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The National Lottery Community Fund (226,066) Co-operative Group (16,503) The Wellcome Trust (16,377) Sport England (15,905) The National Lottery Heritage Fund (10,201) Garfield Weston Foundation (5,922) Lloyds Bank Foundation for England and Wales (5,467) The Henry Smith Charity (4,590) Northern Rock Foundation (4,331) Community Foundation serving Tyne & Wear and Northumberland (4,283) Esmée Fairbairn Foundation (4,194) BBC Children in Need (4,183) Woodward Charitable Trust (2,767) Quartet Community Foundation (2,683) Department for Transport (2,577) The Tudor Trust (2,463) Paul Hamlyn Foundation (2,367) Wolfson Foundation (2,210) Essex Community Foundation (1,876) City Bridge Trust (1,778) Community Foundation for Surrey (1,776) Greater London Authority (1,721) County Durham Community Foundation (1,652) Heart Of England Community Foundation (1,635) The Robertson Trust (1,542) Comic Relief (1,444) Suffolk Community Foundation (1,428) Glasgow City Council (1,365) London Borough of Southwark (1,260) Somerset Community Foundation (1,259) The Clothworkers Foundation (1,257) Guy's and St Thomas' Charity (1,230) Nesta (1,186) Corra Foundation (1,184) London Catalyst (1,174) Oxfordshire Community Foundation (1,139) Birmingham City Council (1,103) CAF (1,004) Masonic Charitable Foundation (895) Power to Change Trust (870) Leeds Community Foundation (869) Sussex Community Foundation (794) Trafford Housing Trust Social Investment (779) Ministry of Justice (774) Two Ridings Community Foundation (765) National Churches Trust (760) Walcot Foundation (755) Devon Community Foundation (715) The Dulverton Trust (680) A B Charitable Trust (665) See Less

Results

Development of fragment-based Hepatitis C (HCV) viral replication inhibitors 21 Jul 2010

Development of fragment-based Hepatitis C (HCV) viral replication inhibitorsAn estimated 170 million people worldwide are infected with HCV with treatment requiring an extended period of therapy and influenced by side effects and low response rates.The Trust has provided £2 million programme related investment to Cambridge based Astex Therapeutics to use their proprietary fragment-based screening approach, Pyramid (TM), to identify and develop novel inhibitors which bind to newly identified regulatory site on a HCV viral protein. Such novel agents would be of significant value in a disease where combination therapy is vital to limiting the emergence of viral resistance.

Amount: £1,000,000
Funder: The Wellcome Trust
Recipient: Astex Therapeutics Limited

Inhibitors of Lysyl Oxidase for the Prevention and Treatment of Invasive and Metastatic Cancer 30 Jul 2010

Inhibitors of Lysyl Oxidase for the Prevention and Treatment of Invasive and Metastatic CancerThe enzyme lysyl oxidase (LOX) regulates cross-linking of structural proteins in the extracellular matrix.LOX also plays a role in stimulating the metastatic spread of cancer through the body. Its expression is increased in hypoxic cancers and is correlated with tumour metastasis and decreased patient survival. In model systems its inhibition significantly decreases cancer metastasis and increases survival. Since metastasis is responsible for over 90 per cent of cancer deaths these data validate LOX as an important therapeutic target in cancer. Professor Caroline Springer and Professor Richard Marais from the Institute of Cancer Research have been awarded Seeding Drug Discovery funding to develop drugs that target LOX. They are applying a medicinal chemistry drug discovery approach underpinned by a strong programme in LOX biology with the aim of producing orally available, small molecular weight drugs that inhibit LOX activity for cancer treatment.See our video: BRAF and cancer: collaborative drug discovery

Amount: £818,674
Funder: The Wellcome Trust
Recipient: Institute of Cancer Research

Alternative complex I as a drug target in malaria 19 May 2010

Summary not available

Amount: £326,240
Funder: The Wellcome Trust
Recipient: Liverpool School of Tropical Medicine

11b-Hydroxysteroid Dehydrogenase Type 1 (11b-HSD1) Inhibition: tissue-specific control of cortisol action 13 Jul 2010

Professor Brian Walker, Professor Jonathan Seckl and Dr Scott Webster, University of Edinburgh have identified 11b-HSD1 as a crucial amplifier of glucocorticoid action in liver, adipose tissue and CNS, have shown its pathophysiological significance in obesity, and have provided preclinical and clinical 'proof of concept' that 11b-HSD1 inhibition improves both Metabolic Syndrome and cognitive function in ageing. Although their work has fuelled intense commercial interest in developing 11b-HSD1 inhibitors for metabolic indications, including type 2 diabetes, the opportunity to improve cognitive function has not yet attracted pharmaceutical companies. Under the latest round of funding, they will select the optimal clinical candidate and aim to progress these to Phase I clinical trials aiming at a memory improvement.

Amount: £1,926,801
Funder: The Wellcome Trust
Recipient: University of Edinburgh

11b-Hydroxysteroid Dehydrogenase Type 1 (11b-HSD1) Inhibition: tissue-specific control of cortisol action 19 May 2010

Professor Brian Walker, Professor Jonathan Seckl and Dr Scott Webster, University of Edinburgh have identified 11b-HSD1 as a crucial amplifier of glucocorticoid action in liver, adipose tissue and CNS, have shown its pathophysiological significance in obesity, and have provided preclinical and clinical 'proof of concept' that 11b-HSD1 inhibition improves both Metabolic Syndrome and cognitive function in ageing. Although their work has fuelled intense commercial interest in developing 11b-HSD1 inhibitors for metabolic indications, including type 2 diabetes, the opportunity to improve cognitive function has not yet attracted pharmaceutical companies. Under the latest round of funding, they will select the optimal clinical candidate and aim to progress these to Phase I clinical trials aiming at a memory improvement.

Amount: £87,450
Funder: The Wellcome Trust
Recipient: University of Edinburgh

11b-Hydroxysteroid Dehydrogenase Type 1 (11b-HSD1) Inhibition: tissue-specific control of cortisol action 19 May 2010

Professor Brian Walker, Professor Jonathan Seckl and Dr Scott Webster, University of Edinburgh have identified 11b-HSD1 as a crucial amplifier of glucocorticoid action in liver, adipose tissue and CNS, have shown its pathophysiological significance in obesity, and have provided preclinical and clinical 'proof of concept' that 11b-HSD1 inhibition improves both Metabolic Syndrome and cognitive function in ageing. Although their work has fuelled intense commercial interest in developing 11b-HSD1 inhibitors for metabolic indications, including type 2 diabetes, the opportunity to improve cognitive function has not yet attracted pharmaceutical companies. Under the latest round of funding, they will select the optimal clinical candidate and aim to progress these to Phase I clinical trials aiming at a memory improvement.

Amount: £195,834
Funder: The Wellcome Trust
Recipient: University of Edinburgh

Development of highly selective beta-1 adrenoceptor antagonists 21 Sep 2010

Development of highly selective beta-1 adrenoceptor antagonists Beta blockers have a serious side-effect of causing airway narrowing, shortness of breath and wheezing, and cannot be taken by patients with both heart and lung diseases. Dr Jillian Baker, Professor Steve Hill, Dr Barrie Kellam and Professor Peter Fischer at the University of Nottingham have been awarded funding to develop highly selective beta-1 antagonists. The programme is based around a lead compound with over 3000-fold beta-1 selectivity and demonstrated activity in an in vivo animal model. Once developed, the group's drug candidate will by definition have less respiratory side-effects and should be able to be given safely to the hundreds of thousands of patients with both heart and lung diseases.

Amount: £660,494
Funder: The Wellcome Trust
Recipient: University of Nottingham

Retinoic acid receptor a agonists for the treatment of Alzheimer's disease 31 Jan 2010

Retinoic acid receptor a agonists for the treatment of Alzheimer's disease. The current licensed treatments for Alzheimer's disease improve the symptoms that people experience but do not alter the progression of the underlying disease changes in the brain.Most of the attempts to develop new treatments have focused on altering deposits of the amyloid protein in the brain, but despite more than a decade of intensive research this has still not yielded any new therapies in the clinic. The studies of Dr Jonathan Corcoran of King's College London highlight a specific retinoic acid receptor (RAR)a agonist as a novel and exciting target for the development of new treatments. This agonist has two mechanisms of action - it regulates amyloid deposits in the brain and also plays a key role in the survival of neurons. In their project they will generate novel RARa agonists for the treatment of Alzheimer's disease.

Amount: £354,795
Funder: The Wellcome Trust
Recipient: King's College London

Optimization and development of novel small molecule inhibitors of beta-amyloid aggregation for the treatment of Alzheimer's disease. 21 Sep 2010

Current treatments for Alzheimer's disease (AD) only produce temporary symptomatic relief and there is a definite unmet medical need for disease-modifying therapies that can significantly delay its progression. Abnormally folded protein species associated with AD have been characterised with regard to their detrimental effects on cognitive function and there is emerging consensus that soluble oligomeric forms of beta-amyloid (Abeta) represent the primary pathological species. Senexis has identified a series of small molecule drug-like compounds which are believed to block the generation of soluble forms of Abeta and their toxic effects. They have clear therapeutic potential and the next phase of optimisation now needs to be undertaken to generate molecules that will be suitable candidates for clinical development for the treatment of AD. The first part of the project will complete the optimisation of key properties of these molecules, including their potency, oral bioavailability and CNS penetration. This will use structure activity relationships generated in the initial programme of the work conducted by Senexis. With this achieved, preliminary safety screening of candidate molecules will be undertaken from which the best one will be selected for pre-clinical development, the successful outcome of which will provide a molecule for clinical evaluation in man.

Amount: £1,196,365
Funder: The Wellcome Trust
Recipient: Senexis Limited

Transthyretin depletion for treatment of hereditary systemic and senile cardiac amyloidosis 15 Feb 2010

Systemic transthyretin amyloidosis is a fatal late onset disease caused by tissue deposition of amyloid fibrils composed of variant and wild type transthyretin. The objective of the project is to construct compounds to trigger the accelerated clearance of plasma transthyretin molecules by the liver by synthesising palindromic ligand-linker-ligand compounds capable of cross-linking transthyretin molecules or oligosaccharide-ligand conjugates that direct hepatic clearance, which could be used as drugs for treating and preventing acquired and hereditary human systemic transthyretin amyloidosis. The aim is to optimise the design, synthesis, and properties of a transthyretin depleting drug and complete the comprehensive safety and efficacy evaluation required prior to administration of a validated candidate compound in humans.

Amount: £831,143
Funder: The Wellcome Trust
Recipient: University College London

Selective glucocorticoid receptor agonists for the treatment of inflammatory conditions. 22 Feb 2010

Research by Professor David Ray and his team at University of Manchester has identified how to modulate the function of the glucocorticoid receptor.The glucocorticoid receptor responds to both natural hormones and synthetic glucocorticoids to inhibit the inflammatory response. Inflammation lies behind many important human diseases, including rheumatoid arthritis, and opening up novel approaches for therapy offers new hope for these chronic, disabling conditions. The award will allow development of new molecules capable of harnessing the glucocorticoid receptor for treatment of multiple inflammatory diseases, without the wide range of side effects that currently limit use of conventional drugs. If successful the research will lead to an orally active drug for use in inflammatory arthritis within five years.

Amount: £444,497
Funder: The Wellcome Trust
Recipient: University of Manchester

Discovery and development of small molecule antagonists of pleckstrin homology domains for the treatment of cancer. 15 Dec 2009

Professor Jeremy Tavare and colleagues at the University of Bristol have been funded to optimise small molecules that inhibit intracellular "signal transduction" systems that become hyperactive in tumour cells. The protein kinase B (PKB/Akt) signalling pathway has been shown to play a central role in the development of numerous different human tumours and has led to intense interest by the pharmaceutical industry to identified inhibitors. However, rather than target the ATP-binding pocket of the kinase domain, Professor Tavares group alternative approach is inhibit the PH domain-mediated responses of PKB. Targeting such PH domain of proteins represents a new approach to drug discovery. If successful, it would become more generically applicable to other targets possessing PH domains that have a range of different biological activities and therapeutic relevance.

Amount: £40,450
Funder: The Wellcome Trust
Recipient: University of Bristol

Development of a novel compound series to treat life-threatening, drug-resistant, Staphylococcal infections through the inhibition of the essential cell division protein, FtsZ. 21 Sep 2010

Drug-resistant Staphylococcal strains represent a growing threat to human health. The emergence of MRSA in particular has received considerable media attention and is attributed to > 1 ,400 of the deaths caused by infections and complicates the treatment of > 7000 patients in UK hospitals per year. With the aid of Trust funding, Prolysis will progress one of their novel antibacterial chemical series that specifically inhibits Staphylococcal cell division through a chemical optimisation programme, preclinical development and into Phase I clinical trials. The project aims to deliver a new targeted therapy for the treatment of Staphylococcal infections acquired in hospitals or the community and to offer a prophylactic treatment for MRSA carriers prior to invasive procedures.

Amount: £464,800
Funder: The Wellcome Trust
Recipient: Biota Europe Ltd

Development of a novel compound series to treat life-threatening, drug-resistant, Staphylococcal infections through the inhibition of the essential cell division protein, FtsZ. 26 Mar 2010

Drug-resistant Staphylococcal strains represent a growing threat to human health. The emergence of MRSA in particular has received considerable media attention and is attributed to > 1 ,400 of the deaths caused by infections and complicates the treatment of > 7000 patients in UK hospitals per year. With the aid of Trust funding, Prolysis will progress one of their novel antibacterial chemical series that specifically inhibits Staphylococcal cell division through a chemical optimisation programme, preclinical development and into Phase I clinical trials. The project aims to deliver a new targeted therapy for the treatment of Staphylococcal infections acquired in hospitals or the community and to offer a prophylactic treatment for MRSA carriers prior to invasive procedures. P~oP

Amount: £277,200
Funder: The Wellcome Trust
Recipient: Biota Europe Ltd

Structural brain changes with learning and recovery from stroke. 22 Mar 2010

The adult brain shows dynamic structural changes with learning and with recovery from damage. Studies in animals are able to characterise such changes with exquisite detail. The vast majority of these studies have focussed on changes occurring in grey matter. We recently provided evidence for learning-related change in the microstructure of white matter pathways of the adult human brain. However, the measures provided by neuroimaging are relatively crude and non-specific and, thus far, have no t been related to specific underlying cellular mechanisms. The current proposal has two main aims: First, to investigate the functional and clinical significance, timecourse, and age-dependence of experience-dependent white matter and grey matter change. Second, to carry out parallel neuroimaging and histological studies in rodents in order to determine mechanisms underlying change detected on imaging. The results of the animal studies will be relevant not only to those with an interest in plas ticity but also to the wider imaging community, as they will shed light on the anatomical basis of structural imaging measures.

Amount: £1,614,561
Funder: The Wellcome Trust
Recipient: University of Oxford

Importance of mammillary body connections for memory. 22 Mar 2010

Parallel programs of work will be carried out using rats and patients to compare and test different hypotheses of mammillary body function. Answering these research questions will involve separating the key inputs that drive mammillary body function and determining the different ways in which they might support memory. A combined rat/human approach will take advantage of the unique benefits provided by each line of research. In rats, I have developed techniques that make it possible to disconn ect selectively all the major afferent and efferent connections of the mammillary bodies. By manipulating these sets of inputs and outputs it will be possible to test which are key for memory function, and why are they important. The application of convergent techniques with rats (electrophysiology, functional gene-imaging, anatomical disconnections, behaviour) will be used to assess system function. Complementary research with patients who have mammillary body damage from different aetiologies will address very similar questions. A key component will be detailed anatomical assessments based on MRI derived information, including diffusion tensor imaging. Again, multiple approaches, including neuropsychological testing and functional imaging, will be used to test various models of mammillary body function.

Amount: £1,089,059
Funder: The Wellcome Trust
Recipient: Cardiff University

Combined genetic and biochemical approaches to uncover and characterize redundant factors involved in late stages of recombinational repair. 22 Mar 2010

Homologous Recombination (HR) provides an error free DNA repair pathway to deal with DNA double strand breaks (DSBs). Such breaks arise from genotoxic agents, but also happen during normal DNA replication. We know very little about late steps of HR, where redundant mechanisms seem to be able to resolve Holliday Junction (HJ) intermediates. It is only very recently that canonical HJ resolvases have been indentified in animals. One of those enzymes is GEN1 which was purified from human cell ext racts. However, its in vivo function remained unclear. Having followed a forward genetic approach, we found that the C. elegans homolog is required for DSB repair and unexpectedly also has a role in DNA damage checkpoint signalling. We propose a series of genetic screens to find further genes that act in the gen-1 DNA damage checkpoint and DSB repair pathways. Furthermore, we aim to undertake synthetic lethal screens to find genes that act in parallel to gen-1 to mediate the processing of late r ecombination intermediates. Finally, we hope to better understand how GEN-1 works by employing purification procedures from worms and from chicken DT40 cells. This cell-line will also be used to generalize genetic interactions and phenotypes we find in worms.

Amount: £1,427,423
Funder: The Wellcome Trust
Recipient: University of Dundee

Pursuing a multi-level understanding of memory and motivation. 22 Mar 2010

The ability to appropriately direct behaviour using our memories is something we take for granted. However, in certain disease-states, such as affective disorders and addiction, our motivational control goes awry and behaviour runs amok. My goal is to understand detailed neural mechanisms of memory and motivation. We will use state-of-the-art genetics, physiology and behaviour to interrogate the relatively simple nervous system of the fruit fly Drosophila at the molecular, cellular and neural ne twork level. We will identify and characterize neural circuits that are modified by experience, and that are required for memory formation, consolidation and retrieval. We will profile gene expression in the relevant neurons before and after training using microarrays and will use neuron-specific transgenic RNA-interference with behavioural assays to find conserved memory-relevant genes. Appetitive memory is only efficiently retrieved in hungry flies and we have discovered the neurons that are c ritical for this motivational control. We will use a combination of genetics, behaviour and physiology to understand the detailed mechanisms that the motivational states of hunger and satiety utilize to conditionally alter neural circuit properties and expression of adaptive behaviour.

Amount: £1,625,197
Funder: The Wellcome Trust
Recipient: University of Oxford