Open Assay Calls

This is an open call for phenotypic assay proposals funded by the Phenomics Discovery Initiative (PDi). PDi is a public-private partnership between industrial pharmaceutical companies and NPSC. PDi seeks to identify, develop, screen and validate innovative phenotypic assays that are relevant to human disease.

Selected proposals are screened free of charge.
The deadline for the next round of selections is 31st January 2017.

Find out more about PDi. *We use the EU commission definition of SME that can be found here.


How to apply?

Phenotypic assays are recruited from academic, clinical and SME communities thorugh an online applications portal.

Assays can be at various stages of development: from an early concept to a screening format (96-well / 384-well). Assays are assessed and selected by the PDi scientific committee, which is made up of a panel of industry and academic experts. Important characteristics for selection are scientific quality, novelty, relevance to human health, feasibility for medium to high-throughput and high-content screening, and value in drug discovery or chemical biology.

  • Selected assays are screened free of charge.
  • All assay results are delivered to the applicant. 

PDi covers the following costs

  • Assay development from concept to high throughput format.
  • Reagents including generation of cell lines and cell/tissue culture.
  • Access to a high quality industry standard compound collection (including annotated reference compounds and approved drugs targeting known pathways), world class high content screening facilities and state of the art chemoinformatics and bioinformatics.

Cell assays/disease models currently being considered

  • Cellular stress assays – Cell stress.
  • Human bronchoepithelial cell air-liquid assays – HBEC.
  • Genetic susceptibility and loss of tolerance in Inflammatory Bowel Disease (IBD) – IBD.
  • Regulatory T cell (Treg) assays– Treg cells.
  • Innovative phenotypic assays - Blue Sky.

If your assay is screened, you can exploit the data generated and the developed assay as you wish

  • You can patent or commercialise the data and/or license it to other parties.
  • You can seek consent from the PDi scientific committee to publish the data immediately, which takes up to 30 days to be granted. The scientific committee can impose a maximum of 90 day delay in publication, should they decide that IP from the project requires protecting.
  • You can use the developed assay on your own compound sets (private screens).
  • If your assay is validated you automatically grant the PDi industry members a licence to use this assay.
  • If the validated assay results are used by PDi industry members in private screens, and you agree to delay publication by 18 months – you will receive a one-off milestone payment of £75,000 from each of the companies using the assay.
  • You can develop collaborations with PDi industry members.
  • Above is a summary of your rights and obligations: Full T&Cs for the consortium can be found here.

How to put your assay proposal forward for consideration? 

You qualify to put an assay forward if you are a member of staff in a university, research institution, hospital or SME.

If you think you have a phenotypic assay that meets PDi requirements, please go to the NPSC online application portal and apply to the call category you are interested in. The site requires registration.

  • The application form is very short and straightforward.
  • We are looking for non-confidential information only at this stage.

If we are interested in accessing more details, we will contact you directly.

This is an open rolling call. Proposals will be selected on a continuous basis.

Blue Sky - High risk, innovative assay proposals

We are looking for proposals for highly novel, high-risk cell-based assays or small model organisms suitable for phenotypic screening, that can provide a step change in our understanding of human disease, and our approach to curing it.

The emphasis in this call is on novelty. The phenotypic assay should provide a novel way to model a disease-state or monitor a novel disease pathway, that can be probed with large libraries of chemical matter. Complex assays are encouraged, that involve human tisue, complex-cocultures, iPS cell lines, organoids etc..

 

 

Cellular stress assays

Assay description, desired readouts and end points

High level brief for the call: We are seeking novel cell-based screening methodologies able to distinguish cells undergoing Endoplasmic Reticulum (ER) stress from normal cells, and able to identify compounds that rectify ER stress responses and restore normal cell function. Ideally, these platforms will be developed using primary human cells or cell lines from tissues of interest, such as neuronal, pancreatic, Gastro Intestinal (GI), to maximize translational value, and allow the comparison of patient-derived healthy versus diseased cells.

The assays should be able to identify phenotypic changes associated with increased ER stress responses in an agnostic manner by leveraging high content imaging-based techniques or genetically encoded reporters of multiple pathways to track and characterize, morphological, subcellular, metabolic and pathway adaptations which generate phenotypic profiles suitable for medium- to high-throughput screening.  

Potential developments of interest

1. Novel unbiased readouts for cells undergoing stress  
  1. Development of biosensors for monitoring misfolded proteins in a cell, by using specific tracer proteins or chaperones; alternatively, developing a method to monitor any improperly folded protein in a cell. The goal would be to screen small molecules for increased clearance of misfolded proteins/aggregates and this could potentially apply to different cellular compartments (i.e. ER, mitochondria, cytosol)
  2. Measurement of the temporal movement and recycling (flux) of mitochondria and ER through autophagosomes, fusion/fission events, subcellular localization (i.e. contact or stress-induced collapse around the nucleus), as the basis of a screen for cell protective molecules. Is the physical location or orientation of the mitochondria/ER altered in response to stress?
  3. High throughput method to monitor ER associated degradation (ERAD) to use as a basis for a screening platform.
  4. ER and mitochondrial calcium perturbations in response to stress. Excess accumulation of mitochondrial calcium is pro-apoptotic and increasing mitochondrial buffering capacity may be protective.
  5. Metabolic changes induced by cellular stress (i.e. metabolic switching and reliance on oxidative phosphorylation versus glycolysis).
  6. Mitochondrial biogenesis readouts.

2. Cell survival assays: Normal screening for cell heath in response to stress is done in short term assays (i.e. 1-2 days). However, monitoring the effects of chronic stress on cellular survival long term would be of great benefit. This would recapitulate sustained physiologic low-level stress.  Ideally this could be done across cell lines representative of target organs/tissues of interest and would be adaptable to high throughput screening methodologies.

3. Survey, identify and categorize misfolded proteins associated with a number of disease states to create a fingerprint that may provide the basis of novel screening approaches. 

4. Epigenetics: Epigenetic modifications contribute to multiple disease states, though this is not well understood as an adaptation mechanism for cells in response to stress.  Readouts for epigenetic modifications in response to stress, and tracking these changes in living cells.

Current knowledge, background, existing comparable assays

Chronic ER stress in response to the accumulation of misfolded proteins and defects in ER-associated protein degradation has been implicated in the pathophysiology of a variety of human disorders, including neurodegeneration, heart disease, inflammatory bowel disease, and immune dysregulation. Cellular stressors may include chemical inducers of ER and mitochondrial stress, genetic interference of protein folding or processing mechanisms, and mutations or physiological conditions associated with disease.

Human bronchoepithelial cell air-liquid assays

Assay description, desired readouts and end points

High-level brief for the call: We are seeking human bronchoepithelial cell (HBEC) air-liquid interface models in 96-well format, which have the potential to be analyzed on a fully automated high-content imaging platform (e.g. Yokogawa, ImageXpress or IN Cell analyzer platforms). These assays will be used to study the interactions of respiratory viruses with HBECs and to test the effect of small molecules on these interactions and associated alterations in inflammatory response.

Protocols of interest could include:

  • novel cell staining methods (nuclei + cell membrane or cell membrane + cell phenotype markers)
  • novel imaging protocols that allow the high-content imaging of these cells with platforms like Yokogawa, ImageXpress or IN Cell analyzer
  • novel methods for culturing these cells

Current knowledge, background, existing comparable assays

Respiratory viruses (Influenza, Respiratory Syncytial Virus (RSV), Rhinovirus…) are a major cause of upper and lower respiratory tract infections, leading to significant morbidity and mortality in humans. For example, viral infections are notorious triggers of symptomatic exacerbations in patients suffering from COPD and asthma.

The human lung epithelium, joining forces with the innate and adaptive immune system, sets up the primary defensive wall against these viral pathogens. However, respiratory viruses have developed strategies to evade the human defense response often leading to severe disease in the infected host. Damage of lung tissue (loss of epithelial cells) ensues from the viral infection itself and the immune response mounted by the host. Epithelial injury and mucus production by epithelial cells impair mucociliary clearance, pave the way for bacterial superinfection and impair gas exchange in the airways, leading to respiratory compromise. Additionally, infected epithelial cells release pro-inflammatory mediators (IL-6, IL-8...) and a damage-associated molecular pattern (DAMP) that can be modulated by the infecting virus. This mechanism contributes further to symptomatic deterioration or eventually respiratory failure. Therefore, there exists a high unmet medical need for novel therapeutics to prevent and treat respiratory viral infections.

The 3-dimensional HBEC air-liquid interface model is a physiologically relevant and established model system to study the effects of respiratory viral infection and is used to test the antiviral activity of RSV inhibitors (1). This model system comprises a multilayered, pseudo-stratified lung epithelial tissue that includes the presence of ciliated epithelial cells, mucus-producing goblet cells, and basal cells; cell types that constitute the bronchoepithelial tissue in humans.

Reference:

  1. Villenave, R., Thavagnanam, S., Sarlang, S., Parker, J., Douglas, I., Skibinski, G., Heaney, L.G., McKaigue, J.P., Coyle, P.V., Shields, M.D. & Power, U.F. (2012). In vitro modeling of respiratory syncytial virus infection of pediatric bronchial epithelium, the primary target of infection in vivo. Proc. Natl. Acad. Sci. U S A. Vol. 109(13): 5040-5045.

Genetic susceptibility and loss of tolerance in inflammatory bowel disease (IBD)

Assay description, desired readouts, and end points

High-level brief for the call: Our primary goal is to identify novel readouts that address the effects of common IBD risk alleles on epithelial/antigen presenting cell and goblet cell/Paneth cell biology in order to identify mechanisms that can promote homeostasis and immune tolerance. We would like to act on this goal in the context of developing assay systems suitable for medium- to high-throughput screening, ultimately using primary human cells to provide readouts specific to IBD pathobiology.

Platforms may include intestinal stem-cell derived 2-D and 3-D culture systems where all epithelial cell types are present; 2-D systems that are enriched for a specific cell type of interest, epithelial/immune cell co-culture, macrophage/DC monoculture.

Potential readouts could include

  • high content imaging
  • secretion of proteins (cytokines, chemokines, mucins, anti-microbial peptides)
  • protein-protein interactions
  • nuclear or membrane translocation
  • trafficking of proteins, protein complexes, or vesicles
  • markers of cell death (apoptosis, necroptosis)
  • altered cellular morphology

Assays of interest are:

  • A bacterial antigen/epithelial cell/dendritic cell co-culture system in 96- or 384-well format would be very desirable for exploration of mechanisms associated with tolerance.
  • Bacterial antigen/macrophage or dendritic cell monoculture systems that are amenable to 384-well high content imaging protocols.
  • Assays that can explore goblet cell and Paneth cell dysfunction in the context of deficits in autophagy.  
  • High throughput screening assays that can differentiate markers of apoptosis and necroptosis.

Current knowledge, background, existing comparable assays

  1. Inflammatory bowel disease (IBD)

Current understanding of the pathobiology of IBD suggests that chronic inflammation arises from a loss of tolerance to host commensal bacteria in the context of both genetic susceptibility and an environmental trigger. Maintenance of an effective epithelial barrier, where there is close association between epithelial cells and dendritic cells (DC), is considered to be central to the maintenance of tolerance. In health, the production of a mucus layer, the release of anti-microbial peptides and the tight regulation of epithelial permeability minimize the opportunity for luminal bacteria to translocate to the sub-epithelial compartment, where they would otherwise induce an adaptive immune response. DCs extend processes across the epithelium and form intimate contacts with epithelial cells. Both epithelial cells and DCs sample the luminal environment and communicate with one another through cell-to-cell contact, and the production of cytokines and chemokines. This crosstalk supports a tolerogenic DC phenotype to commensal bacteria, and in turn promotes a downstream tolerogenic host environment through enhancement of T-regulator function.

Inflammatory bowel disease (IBD), on the other hand, is characterized by impaired barrier function (increased epithelial permeability, decreased mucin and anti-microbial peptide release, increased cell death), impaired epithelial/DC crosstalk and loss of tolerance. Alterations in these processes has been linked to genetic polymorphisms, in particular those that disrupt bacterial molecular pattern recognition and/or impair cellular homeostatic mechanisms. It is hypothesized that adaptive mechanisms will be discovered that may be exploited to overcome these deficits in order to maintain epithelial health and disease remission.

  1. Crohn’s disease (CD)

The most common polymorphisms associated with CD have been identified in three converging pathways; bacterial pattern recognition, autophagy, and the endoplasmic reticulum (ER) stress/unfolded protein response (UPR). Hypomorphic polymorphisms in NOD2, an intracellular receptor involved in bacterial molecular pattern recognition, contributes the largest fraction of genetic risk for CD. The T300A mutation in ATG16L1, an intracellular scaffolding protein, is a close second, and its discovery brought disrupted autophagy and cellular homeostasis to the forefront as an important contributor to CD pathogenesis. The requirement for physical interaction between NOD2 and ATG16L1 for bacterial clearance and innate immune signaling highlights the interdependence of these two pathways. The unfolded protein response (UPR), induced by endoplasmic reticulum stress, is also closely interdependent with autophagy and mutually cross-regulated. Polymorphisms in XBP1 result in reduced capacity to respond to ER stress, resulting in failed clearance of unfolded proteins through autophagic mechanisms leading to the induction of programmed cell death. The intestinal epithelium, situated at the interface between the microbiome and the host, is particularly susceptible to these functional deficits.  

  1. Microbial peptide/epithelial/dendritic cell interactions:

Epithelial cell/DC interactions are important for responses to pattern and damage associated microbial peptides (PAMPs and DAMPs) and for determining downstream immunological responses to pathogens and commensals. NOD2 present on DCs and macrophages senses PAMP and induces autophagy upon binding of antigen. Autophagy is required for lysosomal antigen processing, and generation of MHC Class II antigen-specific T cell responses.   Epithelial cell/DC co-culture systems grown in transwells have shown that mutations associated with abnormalities in molecular pattern recognition (NOD2) and deficiencies in autophagy (ATG16L1) compromise epithelial cell/DC cross-talk, leading to altered antigen processing and enhanced pro-inflammatory signaling. In addition, these defects contribute to chronic inflammation from bacterial persistence due to impaired lysosomal destruction and immune-mediated clearance.

On the other hand, bacterial products derived from “beneficial” commensals can enhance cellular homeostasis and support epithelial barrier function.

  1. Secretory cell pathobiology:

Autophagy has also been linked to epithelial secretion where it is important for directed secretory granule trafficking to the membrane. Up to 40% of CD patients display a disordered Paneth cell phenotype in which secretory granules are reduced in size, absent, or where granule contents are distributed diffusely throughout the cell. This phenotype correlates with the T300A mutation in ATG16L1 and can be recapitulated in mice deficient in autophagy.

In addition, CD patients exhibit a reduction in the thickness of the mucus layer and reduced numbers of goblet cells, with those remaining displaying enlarged mucin containing granules. Originally thought to be an adaptive response to epithelial loss, evidence now suggests that goblet cell hyperplasia is associated with a failure of mucin granule trafficking to the apical membrane and reduced secretion.

In both cases, an inadequate unfolded protein response and induction of ER stress are thought to contribute to secretory dysfunction. A dysregulated oxidative stress response in the context of deficient autophagy was shown to contribute goblet cell dysfunction.

  1. Cell survival:

Cells exposed to unrelenting ER stress will eventually enter caspase-dependent programed cell death in the form of apoptosis. A caspase-independent form of programed cell death, necroptosis, has also been described in patients with IBD. Whereas immune cell processing of apoptotic cells evokes tolerance, necroptotic cells release DAMPs that drive inflammation. Here again, deficiencies in autophagy are thought to increase the likelihood that the death pathway will shift to necroptosis.

Microbial, Epithelial and Immune Interactions in Inflammatory Bowel Disease (IBD)

 
Assay description, desired readouts and end points

High level brief for the call: Our primary goal is to explore epithelial cell function in the context of IBD pathobiology in order to identify adaptive mechanisms that can be exploited to promote epithelial resilience, preserve barrier function, and restore immune tolerance.  To this end, we would like to develop secondary and tertiary assay systems focusing on microbial, epithelial and immune cell interactions using mouse or human primary cells, but ideally those from human.  Platforms may include 2-D and 3-D culture systems where all epithelial cell types are present, or systems that are enriched for specific cell types (stem cells, columnar enterocytes).  The experimental platform should be amenable to modifications that would permit the exploration of a variety of biological processes known to be disrupted in IBD.  
Potential readouts could include secretion of proteins (cytokines, chemokines, mucins, anti-microbial peptides); protein-protein interactions; nuclear or membrane translocation; trafficking of proteins, protein complexes, or vesicles; markers of cell death (apoptosis, necroptosis); altered cellular morphology; molecular readouts (qPCR, microarray, RNAseq, ChIPseq).  Additional approaches are welcome.

 

Current knowledge, background, existing comparable assays

Current understanding of the pathobiology of inflammatory bowel diseases (IBD) suggests that chronic inflammation arises from a loss of tolerance to host commensal bacteria in the context of both genetic susceptibility and an environmental trigger. 
In health, the intestinal epithelium functions as the first line of defense between antigens and microbes in the intestinal lumen and the host.  Epithelial cells sample luminal antigen and become immunologically active, releasing chemokines/cytokines that support epithelial homeostatic function and recruit immune cells.  Dendritic cells (DC) present in the sub-epithelial compartment also sample the luminal environment by extending processes across the epithelial barrier, and in so doing form intimate contacts with epithelial cells.  It has been proposed that crosstalk between epithelial cells and dendritic cells promotes a downstream tolerogenic host environment to commensal bacterial via enhanced T-regulatory function.
Both dendritic cells and mucosal macrophages detect conserved molecular patterns on microbes via pattern recognition receptors which mediate differential responses to commensal or pathogenic bacteria.  Abnormalities in molecular pattern recognition or deficiencies in bacterial or antigen processing can compromise epithelial cell/DC cross-talk, leading to loss of tolerance to commensal microbes, failure of macrophages to effectively clear microbes, and dysregulated pro-inflammatory signaling.  It is hypothesized that susceptibility to inflammatory bowel disease is driven by genetic polymorphisms, and three of the more common risk alleles for IBD (NOD2, ATG16L1, XBP1) are believed to be associated with altered bacterial recognition and processing and cellular homeostasis (autophagy, endoplasmic reticulum stress and the unfolded protein response).  In particular, deficits in autophagy have been linked to wide ranging effects on epithelial and immune cell pathobiology.  We propose that normalization of these processes will improve epithelial barrier function, ameliorate disease, and prevent disease recurrence.

Oncology

 
Assay description, desired readouts and end points

High level brief for the call: We are interested in all assays in the field of oncology, that are relevant to human cancers.
Please apply through the Blue-sky call for proposals, stating the disease area for your assay.

Regulatory T cell (Treg) assays

Assay description, desired readouts, and end points 

High-level brief for the call: The main objectives are to identify a potential surrogate human Treg population, and unique identifying markers/signatures that could serve as readouts for Treg cell differentiation and suppressive capacity.

We are seeking a system capable of testing the effect of small molecules on Treg cell expansion, differentiation and/or function, in particular, but not limited to, measuring Treg suppressive capacity. The assay(s) should allow the detailed analysis of the interaction between Treg and effector/conventional T cells (Tconv) on platform(s) that include high-content imaging and/or transcriptomics/proteomics. One of the main challenges of this task is the limited number of Treg cells that can be isolated from human peripheral blood. This implies that a more scalable approach is desired, while human primary cell-based assay systems are of significant interest, the use of surrogate cell populations such as induced pluripotent stem cells (iPS cells) that can be differentiated into Treg cells for higher throughput screening provide additional advantages. We are also looking for new Treg-specific markers/signatures (signalling and/or transcriptional) to identify bona fide human Tregs. Finally, detailed assessment of small molecule effectors specifically targeting Treg suppressive capacity requires co-culturing Treg cells with Tconv cells. This means that the assays should be able to distinguish the effect of small molecule compounds on Treg versus Tconv cells.  

Current knowledge, background, existing comparable assays
Naturally occurring Treg cells (nTreg) are thymic-derived cells that represent a small population (5-7%) of total CD4+ T cells in human peripheral blood, and express CD25 as well as the transcription factor Foxp3 (forkhead box P3), which is critical for their development and function. They possess potent regulatory activity to suppress excessive activation, proliferation and effector functions. They act on a wide range of immune cells in-vitro and in-vivo, including CD4+ and CD8+ T cells, natural killer (NK), Natural Killer T (NKT) cells, B cells, and antigen-presenting cells. Treg cells are indispensable for the maintenance of tolerance and immune homeostasis. Their dysfunction or absence causes fatal autoimmune disease, immunopathology, and allergy (Sakaguchi 2010, Nat. Imm. Rev.).

The markers typically used to identify Treg cells are CD4, CD25, CD45RA, CD127, Foxp3 and the proliferation marker, Ki67. Phenotypically, these cells are CD4+/CD25hi/CD45RA-/CD127lo/Foxp3hi/Ki67-. However, many of these markers are also expressed by Tconv upon activation. Treg and Tconv also produce different cytokines (eg IL-10 vs IL-2 or IFN-g, respectively), which can be measured by intracellular staining or in supernatants after stimulation. Due to the low numbers or frequencies of nTreg in human peripheral blood, in-vitro assays have been developed to generate larger numbers of “induced” Treg (iTreg) cells from naïve CD4+ T cells. This is achieved by culturing CD4+CD25- T cells for several days with TGF-b +/- IL-2. While the majority of cells cultured under these conditions will upregulate Foxp3, it is unclear whether they have a specific phenotype compared to nTreg.

Currently, the functional study of human Treg-mediated suppression is limited to in-vitro co-culture assays. It should be emphasized that there is no direct evidence that in-vitro suppression assays with nTreg or iTreg directly reflect in-vivo suppressive capacities of Treg. cells. That being said, Treg suppressive capacity can be assessed by culturing Treg with Tconv cells and measuring proliferation (thymidine incorporation or by flow cytometry using CFSE dilution) of, and/or cytokine production (e.g. IL-2 production) by, Tconv cells. Our aims are to exploit and adapt such systems to more automated and higher throughput screening formats.

Ultra high throughput transcriptomics screening platform

Assay description, desired readouts and end points

High level brief for the call: We are seeking novel high throughput cell-based transcriptional platform solutions that allow libraries containing more than 500,000 compounds to be screened at an affordable cost per well. Given the desired throughput, the approach should be applicable in standard 384 or 1536 well format. The method should be sensitive with a sufficiently large dynamic range to accommodate a broad range of differentially expressed transcripts and be highly reproducible. The best method will be selected and funded to develop into a real compound screening campaign in collaboration with Janssen.

Current knowledge, background, existing comparable assays

In drug discovery, phenotypic screening is currently experiencing a renaissance after being replaced by target-based approaches as a result of the advances in molecular biology and genomics. A retrospective study covering the period 1999 to 2008 pointed out that the hypothesis-driven target based screening methods appeared to be less successful in the discovery of new first-in-class small molecules than the unbiased phenotypic approaches1. In the field of oncology, however, the success rate of phenotypic screening was less prominent, and one of the primary reasons was the reliance on simple phenotypic approaches that monitored non-specific drug effects like cytotoxicity or mitotic arrest2

Applying approaches, such as monitoring transcriptional signatures, will enable translation and application of clinically relevant biology to the in vitro early discovery setting. Methods that allow for monitoring gene signatures that represent transition and progression of disease from a normal state have been demonstrated to be effective in the identification of several new chemical compounds3,4. Typically, the obtained gene signature is represented by a set of a few to a hundred genes. These signatures can be applied in a high throughput environment to identify new chemical compounds able to revert the transcriptional disease profiles back to normal states. Many techniques have emerged that allow gene signature based profiling /screening, ranging from interrogating a few genes per sample by qPCR, in the early days, to whole transcriptome RNAseq, in the present day. As these techniques become more mainstream and increasingly sensitive, the primary bottleneck to apply them for a compound screen with a 20-100 gene signature in a high throughput fashion (>500.000) is the high cost per well. Luminex-based assays allow a medium throughput for a highly multiplexed gene panel, at moderate cost5. More versatile techniques making use of a barcoding strategy in combination with Next Generation Sequencing pool multiple samples with a complex gene signature at significantly lower cost4.

References:
  1. Swinney, D.C. & Anthony, J. How were new medicines discovered? Nature Reviews Drug Discovery, volume 10 (2011).
    Moffat, J.G. et al.
  2. Phenotypic screening in cancer drug discovery — past, present and future. Nature Reviews Drug Discovery, volume 13 (2014).
  3. Yamaguchi, T. et al. Identification of JTP 70902, a p15(INK4b)-inductive compound, as a novel MEK1/2 inhibitor. Cancer Science, volume 98 (2007).
  4. Li, H. et al. Versatile pathway centric approach based on high throughput sequencing to anticancer drug discovery. Proceedings of the National Academy of Sciences USA, volume 109 (2012).
  5. Hieronymus, H. et al. Gene expression signature-based chemical genomic prediction identifies a novel class of HSP90 pathway modulators. Cancer Cell, volume 4 (2006).
Apply for a PDi funded assay call

This is an open call for expressions of interest for phenotypic assay ideas.

Call guidelines - How to apply?

We are interested in knowing about highly innovative phenotypic assay ideas from academia, clinicians, and SMEs*.
Assays can be at various stages of development: from an early concept to a working screening format (96-well / 384-well).
We will contact you if we are interested in pursuing a collaboration with you to develop the assay further.
We will select projects according to characteristics such as scientific quality, novelty, relevance to human health, feasibility for medium to high-throughput high-content screening, value in drug discovery or chemical biology.

How to put your assay proposal forward for consideration?

If you think you have a highly novel phenotypic assay please go to the NPSC online application portal and apply to the call category you are interested in. The site requires registration. The application form is very short and straightforward.

We are looking for non-confidential information only at this stage.
If we are interested in accessing more details we will contact you directly.

Deadline for proposals: This is an open rolling call. Proposals will be selected on a continuous basis.
*SME definition is according to EU commission.

Blue sky assays - Highly innovative phenotypic assay ideas

UK-NPSC is seeking ideas from academia, clinicians and SMEs for phenotypic assays that can be executed within its facilities.

We are looking for proposals for highly novel, high-risk cell-based assays or small model organisms suitable for phenotypic screening, that can provide a step change in our understanding of human disease, and our approach to curing it.

The emphasis in this call is on novelty. The phenotypic assay should provide a novel way to model a disease-state or monitor a novel disease pathway, that can be probed with large libraries of chemical matter. Complex assays are encouraged, that involve human tisue, complex-cocultures, iPS cell lines, organoids etc..

Submit an expression of interest

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