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Designing Novel Apolipoprotein A1 Mimetic Peptides As Drug Treatment For Atherosclerosis
Funder
National Health and Medical Research Council
Funding Amount
$60,016.00
Summary
Cardiovascular disease is the formation of atherosclerotic plaques caused by the imbalance between the amount of cholesterol delivered and removed from the arteries. Apolipoprotein A-1 (ApoA-1) is the main protein of high density lipoprotein (HDL) and removes cholesterol out of cell. In this project we are aimed at designing and testing new drugs (ApoA1-mimetic peptides) which will elicit the same anti-atherogenic properties as apoA-1, as a therapeutic agent for prevention of atherosclerosis.
Developing Anti-Inflammatory Drugs Based On Inhibition Of A Human Enzyme
Funder
National Health and Medical Research Council
Funding Amount
$160,000.00
Summary
Human secretory phospholipases A2 have been associated with inflammatory diseases for many years, yet very few truly potent inhibitors of the human enzymes sPLA2 (isoforms IIa, V or X) are known due to a range of problems relating to the lipid nature of substrates, unavailability of enzymes, enzyme assays that do not correlate with in vivo data. Although there remains controversy about which enzyme is responsible in vivo for degrading membrane phospholipids to inflammatory mediators like arachid ....Human secretory phospholipases A2 have been associated with inflammatory diseases for many years, yet very few truly potent inhibitors of the human enzymes sPLA2 (isoforms IIa, V or X) are known due to a range of problems relating to the lipid nature of substrates, unavailability of enzymes, enzyme assays that do not correlate with in vivo data. Although there remains controversy about which enzyme is responsible in vivo for degrading membrane phospholipids to inflammatory mediators like arachidonate, PAF, prostaglandins, leukotrienes, etc. there is a consensus that blockade of phospholipid metabolism would represent a major advance on NSAIDs as antiinflammatory agents. No sPLA2-IIa inhibitor is available yet in man. We aim to create an attractive data package showing proof of concept for a potent new type of antiinflammatory drug. This data will give us an improved negotiating position in our commercialisation of a new drug with potential multi-billion dollar markets as diverse as arthritis, asthma, reperfusion injury, organ transplantation and many other currently intractable human ailmentsRead moreRead less
Macrophage Uncoupling Protein-2 Regulation And Expression In Inflammatory Joint Disease And Hyperoxic Lung Damage
Funder
National Health and Medical Research Council
Funding Amount
$270,013.00
Summary
Oxygen radicals (OR) are made by white blood cells (WBC) when they protect against microbes and cancer cells. However, excessive production also damages normal tissue, for example in lungs that receive too much oxygen (hyperoxic lung damage) or in inflamed joints. One type of WBC, the macrophage has a protein named UCP2, that limit the amount of OR formation. This project aims to find out how macrophages activate UCP2 and whether they do so in inflammatory arthritis and hyperoxic lung damage.
Isolation And Pre-clinical Evaluation Of Small Molecule Anti-inflammatory Compounds From Hookworms
Funder
National Health and Medical Research Council
Funding Amount
$320,891.00
Summary
This project will harness the unique ability of hookworm small molecules (<10 kDa) to modulate inflammation, and exploit these properties to develop novel modalities to treat inflammatory bowel diseases, using millennia of host-parasite coevolution as a guide. The excretory/secretory and somatic extracts will be assessed for their anti-inflammatory properties using TNBS mouse model. Compounds will be separated using HPLC and identified using MS and NMR spectroscopy.
Modulating Interactions Between TNFalpha And IGF-1 Signaling Pathways To Reduce Necrosis Of Dystrophic Muscle
Funder
National Health and Medical Research Council
Funding Amount
$476,515.00
Summary
Duchene Muscular Dystrophy (DMD) is a lethal childhood disease that affects mainly boys. These experiments will test new highly specific anti-inflammatory drugs for the potential clinical treatment of muscular dystrophies, using the mdx mouse model of human DMD. It is essential that the benefits of such anti-inflammatory drugs are fully evaluated in long term studies in mice. Two of these drugs (Enbrel and Remicade) are already in wide clinical use for inflammatory disorders and present attracti ....Duchene Muscular Dystrophy (DMD) is a lethal childhood disease that affects mainly boys. These experiments will test new highly specific anti-inflammatory drugs for the potential clinical treatment of muscular dystrophies, using the mdx mouse model of human DMD. It is essential that the benefits of such anti-inflammatory drugs are fully evaluated in long term studies in mice. Two of these drugs (Enbrel and Remicade) are already in wide clinical use for inflammatory disorders and present attractive options for treatment of DMD patients due to their high specificity of action and relatively few side effects. We have shown that both of these drugs have a striking protective effect and reduce necrosis of dystrophic muscle in the mdx mouse. The benefits of these drugs (and the mouse equivalent cVIq) is due to blocking the action of the key pro-inflammatory cytokine Tumour Necrosis Factor-alpha (TNFa). However, the precise mechanism by which high levels of TNFa increase necrosis of dystrophic muscle is not clear. There are many possible pathways. Identifying which is the key pathway(s), is of central importance to design and target new drugs to treat such lethal muscle diseases. Such modulation of signalling is a major therapeutic goal. To determine which mechanism of TNFa action is responsible for muscle necrosis, experiments will investigate several signalling pathways using specific inhibitors: the drug Pifithrin to inhibit p53; soluble RAGE to block RAGE (Receptor for Advanced Glycation Endproducts); and specific inhibitory peptides to block JNK (c-Jun N-terminal kinase). The application of these inhibitors (drugs), in mice, as future therapies for muscle diseases is novel. These studies will provide much new information on TNFa related signalling that is highly relevant to the potential treatment of many diseases, including muscle wasting that is a major problem in the ageing population and in disuse atrophy and cachexia.Read moreRead less
Design And Evaluation Of Inhibitors Of Phospholipases A2 As Anti-Inflammatory Drugs
Funder
National Health and Medical Research Council
Funding Amount
$317,545.00
Summary
There are at least 16 types of enzymes called phospholipases A2 (PLA2). They are found in venoms of snakes, bees, lizards, cone snails, etc and act as toxic and digestive agents. PLA2 enzymes are also found in cells and tissues of mammals where they carry out a wide range of digestive, maintenance, immune defence, and cell signalling functions. The human pancreas secretes one form of PLA2 into the gut to aid digestion. Human immune cells (macrophages, thymocytes, spleen leukocytes, platelets) us ....There are at least 16 types of enzymes called phospholipases A2 (PLA2). They are found in venoms of snakes, bees, lizards, cone snails, etc and act as toxic and digestive agents. PLA2 enzymes are also found in cells and tissues of mammals where they carry out a wide range of digestive, maintenance, immune defence, and cell signalling functions. The human pancreas secretes one form of PLA2 into the gut to aid digestion. Human immune cells (macrophages, thymocytes, spleen leukocytes, platelets) use other forms of PLA2 in the inflammatory immune response to kill infectious foreign agents like viruses and bacteria. One form of PLA2, known as type IIa, is the main bacteria-killing ingredient of human tears and it is also a chief component of fluid from the joints of patients with arthritis. Type IIa PLA2 is present in abnormally high levels in blood from humans with arthritis, burns, sepsis, ARDS, atherosclerosis, Crohn's disease, malaria, cancer and other chronic illnesses. These high levels can cause injury, tissue damage and pain due to too much inflammation and treatments are needed to stop or decrease effects of this enzyme . For these reasons this and related enzymes are thought to be potential targets for drugs which would act by blocking the functions of such an enzyme. Our group has been using computers to design new chemicals that can selectively fit into this enzyme and stick very tightly. We are determining the three dimensional structures of these chemicals in the enzyme to learn how to make them bind even more tightly. This information is allowing us to synthesize new selective drugs that stop PLA2 from promoting the development of disease. We propose to continue these studies towards developing powerful new antiinflammatory drugs that block the enzyme, and to demonstrate possible benefits of these drugs by testing them in animal models of arthritis, sepsis, adult respiratory distress syndrome (ARDS), period pain, malaria, and cancer.Read moreRead less
Exploring And Targeting The Anti-Inflammatory Signalling Mechanisms Of Interleukin 37
Funder
National Health and Medical Research Council
Funding Amount
$1,018,306.00
Summary
Cytokines are messenger proteins that function as master regulators of biological processes; thus they play central roles in many diseases. The rare cytokines that block inflammation do so by dampening the immune system’s potentially destructive force, making them attractive targets for drug development. We showed that interleukin 37 is a powerful anti-inflammatory cytokine, and will now evaluate its mechanisms of action and its efficacy against several severe diseases, including cancer.
Evaluation Of Orally Active Anti-inflammatory C5a Receptor Antagonists In A Transgenic Rat Motor Neurone Disease Model
Funder
National Health and Medical Research Council
Funding Amount
$533,578.00
Summary
Motor neurone disease is a rapidly progressive and incurable disease, usually ending in death within 3-5 years of diagnosis. The disease usually arrives without warning, and results in a progressive loss of muscle control. There is no effective treatment, and available drugs increase life span by a few weeks at best. There is evidence that the disease involves an inflammatory component, but available anti-inflammatory drugs are ineffective. We have developed a new class of anti-inflammatory drug ....Motor neurone disease is a rapidly progressive and incurable disease, usually ending in death within 3-5 years of diagnosis. The disease usually arrives without warning, and results in a progressive loss of muscle control. There is no effective treatment, and available drugs increase life span by a few weeks at best. There is evidence that the disease involves an inflammatory component, but available anti-inflammatory drugs are ineffective. We have developed a new class of anti-inflammatory drugs, known as C5a antagonists, and in preliminary experiments have shown they are therapeutically effective in a transgenic rat model of motor neurone disease. We propose to investigate in more detail how these drugs work in the rat model, and demonstrate that a specific inflammatory pathway, which we can now block, is responsible for some of the disease's progression. This work may lead to an entirely new class of drugs being used to treat patients with this drastic disease.Read moreRead less
Small Molecule Modulators Of Complement In Metabolism And Obesity
Funder
National Health and Medical Research Council
Funding Amount
$682,820.00
Summary
We have discovered that certain inflammatory proteins in the blood that are produced in the immune response to infection are involved in regulating the storage and burn off of fat in adipose tissue in the abdomen. These proteins bind to the surfaces of both fat and immune cells. We will study the effects of new drugs that compete with these blood proteins for the surfaces of these cells, since our experiments indicate that such drugs can potentially prevent and reverse fat deposition in rats fed ....We have discovered that certain inflammatory proteins in the blood that are produced in the immune response to infection are involved in regulating the storage and burn off of fat in adipose tissue in the abdomen. These proteins bind to the surfaces of both fat and immune cells. We will study the effects of new drugs that compete with these blood proteins for the surfaces of these cells, since our experiments indicate that such drugs can potentially prevent and reverse fat deposition in rats fed a high-fat, high-carbohydrate, diet.Read moreRead less
There is an unmet need for safe and effective anti-inflammatory drugs. Because P38 MAPK intracellular signalling modulates multiple pro-inflammatory cytokine actions, it appears to be an ideal candidate pathway. P38 inhibitors have been limited by their toxicity within hepatocytes. The aim of this program therefore is to develop agents with enhanced P38 MAPK inhibitory effects as well as reduced liver toxicity based on known structure activity relationships.