Pfizer is strongly committed to research in the Inflammation area and supports medical innovation in Europe through this Competitive Investigator Research Awards Programme.
The mission of the Inflammation EUROPE ASPIRE 2016 Research Awards is to support basic science and translational research through a competitive grants program that advances medical knowledge in understanding the role of the JAK-STAT pathways in IMID (Immune Mediated inflammatory Diseases).Of particular interest is the effect of targeted inhibition of the JAK-STAT pathways as related to specific clinical effects examining either at efficacy and/or safety outcomes.
An independent committee of European medical experts in the field of Inflammation will review the research proposals and select the grant recipients.
This program provides research grants for studies designed and conducted by non-Pfizer physicians and scientists.
Intracellular signaling pathways play a critical role in the pathogenesis of immune mediated inflammatory diseases (IMID) such as rheumatoid arthritis (RA). One of these pathways is the Janus Kinase (JAK) -Signal Transducer and Activator of Transcription (STAT) pathway. Basic and clinical research has demonstrated that inhibition of the JAK-STAT pathway results in the reduction of inflammation and may therefore be a potential strategy to reduce the signs and symptoms of several IMID. However, many questions remain with respect to the role that JAK-STAT pathways play in inflammation. Furthermore, increased understanding of exactly how (specific) inhibition of these JAK-STAT pathways may cause a certain clinical effect with respect to efficacy and safety outcomes in IMID is needed.
REQUEST FOR PROPOSALS
Pfizer invites investigators to apply for the Inflammation EUROPE ASPIRE 2016 Research Awards through submission of research proposals with the primary objective to increase our understanding of the role of the JAK-STAT pathways in Rheumatoid Arthritis, Ulcerative Colitis(UC), Psoriasis (PSO) and Psoriasis Arthritis (PSA) and the effect of specific inhibition of the JAK-STAT pathways by targeting JAK on specific clinical effects looking either at efficacy and/or safety outcomes.
UPDATED AREAS OF FOCUS FOR THE 2016 ASPIRE AWARDS
The program focuses on basic and translational research and may include but will not be limited to the following topics:
- Effects of JAK inhibitors in haematopoietic-cell precursors (e.g. via JAK2 inhibition)
- Effect of JAK inhibition on immune cell functions including NK, NKT cells and ILCs
- Long-term effect of JAK inhibition on NK cell numbers and function
- Biological markers of B-cell/T-cell activation in vitro/in vivo and their modifications through the action of JAK inhibitors
- The pleiotropic effect of JAK inhibitors, including anti-oxidant capacity of JAK inhibitors and effects on immune-cell metabolism
- The role of JAK–STAT signalling in metabolic syndrome / diabetes / carotid intima-media wall thickness in animal models treated with JAK inhibitors
- The role of JAK–STAT signalling in the immune response to infection (e.g. viral/herpes zoster, tuberculosis)
- Treatment with JAK inhibitors in animal models of lipid metabolism and increases in HDL/LDL
- Effects of inhibiting specific JAK isoforms versus non-selective pan-JAK inhibition
- The effects of inhibiting specific JAK isoforms on clinical safety/efficacy (e.g. monotherapy) outcomes and specific markers of effect (biological or biochemical)
- The role of JAK–STAT signalling and itching in psoriasis (e.g. via animal models treated with JAK inhibitors)
- The role of JAK pathways in the pathophysiology and immunology of psoriatic arthritis
- The role of JAK pathways in the pathophysiology and immunology of ulcerative colitis
- Cross-talk between the JAK–STAT pathway and other signalling pathways, including the IL-12/IL-23 signalling pathway
- The interaction between the JAK pathway and the IL-17 axis / TH17-cells
- The relationship between the JAK pathway and the biology of relevant cytokines (e.g. TNF)/chemokines (e.g. IP-10)
- Investigation into how JAK inhibitors affect SOCS activity and other regulatory feedback mechanisms
- Involvement of the JAK pathway in CRP production
- JAK–STAT signalling inhibition on the modulation of pro-inflammatory genes such as in RA cartilage erosion and synovitis
- Inhibition of bone-turnover markers in arthritis-induced animal models treated with JAK inhibitors, and their role in bone erosion and cartilage degeneration (synovial tissue biomarkers)
Effect of JAK inhibition on immune cells
Role of JAK–STAT signalling
Role of JAK isoforms
Role of JAK pathway in different diseases
Interaction of JAK-STAT pathway
Proposals that include the generation of pure clinical (human) data will not be considered for the 2016 ASPIRE awards.
Within the proposed topics, investigators are expected to generate in-vitro, in-vivo (animal model) data with the primary objective of further understanding the role of the JAK-STAT pathways in Rheumatoid Arthritis, Ulcerative Colitis(UC), Psoriasis (PSO) and Psoriasis Arthritis (PSA) and the effect of specific inhibition of the JAK-STAT pathways by targeting JAK on specific clinical effects looking either at efficacy and/or safety outcomes.
CRITERIA FOR SELECTION- Independent, External Review Committee
The ASPIRE applications will be reviewed by an independent, external review committee comprised of medical and scientific experts. Grants will be awarded based upon:
- Scientific merit of the research proposal
- Qualifications of the applicant
- Relevance of proposed research to the program's mission
- Evidence of the applicant's commitment to an academic research career
- Evidence of a suitable research environment
Pfizer is funding awards of 60,000 Euros each. It is expected that the results will be presented at scientific meetings and published in peer reviewed journals.
DEADLINE FOR APPLICATION AND KEY DATES
- Application submission start: January 1st 2016
- Application deadline: February 29th 2016 EXTENDED to March 7th 2016
- Award announcement: May 2016