PrIMe News

PrIMe graduate student identifies gene essential for effective pain treatment in dogs

November 8, 2016
Tramadol is one of the most widely prescribed drugs for treatment of mild to moderate pain in dogs.  However, there is growing evidence that this drug may not work well in some patients because of genetic differences.  Dr. Tania E. Perez-Jimenez (DVM, MS), a graduate student in Dr. Michael Court’s Pharmacogenomics laboratory, has identified a gene that is essential for “turning on” the pain relieving effects of tramadol in dogs.  The gene called CYP2D15 produces an enzyme that converts tramadol into M1.  Tramadol by itself lacks any pain relieving effects and must first be converted into M1 in the liver before it can alleviate pain.  A related gene in humans (CYP2D6) produces a similar enzyme that is essential for forming M1 from tramadol in people.  However, tramadol is ineffective for treating pain in 5 to 10% of people because they have a mutation in CYP2D6 and do not produce sufficient amounts of M1.  Consequently, the next step in the project is to determine whether there are mutations in the canine CYP2D15 gene that could also explain why some dogs do not achieve adequate pain relief from tramadol.   Dr. Perez’s discoveries were recently reported in the journal Drug Metabolism and Disposition (PMID: 27758804), and were funded by a Morris Animal Foundation Training Fellowship and the William R. Jones Endowment at WSU.
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