Okadaic acid ammonium salt, a marine toxin, serves as an inhibitor of protein phosphatases (PP), displaying a higher affinity for PP2A (IC50 = 0.1-0.3 nM) alongside inhibitory effects on PP1 (IC50 = 15-50 nM), PP3 (IC50 = 3.7-4 nM), PP4 (IC50 = 0.1 nM), and PP5 (IC50 = 3.5 nM), but does not affect PP2C. By inhibiting PPs, this compound promotes protein phosphorylation, acts as a tumor promoter, and is involved in inducing tau phosphorylation.

PP1:15-50 nM (IC50), PP4:0.1 nM (IC50), PP3:3.7-4 nM (IC50), PP2B:4000 nM (IC50), PP5:3.5 nM (IC50), PP2A:0.1-0.3 nM (IC50), PP7:＞1000 nM (IC50)

Okadaic acid ammonium salt at concentrations ranging from 0-100 nM and exposure times of either 24 or 48 hours has been shown to inhibit the proliferation of AGS, MNK-45, and Caco 2 cell lines[3]. Moreover, at a specific concentration of 10 nM and an incubation period of 8 hours, this compound enhances Drp1 phosphorylation and mitochondrial fission in rat cortical neurons[4]. These findings are supported by a Cell Proliferation Assay conducted on the aforementioned cell lines, with the results clearly indicating a suppression in their proliferation rates under the specified conditions[3].

When administered unilaterally to the lateral amygdala in female wild-type C57BL/6 mice aged 6 to 8 months, okadaic acid ammonium salt at a dosage of 100 μM induces Tau phosphorylation and protein aggregation in anatomically distinct regions of the brain 24 hours after injection.