The chemical composition of Sinningia species has been studied in the last few years. Flavonoids were Regorafenib isolated from S. cardinalis, and ethylcyclohexane derivatives and anthraquinones were identified in S. speciosa. In S. allagophylla, lapachenol, 8-methoxylapachenol, anthraquinones, and naphthoquinones were found. S. aggregata produces essential oil, anthraquinones, and aromatic compounds with a new skeleton named aggregatin A-D. Although the chemical composition of these plants is beginning to be known, few studies have investigated the pharmacological properties of the newly identified compounds. We recently found that an ethanolic extract from S. allagophylla exerted antinociceptive effects, an action related, at least partially, to the presence of 8-methoxylapachenol. Anthraquinones were also found in these species, a class of compounds usually associated with antiinflammatory and antinociceptive activity in other species. These observations prompted us to investigate the possible antinociceptive, antiinflammatory and antipyretic activity of the ethanolic extract obtained from the tuber of S. aggregata. Once the antinociceptive activity of the ESa was identified, we further investigated the activity of the fractions and isolated compounds obtained from the ESa. We identified antinociceptive effects in one of these compounds, aggregatin D, and evaluated its effectiveness against nociception induced by several mediators and ion channels agonists, and nitric oxide production to obtain some indications about its mechanism of action. The present study showed that the ethanolic extract obtained from the tubers of S. aggregata has important antinociceptive activity, in which it blocked the inflammatory phase of overt nociception induced by formalin and mechanical hyperalgesia induced by carrageenan. However, the ESa did not exert an antiinflammatory or antipyretic effect. A new compound identified in this plant, AgD, shared this antinociceptive activity, likely acting at peripheral sites. Additionally, AgD blocked mechanical hyperalgesia induced by BK, TNF-��, IL-1��, CINC-1, PGE2 and dopamine but not forskolin, dbcAMP, capsaicin, cinnamaldehyde, menthol, or acidic saline. The analgesic effect of AgD also did not appear to involve the NO/cGMP/K+ channel pathway. The ESa was effective against inflammatory nociception. However, ESa, at least at the doses tested, does not act similarly to NSAIDs or glucocorticoids, because these drugs effectively inhibit edema formation, neutrophil MLN4924 migration and fever.