(A) Box plots of triethylamine (TEA) thresholds. The addition of Timberol® does not significantly alter the TEA threshold. (B) Scatterplots of individual thresholds with TEA.

<p>(A) Box plots of triethylamine (TEA) thresholds. The addition of Timberol® does not significantly alter the TEA threshold. (B) Scatterplots of individual thresholds with TEA.</p

Blocking effect of Timberol® is exclusively mediated by hTAAR5.

<p>Each response was normalized to corresponding agonist alone. Left: Concentration-response curves (n = 3) of (A) azelaic acid and MOR42-3 and (B) nonanoic acid and hOR51E1. Right: Blocking effects (n = 3) of Timberol® (30 μM) on (A) MOR42-3-mediated responses to azelaic acid and (B) hOR51E-mediated responses to nonanoic acid. No significant blocking effects were observed. Gray bars represent the blocking effect of Timberol® (30 μM) on hTAAR5-mediated responses to TMA in a concentration close to calculated EC₅₀.</p

(A) Box plots of TMA thresholds. In the presence of Timberol®, the threshold of TMA was shifted to a higher concentration compared to TMA alone or in the presence of Ambrocenide® and Mugetanol.* p<0.05. (B) Scatterplots of individual thresholds with TMA.

<p>(A) Box plots of TMA thresholds. In the presence of Timberol®, the threshold of TMA was shifted to a higher concentration compared to TMA alone or in the presence of Ambrocenide® and Mugetanol.* p<0.05. (B) Scatterplots of individual thresholds with TMA.</p

Blocking effect of Timberol® is mediated by hTAAR5.

<p>Timberol® (100 μM) was either applied alone (normalized to unstimulated control) or in a mixture with 10 μM forskolin (normalized to forskolin alone) (n = 3–6). Timberol® did not affect measured luciferase activity (p>0.05).</p