SOURCES SOUGHT
R -- Pharmacologic Characterization Support Services - Sources Sought 4627643
- Notice Date
- 6/30/2017
- Notice Type
- Sources Sought
- NAICS
- 541690
— Other Scientific and Technical Consulting Services
- Contracting Office
- Department of Health and Human Services, National Institutes of Health, National Institute on Drug Abuse, 6001 Executive Boulevard, Room 4211, MSC 9559, Bethesda, Maryland, 20892-9559, United States
- ZIP Code
- 20892-9559
- Solicitation Number
- HHS-NIH-NIDA-SSSA-SS-17-484
- Archive Date
- 7/22/2017
- Point of Contact
- Danielle R. Brown, Phone: 301 480 2385, Rachelle Trice, Phone: 3015941928
- E-Mail Address
-
danielle.brown2@nih.gov, rachelle.trice@nih.gov
(danielle.brown2@nih.gov, rachelle.trice@nih.gov)
- Small Business Set-Aside
- N/A
- Description
- Pharmacologic Characterization Support Services Sources Sought 4627643 The purpose of this acquisition is to procure commercial support services to aid in the pharmacological characterization of the TNF-alpha synthesis inhibitors that have been generated within the Drug Design & Development Section of the Intramural Research Program of NIA. Support is required to define which specific compounds, among the many dozens of novel agents generated, have appropriate features to effectively provide anti-inflammatory actions in both animal and ex vivo models predictive of human activity. Clinical/preclinical studies indicate that basal inflammatory status increases as a function of normal aging, and development of a mild pro-inflammatory state closely associates with major degenerative diseases in the elderly. Accordingly, levels of brain pro-inflammatory cytokines become elevated with age in rodents and humans, and several regulatory molecules and anti-inflammatory cytokines decline. Microglia cells within the brain, as a source of these pro- and anti-inflammatory molecules, are thereby implicated as the major culprit of this neuro-inflammation. Hence, correcting the overproduction of pro-inflammatory cytokines by microglia may mitigate a broad number of neurodegenerative disorders prevalent in the elderly. Tumor necrosis factor-alpha (TNF-alpha), a vital pro-inflammatory cytokine, is generated and released by microglial cells during their activated M1 (pro-inflammatory) state as part of the innate immune system response to initiate healing following a physiological insult. If elevated TNF- production is not appropriately time-dependently reduced by microglial transition to a M2 (anti-inflammatory) phase, dysregulated TNF-alpha synthesis initiates a self-propagating cycle of unchecked inflammation. The pharmacological inhibition of this cycle may benefit disorders with a neuro-inflammatory component. To achieve this, the Drug Design & Development Section within the Intramural Research Program of NIA has synthesized a broad series of TNF-alpha synthesis inhibitors as both pharmacological probes to understand the role of TNF-alpha in disease processes such as Alzheimer's Disease and Parkinson's Disease, and as drug candidates to treat them. Please see the attached Sources Sought notice for further information. All capability statements are to be sent to the Contract Specialist, Danielle R. Brown, via email at danielle.brown2@nih.gov by Friday, July 7, 2017 at 12PM, EST.
- Web Link
-
FBO.gov Permalink
(https://www.fbo.gov/spg/HHS/NIH/NIDA-01/HHS-NIH-NIDA-SSSA-SS-17-484/listing.html)
- Place of Performance
- Address: 251 Bayview Boulevard, Baltimore, Maryland, 21224, United States
- Zip Code: 21224
- Zip Code: 21224
- Record
- SN04565548-W 20170702/170630235358-967750c633a089887ce50f34f40af52e (fbodaily.com)
- Source
-
FedBizOpps Link to This Notice
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