Eicosatetraynoic Acid is nonspecific inhibitor of cyclooxygenases and lipoxygenases [1].

Cyclooxygenase (COX) is the key enzyme required for the conversion of arachidonic acid to prostaglandins. Two cyclooxygenase isoforms have been identified: COX-1 and COX-2. The COX-1 enzyme is produced constitutively (i.e., gastric mucosa) and COX-2 is inducible (i.e., sites of inflammation). Cyclooxygenase has been involved in different physiological situations and disease processes ranging from inflammation to cancer [2]. Lipoxygenases belong to a family of non-heme and iron-containing enzymes and serve diverse roles as autocrine signals that regulate the function of their parent cells, paracrine signals that regulate the function of nearby cells, and endocrine signals that regulate the function of distant cells [3].

In human platelet, Eicosatetraynoic acid inhibited 12-LO and COX-1 with IC50 values of 4 μM and 8 μM, respectively [1]. Eicosatetraynoic acid acted as a PPAR ligand which activated PPARα and PPARγ chimeras at concentrations of 10 μM [4].

References:
[1] Hammarstrm S.  Selective inhibition of platelet n—8 lipoxygenase by 5, 8, 11-eicosatriynoic acid[J]. Biochimica et Biophysica Acta (BBA)-Lipids and Lipid Metabolism, 1977, 487(3): 517-519.
[2] Dubois R N, Abramson S B, Crofford L, et al.  Cyclooxygenase in biology and disease[J]. The FASEB journal, 1998, 12(12): 1063-1073.
[3] Feussner I, Wasternack C.  The lipoxygenase pathway[J]. Annual review of plant biology, 2002, 53(1): 275-297.
[4] Kliewer S A, Lenhard J M, Willson T M, et al.  A prostaglandin J2 metabolite binds peroxisome proliferator-activated receptor γ and promotes adipocyte differentiation[J]. Cell, 1995, 83(5): 813-819.