[7] The systemic administration of acromelic acid A in rats results in selective loss of interneurons in the lower spinal cord, without causing neuronal damage in the hippocampus and other regions.

[6] Comparative studies reveal acromelic acid B, an isoform of A, to exhibit reduced allodynia effects in mice models.

[6] Conversely, limited information exists regarding ACROs C, D, and E, though their analogous structure suggests similar functionalities to varying extents.

Further research into these compounds is needed, but not without challenges; the synthesis of acromelic acid A presents difficulties for large-scale production required for comprehensive biological studies.

One way to do this, as outlined by Katsuhiro Konno et al. (1986), initiates with the successive protection of imino and carboxyl groups of L-alpha-kainic acid, followed by a reduction and silylation.

[12] The yield of this elaborated synthesis is notably low, as expected due to the numerous synthetic steps, which in turn also hinders large-scale biological studies on acromelic acid A.

[14] The construction of the pyridone ring is achieved from a catechol through an oxidative cleavage recyclization strategy, akin to the previously described method.

[13] Acromelic acids A and B were synthesized from 2,6-dichloropyridine, with the pyrrolidine ring constructed via Ni-catalyzed asymmetric conjugate addition, followed by intramolecular reductive amination.

[15] However, over the years, a new type of non-NMDA receptor was thought to be the target of acromelic acid A, as the observed effects couldn't completely be explained by AMPA binding.

Furthermore, at a higher dose of 500 ng/kg, injection of acromelic acid A induced strong spontaneous agitation, scratching, jumping and  tonic  convulsion  and  caused  death  within  15 min.

However, after accidental ingestion of Clitocybe acromelalga, violent pain and marked reddish edema in hands and feet were observed after several days and continued for a month.