Efficacy of ABT-116, an antagonist of transient receptor potential vanilloid type 1, in providing analgesia for dogs with chemically induced synovitis.
OBJECTIVE
To investigate the ability of ABT-116 (a proprietary antagonist of transient receptor potential vanilloid type 1) administered at 2 doses to attenuate lameness in dogs with experimentally induced urate synovitis.


METHODS
8 purpose-bred mixed-breed dogs.


METHODS
In a 4-way crossover study, dogs orally received each of low-dose ABT-116 treatment (LDA; 10 mg/kg), high-dose ABT-116 treatment (HDA; 30 mg/kg), firocoxib (5 mg/kg), and no treatment (nontreatment) once a day for 2 days, in a randomly assigned order. Synovitis was induced on the second day of each treatment period by intra-articular injection of either stifle joint with sodium urate, alternating between joints for each treatment period, beginning with the left stifle joint. Ground reaction forces, clinical lameness scores, and rectal temperature were assessed before the injection (baseline) and at various points afterward.


RESULTS
Lameness scores at the 2-, 6-, and 12-hour assessment points were higher than baseline scores for HDA and nontreatment, whereas scores at the 2- and 6-hour points were higher than baseline scores for LDA. For firocoxib, there was no difference from baseline scores in lameness scores at any point. Compared with baseline values, peak vertical force and vertical impulse were lower at 2 and 6 hours for HDA and nontreatment and at 2 hours for LDA. No changes in these values were evident for firocoxib. The HDA or LDA resulted in higher rectal temperatures than did treatment with firocoxib or nothing, but those temperatures did not differ among treatments.


CONCLUSIONS
HDA had no apparent effect on sodium urate-induced lameness; LDA did attenuate the lameness but not as completely as firocoxib treatment. High rectal temperature is an adverse effect of oral ABT-116 administration that may be of clinical concern.
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA.
Curtis J
CJ
Cathcart
Spencer A
SA
Johnston
Lisa R
LR
Reynolds
Sami
S
Al-Nadaf
Steven C
SC
Budsberg
D015107:4-Butyrolactone / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000698:Analgesia / Q000662:veterinary; D000818:Animals; D018592:Cross-Over Studies; D052246:Cyclooxygenase 2 Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D004283:Dog Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005260:Female; D007191:Indazoles / Q000627:therapeutic use*; D007270:Injections, Intra-Articular / Q000662:veterinary; D007794:Lameness, Animal / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D010671:Phenylurea Compounds / Q000627:therapeutic use*; D013264:Stifle / Q000473:pathology; D013450:Sulfones / Q000008:administration & dosage / Q000627:therapeutic use*; D013585:Synovitis / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology / Q000662:veterinary*; D050916:TRPV Cation Channels / Q000037:antagonists & inhibitors*; D014527:Uric Acid
C551310:ABT 116; D052246:Cyclooxygenase 2 Inhibitors; D007191:Indazoles; D010671:Phenylurea Compounds; D013450:Sulfones; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D014527:Uric Acid; D015107:4-Butyrolactone; C487384:firocoxib