| ID | Title | Body | Facebook Description | Facebook image | Facebook Title | Facebook Video | Twitter Description | Twitter Image | Twitter Title | Meta tags |
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| 200 | Development of Nogo Receptor Decoy for the Treatment of Spinal Cord Injury | Spinal cord injuries (SCIs) cause paralysis and loss of feeling in some or most of the body. Many people with SCIs are permanently disabled, relying on wheelchairs and other assistive devices for their entire lives. An estimated 17,700 SCIs occur every year in the United States, and approximately 288,000 Americans are living with SCIs. The cost of care for SCI patients is high. The spinal cord consists of bundles of nerve fibers, called axons, that carry signals up and down the spinal cord and to the rest of the body. Complete recovery from SCI is normally not possible because these axons are usually damaged and cannot regrow in adults. The investigators are working on a drug that stimulates spinal cord axon growth and restores neurological function after SCI. This project’s aim is to further develop this therapy to prepare it for testing in human clinical trials. Scientific Synopsis ReNetX is developing a therapeutic Nogo Receptor Decoy protein, AXER-204 [NgR(310)ecto-Fc], to promote the recovery of neurological function through axonal fiber growth after SCI. In nearly all neuropathies, a substantial portion of brain and spinal cord is preserved. If the remaining healthy tissue can be “rewired” with appropriate axonal connections, improved neurological function can occur. Partial recovery from SCI may take place within the first few weeks after the injury. Additional recovery beyond that period is limited. This is because axonal growth, which is needed for greater recovery, is virtually nonexistent in the adult spinal cord. Treatment for chronic SCI, therefore, consists primarily of physical and/or occupational therapy. To date, no therapeutic approved by the Food and Drug Administration (FDA) promotes new connections between surviving nerve cells. As a result, a significant unmet medical need exists for therapeutics that stimulate neurological recovery. It has been demonstrated that NgR(310)ecto-Fc stimulates corticospinal and raphespinal axon growth. Additionally, it has been shown that functional recovery can be achieved in acute, subacute and chronic spinal contusion injuries with NgR(310)ecto-Fc therapy. Preclinical studies that demonstrate efficacy in an animal model of chronic SCI provide the basis for launching clinical trials of NgR(310)ecto-Fc therapy. The goal of this project is to execute key activities necessary to support an Investigational New Drug (IND) application to the FDA for clinical evaluation of NgR(310)ecto-Fc for the treatment of chronic SCI. The ultimate goal is to allow victims of chronic SCI to regain function and to improve their quality of life. Lead Collaborator ReNetX Bio, New Haven, Connecticut George D. Maynard, Ph.D. Public Health Impact ReNetX Bio will develop AXER-204 to promote recovery of neurological function through growth of axonal fibers after SCI. Outcomes BrIDGs program scientists collaborated in completing CMC development, manufacture of clinical product, pharmacokinetic studies and IND-directed toxicology studies. An IND has been cleared by FDA, and clinical trials have been initiated to establish the safety, tolerability, pharmacokinetics and efficacy of AXER-204 in participants with chronic SCI. See ClinicalTrials.gov, NCT03989440. | ||||||||
| 199 | Development of Neurosteroids for Lysosomal Storage Disorders | Niemann-Pick disease type C is a very rare inherited inability to metabolize cholesterol and other fats. Because of this inability, cholesterol accumulates in the liver and the spleen and other fats accumulate in the brain, causing progressive neurodegeneration. In most cases, neurological symptoms appear between the ages of 4 and 10 years, but the disease may not appear until a person is an adult. Progression is slower the later the symptoms appear, but Niemann-Pick C is always fatal. The majority of children with the disease die before the age of 20. No treatment is known. The researchers are developing a therapy for children with Niemann-Pick C based on a neurosteroid, a hormone that acts on the growth and differentiation of brain cells and is produced in the nervous tissue. The drug has shown activity in both increasing brain cell survival and reducing the accumulation of fats in the brain that causes the brain degeneration. Scientific Synopsis Niemann-Pick disease type C is a fatal, autosomal recessive, childhood-onset neurodegenerative disorder for which there is no treatment. It is a lysosomal lipid storage disease characterized by defective trafficking of intracellular cholesterol and lysosomal accumulation of unesterified cholesterol, gangliosides and other lipids. Neurosteroids, synthesized from cholesterol in the nervous system, affect growth and differentiation of neurons. We showed that post-embryonic neurosteroid synthesis is altered in a time- and region-specific fashion in the BALB/c Niemann-Pick C mouse and that neurons and glia expressing steroidogenic enzymes are lost in the Niemann-Pick C mouse. In particular, the synthesis of the GABA-ergic neurosteroid allopregnanolone (ALLO) is substantially diminished at birth when the rodent brain is still undergoing maturation and decreases further over time. Our data show that appropriately timed treatment of Niemann-Pick C mice with ALLO increases the lifespan of these mice and delays the onset of neurological impairments that are hallmarks of this disease in mice — tremor, ataxia, and hindlimb dysfunction. Furthermore, ALLO treatment of Niemann-Pick C mice significantly increases cerebellar Purkinje and granule cell survival and substantially reduces accumulation of cortical gangliosides GM1, GM2 and GM3. Our recent data indicate that this treatment is not limited to Niemann-Pick C, as two other lysosomal storage disorders are treated effectively with ALLO. To obtain data necessary for submission of an Investigational New Drug (IND) application to the FDA to treat children with Niemann-Pick C with ALLO, we have established the pharmacokinetics and pharmacodynamics of ALLO in neonatal, juvenile and adult wild-type and Niemann-Pick C mice and optimized ALLO treatment in Niemann-Pick C mice. Submission of our pre-IND document and type B meeting with the FDA has provided direction for our safety and toxicology studies in animals and in vitro, needed for IND submission. We are requesting program support to complete these safety and toxicity studies and for preparation of GMP allopregnanolone for use in these studies and in phase I clinical trials. The use of neuroactive steroids in the treatment of degenerative brain diseases has not been described previously. We believe that other brain diseases, including but not limited to congenital storage diseases, may benefit from similar treatments with neuroactive steroids. Thus, this proposal is directed toward obtaining preclinical safety and toxicity data necessary to file an IND for the treatment of a broad group of disorders with a novel class of drugs, with Niemann-Pick C as the model disease. Lead Collaborator University of California, San Francisco Synthia Mellon, Ph.D. Public Health Impact The allopregnanolone treatment that we have developed in mouse models of Niemann-Pick disease type C also shows significant benefits in two unrelated mouse models of human lysosomal storage disorders, Sandhoff disease and Sanfilippo disease. Currently, there are no treatments for any of these three lysosomal storage disorders, and thus allopregnanolone treatment represents a major advance in treatment of three different orphan diseases. Outcomes As a result of BrIDGs support, the lead collaborator was able to file an IND application in December 2017, which was cleared by the Food and Drug Administration. BrIDGs support is completed and the collaboration on this project is now concluded. Project Details Formulation development Manufacture of GMP drug product Pharmacokinetic studies IND-directed toxicology | ||||||||
| 198 | Development of Minihepcidins for the Treatment of Beta Thalassemia | Beta thalassemia is a rare, inherited blood disorder that causes severe anemia and damage to organs. The only current treatment is blood transfusions, and patients often must have many of these procedures. Repeated transfusions can cause too much iron to build up in the body. Patients with beta thalassemia also have reduced levels of a hormone called hepcidin, which helps the body use iron properly. A buildup of iron from transfusions combined with low levels of hepcidin can cause "iron overload," which can damage the heart, liver and other tissues. The goal of this project is to produce a treatment that increases levels of hepcidin and lowers the damaging effects of iron in patients with beta thalassemia. Scientific Synopsis Patients with beta thalassemia suffer from anemia, which is often severe, and iron overload, which causes damage to the heart, liver and endocrine tissues. Current treatment of beta thalassemia consists of blood transfusions to correct the anemia and chelation agents to remove iron from the body. Although this therapeutic approach can prevent premature death in childhood or early adulthood, it does not modify the underlying disease process. These treatments do not provide consistent, long-term benefits for patients and can confer significant toxicity. Beta thalassemia causes defects in red blood cell production by bone marrow as well as reduced red blood cell survival time. These factors contribute to the development of anemia and lead to reductions in the iron regulatory hormone hepcidin. Low hepcidin levels allow too much iron to be absorbed from the diet, resulting in severe iron overload. Excess iron in the developing red blood cells contributes to the failure of cell production. These events create a vicious cycle in which too much iron contributes to low red blood cell production, which in turn increases the amount of iron that can cause cellular damage. Increasing the amount of hepcidin activity in the body is one approach to breaking the cycle of excess iron and red blood cell destruction in beta thalassemia. Increasing hepcidin can restrict the flow of iron to the developing red blood cell, reducing cell damage and death and improving the production of these cells. The increased hepcidin levels also can restrict the amount of iron absorbed from the diet and prevent the development of iron overload. The investigator is developing minihepcidins, which are novel peptides that possess the biological activities of hepcidin and can be used to increase hepcidin activity. Studies in animal models of beta thalassemia have found that treatment with a minihepcidin can reduce red blood cell damage and rapidly decrease severity of anemia. If similar effects are seen in patients, minihepcidins could become a new type of disease-modifying agent for the treatment of beta thalassemia. Lead Collaborator Merganser Biotech LLC, Newtown Square, Pennsylvania Brian MacDonald, Ph.D. Public Health Impact A disease-modifying therapy such as minihepcidin could transform the treatment of beta thalassemia by reducing or eliminating the need for transfusions and chelation therapy. It may also provide consistent, long-term improvements in the quality of life of these patients as a result of reducing the level of anemia. Outcomes During the course of the project, the lead collaborators at Merganser Biotech successfully raised private funding. This enabled them to take full control of the project and continue the remaining preclinical development with internal resources. The collaborators filed an Investigational New Drug (IND) application, which was cleared by the Food and Drug Administration, allowing clinical trials to begin. Project Details Formulation development Pharmacokinetic/absorption, distribution, metabolism, and excretion (PK/ADME) studies IND-directed toxicology | ||||||||
| 197 | About Chemistry Technology | The aim of NCATS' Chemistry Technology program is to provide cutting-edge resources to enable the broader biomedical research community to pursue basic and translational studies in a faster and more in-depth manner. To achieve this, chemistry technology scientists at NCATS engage in a variety of innovative translational research activities, including: Design and synthesis of bioactive small molecules. Development of mechanistically defined small molecule libraries to analyze the concurrent biological pathways of drug signatures and to understand the molecular basis of drug response. Design and implementation of systems-based phenotypic drug screening, which seeks to identify substances that can alter the observable characteristics of a target of interest. Identification of genetic predictors (e.g., somatic mutations, amplifications) of drug sensitivity and/or drug resistance. The program is highly collaborative and supports projects and platforms that are currently underdeveloped or brand new. Learn more about these projects. The development of high-quality molecular probes is an integral effort of chemical biology, a rapidly developing field aimed at better understanding the molecular basis of diseases. The modification of bioactive molecules can also lead to the development of reagents designed to identify the target(s) accounting for a specific observed phenotype. | ||||||||
| 196 | Development of Exendin-(9-39) for the Treatment of Congenital Hyperinsulinism | Congenital hyperinsulinism is a rare, inherited disease affecting about 1 in 25,000 to 1 in 50,000 infants. In this disorder, the beta cells (cells that produce insulin) in the pancreas produce too much insulin and at the wrong time, leading to low blood sugar. Four types of congenital hyperinsulinism are known, caused by different genetic mutations. The disease can be difficult to identify in babies because the symptoms include irritability, sleepiness, lethargy and excessive hunger, but in severe cases, it can be life threatening, with seizures and coma. Current treatments include feeding more sugar, medication to control insulin secretion and surgery to remove part of the pancreas. These researchers are working on a drug to treat one type of congenital hyperinsulinism that does not respond to any current medication and is typically treated by near-total removal of the infant’s pancreas. The new drug acts by blocking the activity of a protein called glucagon-like peptide-1 receptor, reducing insulin secretion. Scientific Synopsis Congenital hyperinsulinism due to mutations in the KATP channel (KATPHI) is characterized by severe hypoglycemia unresponsive to available medical therapy. Currently, most patients require a near-total pancreatectomy to control the hypoglycemia, resulting in prolonged hospital stays and high risk for life-threatening complications. Antagonism of the glucagon-like peptide-1 receptor by exendin-(9-39) results in elevation of fasting blood glucose levels in mice, in baboons and in healthy human subjects. Our preliminary data demonstrate that exendin-(9-39) inhibits insulin secretion and corrects fasting hypoglycemia in a mouse model of congenital hyperinsulinism (SUR-1−/− mice). In isolated islets from these mice, exendin-(9-39) suppresses baseline and amino acid–stimulated insulin secretion. Preliminary results from a pilot study show that an intravenous infusion of exendin-(9-39) in adult human subjects with KATPHI suppresses insulin secretion and raises fasting blood glucose levels. Our long-term objective is to develop exendin-(9-39) as a new therapy for the treatment of congenital hyperinsulinism. Our overall hypothesis is that antagonism of the GLP-1 receptor by exendin-(9-39) will increase fasting blood glucose levels, prevent protein-induced hypoglycemia and decrease glucose requirement to maintain euglycemia in subjects with KATPHI as a result of suppressed insulin secretion and increased glucagon levels. The assistance requested in this proposal will allow us to proceed with further preclinical and clinical studies in the pathway of development of this potential new treatment. Although congenital hyperinsulinism due to mutations in the KATP channel is a rare disease affecting approximately 1:20,000 to 1:50,000 children in this country, this devastating disease and its current treatment (near-total pancreatectomy) are associated with severe, life-threatening complications that could be prevented with effective medical therapy. The development of exendin-(9-39) as a therapeutic agent for this disorder would represent a major breakthrough in the field. Furthermore, the outcomes of this translational research project may have implications for treatment of other forms of hyperinsulinism and other forms of hypoglycemia in which GLP-1 may play a role, including post-prandial hypoglycemia after Nissen fundoplication and gastric bypass surgery. Lead Collaborators Children’s Hospital of Philadelphia Diva D. De Leon, M.D. Children’s Hospital of Philadelphia/University of Pennsylvania Charles A. Stanley, M.D. Public Health Impact Currently, there is no effective medical therapy for subjects with congenital hyperinsulinism due to mutations in the KATP channel. Our preliminary results show very promising effects of antagonism of the GLP-1 receptor by exendin-(9-39) on glucose homeostasis of mice and human subjects with KATP channel mutations. Outcomes Work on this project is complete. The investigators used BrIDGs data to amend an Investigational New Drug (IND) application that was cleared by the Food and Drug Administration, allowing clinical trials to begin. Project Details Synthesis of Good Manufacturing Practice (GMP) and non-GMP material Formulation development Pharmacokinetic/absorption, distribution, metabolism, and excretion (PK/ADME) studies IND-directed toxicology | ||||||||
| 195 | Development of Bone Morphogenetic Protein Inhibitors to Treat Blood and Bone Disorders | Bone morphogenetic protein (BMP) is a protein essential for normal bone growth and other functions in the body. Gene defects that cause too much BMP activity can lead to two diseases: fibrodysplasia ossificans progressive (FOP) and anemia of inflammation (AI). FOP is a rare, inherited and deadly disease in which muscles and tendons turn to bone, making movement difficult. AI is a more common condition in which too much BMP activity in the liver causes anemia. No completely effective treatments exist for either disease. The investigators are developing a drug that inhibits BMP activity and could be used to treat FOP and AI. This project’s aim is to prepare the drug for testing in humans. Scientific Synopsis BMP signals have been known for decades to play essential roles in normal embryonic development. More recently, it has been recognized that BMP signals also play important roles in adults. In fact, excessive BMP signaling has been shown to contribute to the pathophysiology of two distinct diseases. The first of these, FOP, is caused by activating mutations in a gene encoding one of the type I BMP receptors. The second disease, AI, is a common condition in which chronic inflammation leads to anemia through excess BMP signaling in the liver. There are no available treatments for FOP patients, and therapies for AI are not effective enough and have negative side effects. As the significance of BMP signaling for these two diseases has become known, development of BMP signaling inhibitors has emerged as an important goal. In 2008, the first small molecule inhibitor of BMP signaling was reported. The compound, dorsomorphin, blocks BMP signaling by inhibiting type I BMP receptors. Through medicinal chemistry optimization, dorsomorphin derivatives were developed, including LDN-193189, a compound with much greater potency (~5 nM in cells) and specificity than the parent compound. LDN-193189 is well tolerated in mice, has low toxicity and is orally available. Most importantly, LDN-193189 has proven to be efficacious in treating FOP and AI in mouse models of these diseases. The overall objective of this research project is to advance the development of LDN-193189 in preparation for clinical testing in patients with FOP and AI. The planned developmental steps are applicable to both diseases, leading to efficient use of resources and increased likelihood that LDN-193189 will find successful clinical application in treating patients with these debilitating diseases. Lead Collaborators Brigham and Women’s Hospital, Boston Paul B. Yu, M.D., Ph.D. Massachusetts General Hospital (General Hospital Corp.), Boston Donald B. Bloch, M.D. Kenneth D. Bloch, M.D. Gregory D. Cuny, Ph.D. Randall T. Peterson, Ph.D. Public Health Impact Two very different diseases, a rare but fatal bone overgrowth disease and a common form of anemia, share a similar underlying cause: over-activation of signals from BMPs. This project will advance development of a newly discovered drug candidate that blocks BMP signaling and will prepare the compound for testing in patients with these diseases. Outcomes Initial toxicology studies indicated that LDN-193189 was not a suitable candidate for further Investigational New Drug (IND)-directed development. The lead collaborators proposed a new collaboration with the Therapeutics for Rare and Neglected Diseases (TRND) program to improve the compound through additional medicinal chemistry. BrIDGs support for this project was concluded and the project transferred to TRND. Project Details Synthesis of Good Manufacturing Practice (GMP) and non-GMP material Formulation development Pharmacokinetic/absorption, distribution, metabolism, and excretion (PK/ADME) studies IND-directed toxicology | ||||||||
| 194 | Functional Genomics Lab Projects | Project AreasCancerDrug enhancer/resistance screensDNA-damaging agentsImmunotoxinsMolecular targets in cancerBreast cancerMelanomaCancer-related pathwaysNF-κBMigrationInfectious diseasesViral infection and replicationPoxvirusHIVEbola virusHepatitis C virusImmune responseFundamental cell biologyDNA replicationReprogramming/differentiationOther disease-related phenotypesParkinson’s diseaseDiabetesFragile X syndrome | ||||||||
| 193 | Work with the Functional Genomics Lab | NIH investigators are eligible to collaborate with the Functional Genomics Lab at NCATS and access screening facility resources. Open application cycles occur once each year and last about two months. During these cycles: NIH investigators work with Functional Genomics Lab experts at NCATS to develop an assay. Review the latest version of the Assay Guidance Manual. The NIH investigator submits a letter of intent for review to his or her Institute or Center and a proposal to the Functional Genomics Lab for independent peer review by a proposal selection committee. Rejected proposals can be revised to address key concerns and resubmitted for additional review. Following proposal approval, NCATS staff and the NIH investigator work together to develop and execute a project plan. NIH investigators interested in collaborating with the Functional Genomics Lab should contact Ken Cheng, Ph.D., to get started. Learn more about how the Functional Genomics Lab works. | ||||||||
| 192 | Development of an ApoA-1 Mimetic Peptide for Treatment of Atherosclerosis | Coronary heart disease (CHD) is the buildup of a waxy substance called plaque in the arteries that supply blood to the heart. Plaque builds up over time and can eventually narrow arteries and reduce blood flow to the heart, leading to abnormal heart rate, heart attack or heart failure. CHD is the most common type of heart disease and the primary cause of death for men and women in the United States. Having high levels of low-density lipoprotein (LDL) cholesterol — “bad” cholesterol — and low levels of high-density lipoprotein (HDL) cholesterol — “good” cholesterol — increases risk for CHD. Currently, drugs that lower LDL cholesterol are used to help prevent CHD, but they are not completely effective. Scientists have recently explored the therapeutic effects of giving HDL cholesterol to patients with CHD at high risk for a heart attack. These investigators are developing a drug that mimics the effects of apoA-1, a building block of HDL cholesterol. The drug would increase HDL levels in the blood to treat and prevent CHD. Scientific Synopsis It has become increasingly evident that therapeutic agents for raising HDL would be a useful addition to our current treatment approach for preventing CHD because our existing drugs that lower LDL are not fully adequate for preventing CHD. The recent unraveling of some of the complexities of HDL metabolism has led to the identification of key proteins involved in the biogenesis of HDL, giving new hope and ideas for drug targets. In spite of this, therapies using small molecules to raise HDL have been elusive. Recently, a potential new treatment strategy for CHD, called acute HDL therapy, has been described. The strategy involves a weekly intravenous infusion of HDL into patients with acute coronary syndrome. A five-week course of this therapy has been shown to rapidly reduce atherosclerotic plaques, as assessed by intravascular ultrasound. The goal of acute HDL therapy is to stabilize patients at great risk for developing a heart attack and to concurrently start them on conventional lipid lowering drugs and other agents for reducing the risk for heart attack. This project describes a short synthetic peptide mimic of apoA-1, referred to as the 5A peptide, which potentially can be used instead of recombinant apoA-1 in acute HDL therapy. As described below, peptide 5A has several potential advantages over the use of recombinant apoA-1. Peptide 5A is being developed for treatment and prevention of atherosclerotic cardiovascular disease. The 5A attenuates the development of atherosclerotic plaque in preclinical models of atherosclerosis, including APOE-deficient mice, and impairs macrophage recruitment and foam cell formation in the rabbit collar model. In vitro assays have demonstrated that 5A specifically interacts with the cholesterol efflux transporter ABCA1 and catalyzes the efflux of cholesterol from macrophages. Furthermore, the investigators have shown that 5A accelerates the in vivo efflux of cholesterol from tissues to plasma lipoproteins in animal models. This feature of the peptide will be used to inform first-in-human studies following Investigational New Drug (IND) approval from the Food and Drug Administration for rapid assessment of therapeutic proof-of-concept. Lead Collaborator National Heart, Lung, and Blood Institute, Bethesda, Maryland Alan T. Remaley, M.D., Ph.D. Public Health Impact Peptide 5A has been shown to reduce atherosclerosis and replicate many of the known benefits of HDL in animal studies, making it an excellent candidate therapy. In spite of good therapies for lowering LDL, atherosclerosis remains a major cause of death worldwide. Outcomes BrIDGs program scientists completed formulation development, manufacture of Good Manufacturing Practice (GMP) drug product, and IND-directed toxicology studies. As a result of BrIDGs support, the collaborators successfully filed an IND application with the Food and Drug Administration, allowing clinical trials to begin. See ClinicalTrials.gov, NCT04216342. | ||||||||
| 191 | Functional Genomics Lab Resources | The Functional Genomics Lab experts at NCATS employ scientific resources that include a variety of commercially available siRNA screening libraries; tools for data tracking, storage and analysis; and a fully automated, large-scale screening platform. Screening Libraries Software and Analysis Tools Assays Robotic Platform High-Content Imaging and Analysis Platforms (in progress) Screening Libraries Ambion Silencer Select Human Genome-Wide siRNA library targeting ~22,000 genes with three individual siRNAs per gene Ambion Silencer Mouse Genome-Wide siRNA library targeting ~17,000 genes with three individual siRNAs per gene Dharmacon siGENOME and Dharmacon ON-TARGETplus Human Genome-Wide siRNA libraries (Thermo Scientific), with pools of four siRNAs targeted against each of ~16,000 genes in the library; “druggable genome” subsets included for focused screening of potentially druggable targets microRNA mimic and inhibitor libraries Ambion Silencer Select Human Druggable Genome siRNA Library V4 Dharmacon Human ON-TARGETplus siRNA Transcription Factors Library Dharmacon Human ON-TARGETplus Epigenetics siRNA Library Ambion Silencer Select Human Ubiquitin 96 siRNA Library Software and Analysis Tools RNAi Data Viewer This tool allows users to view plates, check stats, screen data and perform a variety of analyses. Access user data (restricted). Assays Simple phenotypes Examples: viability, cytotoxicity Assays that explore one aspect of morphology or function/loss of function. Pathway reporter assays Examples: luciferase, beta-lactamase Assays using a specific read-out mechanism to “report” data, or “reporter assays.” Complex phenotypes Examples: high-content imaging, cell cycle, translocation Assays that explore more than one aspect of morphology or function/loss of function, usually a process with two or more steps. 3-D physiologically relevant models Representation of 2-D and 3-D RNAi invasion screening data. The two panels are shown 24 hours after Matrigel addition. The left panel shows a well with a breast cancer organoid with an siRNA targeting MMP9 (siMMP9). The right panel shows a 3-D organoid targeted with a non-targeting siRNA AN2. These two siRNAs will be used as negative and positive controls for data analysis. Robotic Platform Liquid handlers, washers and dispensers EnVision and Pharastar Multilabel Reader (PerkinElmer) Measures luminescence, fluorescence, fluorescence polarization, absorbance and time-resolved fluorescence ImageXpress Micro XL confocal high-content imager (Molecular Devices) Automated microscope used for the acquisition and analysis of cell-based images in relatively high throughput Schematic illustration of the RNAi robotic platform. Photograph of the RNAi robotic platform. |
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