The National Institutes of Health issued last week a request for applications for research projects focused on the development of therapeutics, including those based on siRNA, for biodefense applications.
The NIH also recently reissued requests for applications for two other funding opportunities, one focused on the use of mouse models to study joint degeneration and one exploring the relationship between Fragile X syndrome and autism and both with RNAi components.
Under the biodefense program, which is being supported by the National Institute of Allergy and Infectious Diseases, the NIH said it expects to award up to $10 million a year for up to five years to fund between 10 and 15 research projects developing therapeutics and diagnostics for biodefense category B pathogens. These pathogens include ricin toxin from Ricinus communis; Staphylococcus enterotoxin B; Listeria monocytogenes; West Nile virus; and Burkholderia pseudomallei.
"Developing biodefense therapeutics against NIAID Category B threats is a key national priority."
"The objective of this program is to support translational research and advanced product development, i.e. beyond basic research," the NIH said. "Projects may include, but not be limited to, identification of diagnostic or therapeutic targets; the adaptation of technologies or products to category B biodefense applications; optimization of products; process development, early validation and testing; preclinical evaluation; scale-up, and production of materials sufficient for preclinical regulatory requirements and clinical phase I testing or field trials."
The NIH added that "developing biodefense therapeutics against NIAID Category B threats is a key national priority," and that it is encouraging projects involving the preclinical development of "novel therapeutic technologies" such as siRNA.
The NIH said that since a key component of the funding opportunity is the development of partnerships, all grant recipients will be required to partner with an NIH project scientist. "In addition, cooperative applications between researchers in academia and/or industry that bring together expertise in different aspects of research and product development are strongly encouraged, but not required," the institute said.
The NIH also noted that "while clinical development strategies may be included within an overall product development plan, this [funding opportunity] will not support clinical trials." Because of this, funded research is not required to result in a final product, but the NIH said it expects "proposals to make significant progress along the preclinical research and product development pathway."
Letters of intent for this funding opportunity are due by Oct. 27, with final applications due a month later. The earliest anticipated start date for funded research is July 2007.
In the first reissued RFA, the NIH said it will provide up to $275,000 per two-year project investigating the biological mechanisms underlying non-inflammatory joint degradation, or osteoarthritis, using genetically modified mouse models.
"Inflammatory processes are evident in late stages of osteoarthritis, and are likely to be major contributors to the chronic pain that is the most common symptom of the condition," the NIH said. "However, for the purpose of this initiative, osteoarthritis is distinguished from diseases, such as rheumatoid arthritis, in which inflammation arising from autoimmunity is the primary cause of tissue damage.
"The root causes of joint degeneration in osteoarthritis remain unclear … [and this funding opportunity] is intended to accelerate the characterization of new models and the testing of hypotheses that could lead to improved diagnosis and treatment of osteoarthritis," the institute added.
The NIH said that candidate research projects will focus on identifying "specific genes, proteins, and biochemical pathways that contribute to joint degeneration. Information to be gained will include the timing and anatomical location of events that lead to joint degeneration, the functional characterization of proteins identified as causal factors, and the definition of pathways by which particular gene products contribute to joint degeneration."
Key objectives of the initiative include the characterization of new models; the development and testing of hypotheses that arise from the properties of new and existing models; and the definition of functional roles for specific molecular entities identified as contributing to joint degeneration.
Among the research topics suggested by the NIH is the testing of models of joint degeneration by specific antagonism of biological functions using antisense … or RNAi approaches.
The National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute on Aging, and the National Institute of Dental and Craniofacial Research are participating in the initiative, which was first issued in August 2004.
The deadline for applications is October 1.
The second reissued RFA, the NIH said it will provide up to $50,000 a year for projects aimed at "characterizing, understanding, and treating etiological and pathophysiological mechanisms common to both Fragile X syndrome and autism."
"Researchers have argued that autism and autistic symptoms in FXS reflect a common etiological or pathophysiological pathway underlying the two conditions," the NIH added. "Ongoing basic neuroscience research on FXS in model systems like the mouse and fly are providing a wealth of information at multiple levels … to delineate the neurobiology of this disorder. Studies [supported under this initiative] should dissect components of the neurobiology of autism, especially in patients with both FXS and autism, and identify novel targets for new drugs to treat both disorders."
The NIH said that possible areas of investigation include studies of RNA and microRNAs, including microRNA-mediated translational regulation by the Fragile X Mental Retardation protein, which is not expressed in people with FXS.
This funding opportunity was first issued in May 2005. The deadline for grant applications is Oct. 1.
Doug Macron ([email protected])