypeptide constructs and uses thereof as scavenging agents of organophosphate compounds are described.
Israel Institute for Biological Research | Date: 2012-07-18
The invention provides an isolated Bacillus cereus sensu lato strain, selected from Bacillus anthracis, Bacillus cereus and Bacillus thuringiensis, in which the htrA gene or any part thereof is silenced, and vaccines comprising the same.
Israel Institute for Biological Research | Date: 2010-01-07
Compositions comprising at least one decontaminating agent, and being in a form of a gel, are disclosed herein, as well as processes for producing the compositions by contacting a solution containing the decontaminating agent(s) with at least one gelling agent. The compositions are useful in decontamination. The decontamination efficacy of the compositions can be enhanced by adding a solid hypochlorite salt to the composition. Systems are further disclosed herein which are designed for mixing the decontaminating agent(s) with the gelling agent(s) when and where needed, and for propelling the mixed solutions onto a surface to be contaminated. Methods employing the compositions for decontamination are also disclosed.