Kevin J Gaffney
- Assistant Research Professor, Pharmacology
- Ph.D. Computational and Medicinal Chemistry
- University of Southern California, Los Angeles, California, United States
- Adventures in medicinal chemistry: design and synthesis of small molecule biological modulators
- University of Southern California, Los Angeles, California (2013 - 2017)
My research seeks to combine my Ph.D. work in computational drug design and synthetic chemistry with my post-doctoral work in pharmacology to develop novel GPCR-targeting therapeutics and characterize their biological efficacy to deliver the drugs to patients in need.
No activities entered.
- Soto, M., Gaffney, K. J., & Rodgers, K. E. (2019). Improving the Innate Immune Response in Diabetes by Modifying the Renin Angiotensin System. Frontiers in immunology, 10, 2885.More infoPatients with Type 2 Diabetes Mellitus (T2DM) suffer from a higher incidence and severity of pulmonary infections. This is likely due to immune impairment and structural abnormalities caused by T2DM-induced oxidative stress (OS) and chronic inflammation. Modulation of the Renin Angiotensin System (RAS) through blockade of the actions of angiotensin II (AII), or inducing the protective pathway, has the potential to reduce these pathological pathways. The effects of Angiotensin 1-7 [A(1-7)] and NorLeu-A(1-7) [NorLeu], ligands of the protective RAS, on the innate immune response were evaluated in the mouse model of T2DM. Only NorLeu treatment reduced the structural pathologies in the lung caused by T2DM. A decreased in bactericidal activity and phagocytosis in diabetic animals was also observed; both A(1-7) and NorLeu treatment restored these functions. Myeloid progenitor CFUs were reduced and neutrophil/progenitor OS was increased in saline-treated mice, and was reversed by A(1-7) and NorLeu treatment. These results demonstrate the adverse effects of diabetes on factors that contribute to pulmonary infections and the therapeutic potential of protective RAS peptides. Overall, RAS-modification may be a viable therapeutic target to treat diabetic complications that are not addressed by glucose lowering drugs.
- Gaffney, K. J., Rodgers, K. E., Weinberg, M., & Soto, M. H. (2018). Development of angiotensin II (1-7) analog as an oral therapeutic for the treatment of chemotherapy-induced myelosuppression. Haematologica, haematol.2018.193771.
- Gaffney, K. J. (2015). Molecular characterization of the boron adducts of the proteasome inhibitor bortezomib with epigallocatechin-3-gallate and related polyphenols.. Organic & biomolecular chemistry.
- Gaffney, K. J. (2014). Abstract 1811: Evaluation of anti-CXCR2 small molecule inhibitors as novel chemotherapy targeting the Interleukin-8 pathway in colorectal cancer. Cancer Research.
- Gaffney, K. J. (2012). Inhibition of the function of class IIa HDACs by blocking their interaction with MEF2. Nucleic Acids Research.
- Gaffney, K. J. (2012). Preferential killing of triple-negative breast cancer cells in vitro and in vivo when pharmacological aggravators of endoplasmic reticulum stress are combined with autophagy inhibitors.. Cancer letters.
- Gaffney, K. J. (2011). Enhancement of photodynamic therapy by 2,5-dimethyl celecoxib, a non-cyclooxygenase-2 inhibitor analog of celecoxib. Cancer Letters.
- Gaffney, K. J. (2010). Antiangiogenic Activities of 2,5-Dimethyl-Celecoxib on the Tumor Vasculature. Molecular Cancer Therapeutics.
- Gaffney, K. J. (2010). Cytotoxic effects of celecoxib on Raji lymphoma cells correlate with aggravated endoplasmic reticulum stress but not with inhibition of cyclooxygenase-2. Leukemia Research.
- Gaffney, K. J. (2009). Enhanced killing of chemo-resistant breast cancer cells via controlled aggravation of ER stress. Cancer Letters.
- Gaffney, K. J. (2009). Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. Blood.
- Gaffney, K. J. (2008). COX-2 inhibition is neither necessary nor sufficient for celecoxib to suppress tumor cell proliferation and focus formation in vitro. Molecular Cancer.