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5. OATP1B2 deficiency protects against paclitaxel-induced neurotoxicity

Author

Leblanc, A.F. (Alix F.), Sprowl, J.A. (Jason), Alberti, A. (Alfredo), Chiorazzi, A. (Alessia), David Arnold, W. (W.), Gibson, A.A., Hong, K.W. (Kristen W.), Pioso, M.S. (Marissa S.), Chen, M. (Mingqing), Huang, K.M. (Kevin M.), Chodisetty, V. (Vamsi), Costa, O. (Olivia), Florea, T. (Tatiana), Bruijn, P.J. (Peter) de, Mathijssen, A.H.J. (Ron), Reinbolt, R.E. (Raquel E.), Lustberg, M.B. (Maryam B.), Sucheston-Campbell, L.E. (Lara E.), Cavaletti, G. (Guido), Sparreboom, A. (Alex), Hu, S. (Shuiying), Leblanc, A.F. (Alix F.), Sprowl, J.A. (Jason), Alberti, A. (Alfredo), Chiorazzi, A. (Alessia), David Arnold, W. (W.), Gibson, A.A., Hong, K.W. (Kristen W.), Pioso, M.S. (Marissa S.), Chen, M. (Mingqing), Huang, K.M. (Kevin M.), Chodisetty, V. (Vamsi), Costa, O. (Olivia), Florea, T. (Tatiana), Bruijn, P.J. (Peter) de, Mathijssen, A.H.J. (Ron), Reinbolt, R.E. (Raquel E.), Lustberg, M.B. (Maryam B.), Sucheston-Campbell, L.E. (Lara E.), Cavaletti, G. (Guido), Sparreboom, A. (Alex), and Hu, S. (Shuiying)

Abstract

Paclitaxel is among the most widely used anticancer drugs and is known to cause a dose-limiting peripheral neurotoxicity, the initiating mechanisms of which remain unknown. Here, we identified the murine solute carrier organic anion–transporting polypeptide B2 (OATP1B2) as a mediator of paclitaxel-induced neurotoxicity. Additionally, using established tests to assess acute and chronic paclitaxel-induced neurotoxicity, we found that genetic or pharmacologic knockout of OATP1B2 protected mice from mechanically induced allodynia, thermal hyperalgesia, and changes in digital maximal action potential amplitudes. The function of this transport system was inhibited by the tyrosine kinase inhibitor nilotinib through a noncompetitive mechanism, without compromising the anticancer properties of paclitaxel. Collectively, our findings reveal a pathway that explains the fundamental basis of paclitaxel-induced neurotoxicity, with potential implications for its therapeutic management.

Published
2018
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6. Open-label trial of ranolazine for the treatment of paramyotonia congenita.

Author

Lorusso, Samantha, Kline, David, Bartlett, Amy, Freimer, Miriam, Agriesti, Julie, Hawash, Ahmed A., Rich, Mark M., Kissel, John T., and David Arnold, W.

Subjects
COMPARATIVE studies, ELECTROMYOGRAPHY, GRIP strength, RESEARCH methodology, MEDICAL cooperation, MYOTONIA, PAIN, RESEARCH, RESEARCH funding, STIFF-person syndrome, EVALUATION research, SEVERITY of illness index, SODIUM channel blockers, MUSCLE weakness, DISEASE complications
Abstract

Introduction: Paramyotonia congenita (PMC) is a nondystrophic myotonic disorder that is believed to be caused by a defect in Nav 1.4 sodium channel inactivation. Ranolazine, which acts by enhancing slow inactivation of sodium channels, has been proposed as a therapeutic option, but in vivo studies are lacking.Methods: We conducted an open-label, single-center trial of ranolazine to evaluate efficacy and tolerability in patients with PMC. Subjective symptoms of stiffness, weakness, and pain as well as clinical and electrical myotonia were evaluated. Baseline measures were compared with those after 4 weeks of treatment with ranolazine.Results: Ranolazine was tolerated well without any serious adverse events. Both subjective symptoms and clinical myotonia were significantly improved. Duration of myotonia was reduced according to electromyography, but this change was not statistically significant in all tested muscles.Discussion: Our findings support the use of ranolazine as a treatment for myotonia in PMC and suggest that a randomized, placebo-controlled trial is warranted. Muscle Nerve 59:240-243, 2019. [ABSTRACT FROM AUTHOR]

Published
2019
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7. Electrophysiological biomarkers in spinal muscular atrophy: proof of concept

Author

David Arnold, W., primary, Porensky, Paul N., additional, McGovern, Vicki L., additional, Iyer, Chitra C., additional, Duque, Sandra, additional, Li, Xiaobai, additional, Meyer, Kathrin, additional, Schmelzer, Leah, additional, Kaspar, Brian K., additional, Kolb, Stephen J., additional, Kissel, John T., additional, and Burghes, Arthur H. M., additional

Published
2013
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