Table 1.

Overview of proposed molecular targets or mechanisms of action for CA. AhR—aryl hydrocarbon receptor; CA—cinnabarinic acid; ca.—circa (about); IC₅₀—half-maximal inhibitory concentration; IDO—indoleamine-2,3-dioxygenase; IL22—interleukin 22; K_i—the inhibitor constant; mGlu4—metabotropic glutamate receptor type 4; ROS—reactive oxygen species.

Molecular Target/Mechanism	CA Activity (Summary of Data Found in References)	References
IDO inhibition	IC50 ≈ 2 μM	[77]
	Ki value at 326 nM IC50 was equal to 0.46 μM	[76]
mGlu4 receptor orthosteric agonist	100 μM CA increases [3H]Ins5 formation by ca. 35% (it is 5× less efficacious than the full mGlu4 agonist ACPT-I); CA binds within the glutamate-binding pocket.	[74]
AhR agonist; production of IL22	CA increases (1 μM) the production of IL22 in human and mouse CD4+ T cells through AhR (the blocking of this receptor prevents the IL22 increase).	[78]
Inhibition of mitochondrial respiration	Complete inhibition at 5 μM; 0.5 μM of CA leads to 50% inhibition of state III respiration.	[84]
	CA is at least 20× more efficient at inhibition than 3-hydroxyanthranilic acid.	[82]
ROS generation	CA brings about the rapid induction of ROS generation (ca. 15 min, with return to the control level after 4 h).	[85]
Apoptosis	Induction: CA holds at least 10× higher apoptosis-inducing properties when compared with 3-hydroxyanthranilic acid. The caspase-3 activity is upregulated in the thymocytes within 6 h after simulation with 30 μM of CA.	[85]
	Antiapoptotic properties: CA alleviates caspase-3 or caspase-3/7 upregulation in ethanol-treated hepatocytes/liver lysates. No direct effect of CA itself is indicated.	[86,87]