Todd W Vanderah, PhD

Links

Biography

Dr. Vanderah is a Professor and Head of Pharmacology, College of Medicine, at the University of Arizona. He has worked in the area of Neuropharmacology for over 20 years that has resulted in 170 peer-reviewed publications and continual NIH funding since his appointment and is the author of three Neuroscience Text Books. Dr. Vanderah did his PhD in Pharmacology and Toxicology at the UofA. He did his Post-doctoral Fellowship at the University of Colorado where he learned electrophysiology studying the effects of alcohol on ion channels/G-proteins. He worked for 4.5 years with a small pharmaceutical company, Ferring Inc., where he developed several novel drugs that are commercially available.

Cancer Focus

Dr. Vanderah's research focuses on identifying novel molecular targets on pain pathways in order to attenuate acute and chronic pain while reducing unwanted side effects. Studies include trying to identify the source of metastatic bone cancer pain and treatments that may inhibit such pain. His studies have investigated several novel mechanisms that may drive pain in long-bones of the body due to cancer including a transporter termed system Xc. His studies have investigated novel synthetic cannabinoids that are non-psychotropic but act to inhibit pain and may slow bone loss. Currently, Dr. Vanderah is working with Dr. Chalasani to run a clinical trial with a cannabinoid in advanced metastatic pain patients.

Research Program Role

Cancer Biology Program

Display Name

Todd W Vanderah, PhD

Publications

Peripherally restricted cannabinoid 1 receptor agonist as a novel analgesic in cancer-induced bone pain.

Zhang H, Lund DM, Ciccone HA, Staatz WD, Ibrahim MM, Largent-Milnes TM, Seltzman HH, Spigelman I, Vanderah TW. 2018. Peripherally restricted cannabinoid 1 receptor agonist as a novel analgesic in cancer-induced bone pain. Pain. 159:1814–1823. doi:10.1097/j.pain.0000000000001278.

Long-lasting antinociceptive effects of green light in acute and chronic pain in rats.

Ibrahim MM, Patwardhan A, Gilbraith KB, Moutal A, Yang X, Chew LA, Largent-Milnes T, Malan TP, Vanderah TW, Porreca F, et al. 2017. Long-lasting antinociceptive effects of green light in acute and chronic pain in rats. Pain. 158:347–360. doi:10.1097/j.pain.0000000000000767.

Disease modification of breast cancer-induced bone remodeling by cannabinoid 2 receptor agonists.

Lozano-Ondoua AN, Hanlon KE, Symons-Liguori AM, Largent-Milnes TM, Havelin JJ, Ferland HL, Chandramouli A, Owusu-Ankomah M, Nikolich-Zugich T, Bloom AP, et al. 2013. Disease modification of breast cancer-induced bone remodeling by cannabinoid 2 receptor agonists. J Bone Miner Res. 28:92–107. doi:10.1002/jbmr.1732.

Inhibition of p38-MAPK signaling pathway attenuates breast cancer induced bone pain and disease progression in a murine model of cancer-induced bone pain.

Sukhtankar D, Okun A, Chandramouli A, Nelson MA, Vanderah TW, Cress AE, Porreca F, King T. 2011. Inhibition of p38-MAPK signaling pathway attenuates breast cancer induced bone pain and disease progression in a murine model of cancer-induced bone pain. Mol Pain. 7:81. doi:10.1186/1744-8069-7-81.

CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids.

Ibrahim MM, Porreca F, Lai J, Albrecht PJ, Rice FL, Khodorova A, Davar G, Makriyannis A, Vanderah TW, Mata HP, et al. 2005. CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci U S A. 102:3093–8. doi:10.1073/pnas.0409888102.

Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS.

Ibrahim MM, Deng H, Zvonok A, Cockayne DA, Kwan J, Mata HP, Vanderah TW, Lai J, Porreca F, Makriyannis A, et al. 2003. Activation of CB2 cannabinoid receptors by AM1241 inhibits experimental neuropathic pain: pain inhibition by receptors not present in the CNS. Proc Natl Acad Sci U S A. 100:10529–33. doi:10.1073/pnas.1834309100.

Tonic descending facilitation from the rostral ventromedial medulla mediates opioid-induced abnormal pain and antinociceptive tolerance.

Vanderah TW, Suenaga NM, Ossipov MH, Malan TP, Lai J, Porreca F. 2001. Tonic descending facilitation from the rostral ventromedial medulla mediates opioid-induced abnormal pain and antinociceptive tolerance. J Neurosci. 21:279–86.

Dynorphin promotes abnormal pain and spinal opioid antinociceptive tolerance.

Vanderah TW, Gardell LR, Burgess SE, Ibrahim M, Dogrul A, Zhong CM, Zhang ET, Malan TP, Ossipov MH, Lai J, et al. 2000. Dynorphin promotes abnormal pain and spinal opioid antinociceptive tolerance. J Neurosci. 20:7074–9.