Pain is the primary reason people seek medical care, with chronic pain affecting ~ 20% of people in the United States. However, many existing analgesics are ineffective in treating chronic pain, while others have undesirable side effects. In this study, we used a sensitized thermal place aversion assay in larval zebrafish to screen a small molecule library to identify potential novel analgesics. From this behavioral screen, we discovered a small molecule we termed Analgesic Screen 1 (AS1), which surprisingly elicited attraction to noxious heat. AS1 was similarly able to reverse the negative hedonic valence of other aversive stimuli, eliciting attraction to both a painful chemical irritant as well as non-painful dark environments. Interestingly, AS1 did not appear to be inherently rewarding, and targeting molecular pathways canonically associated with analgesia neither replicated nor reversed the effects of AS1. A neuronal imaging assay using the neural activity marker phosphorylated-ERK revealed that distinct clusters of dopaminergic neurons, as well as forebrain regions located in the teleost equivalent of the basal ganglia, were highly upregulated in the specific context of AS1 and aversive heat. Through a combination of behavioral assays and pharmacological manipulation of dopamine circuitry, we determined that AS1 acts via D1 dopamine receptor pathways to elicit attraction to noxious stimuli. Together, our results suggest that AS1 relieves an aversion-imposed “brake” on dopamine release, and that this unique mechanism may provide valuable insight into the development of new valence-targeting analgesic drugs. Funded by NINDS grant #1R21NS096635, NIDCR grant #1R01NS115747-01A1, NIDCR grant #T90DE021984.