The cation channel TRPA1 plays an important role in the perception of pain. One of its major functions is to act as a sensor for irritating and potentially hazardous electrophilic substances. TRPA1 involvement has been demonstrated for several diseases. However, for TRPA1 in particular, species differences are pronounced and limit translational research. Therefore, a human TRPA1-specific pain model was established. Our own previous study used carvacrol as TRPA1-agonist. While there is no doubt about TRPA1 activation, the required concentration was high, and a specific antagonist only allowed for a partial (31%) inhibition (Schwarz et al., 2017). JT010 is the most potent published and commercially available agonist, a half-maximal activation in the nanomolar range was reported (Takaya et al., 2015). Using this substance and the so far most potent available antagonist A-967079 we established the first TRPA1-specific pain model. With approval of the ethics committee, 16 subjects were tested in two sessions in a double-blind manner. The first session introduced to the experimental paradigm and contained an in injection of phosphate buffered synthetic interstitial fluid, without addition as control and with capsaicin as a painful reference. Intracutaneous injections into the volar forearm were rated every five seconds. In a second session, multiple concentrations of JT010 with and without antagonist were applied in a double-blind manner with a pre-randomized sequence. JT010 caused a higher pain rating than control injections (p < 0.001, t-test). Pain ratings peaked after 30 s and fully subsided in less than five minutes. The JT010-induced pain was concentration-dependently inhibited by the TRPA1 antagonist, almost complete inhibition (98%) could be achieved. This specific model provides a new tool to validate new drug candidates with respect to their efficacy in humans.