MY33-3 is a powerful and specific inhibitor of receptor protein tyrosine phosphatase (RPTP)β/ζ, demonstrating an IC50 value of approximately 0.1 μM. Moreover, MY33-3 exhibits inhibitory activity against PTP-1B with an IC50 value of about 0.7 μM. Additionally, MY33-3 has been shown to effectively decrease ethanol consumption and alleviate neuroinflammation and cognitive dysfunction induced by Sevoflurane.

PTP1B:0.7 μM (IC50), RPTPβ/ζ:0.1 μM (IC50)

MY33-3, at a concentration of 1 μM with a pretreatment time of 5 minutes, inhibits the ethanol-induced activation of TrkA and ALK in SH-SY5Y cells without altering the overall protein levels of TrkA and ALK. Furthermore, MY33-3, within a concentration range of 0.1-10 μM over 24 hours, reduces LPS-induced nitrite production and the increase of iNOS in BV2 microglial cells. In a cell viability assay conducted on SH-SY5Y cells with a 1 μM concentration of MY33-3 pretreated for 5 minutes and co-treated for 15 minutes, the compound decreased the ethanol-induced activation of TrkA and ALK, indicating no significant effect on the total protein levels of TrkA or ALK.

Administered orally (p.o.) at a dosage of 60 mg/kg on days 3 and 4, MY33-3 notably decreases ethanol consumption in male C57BL/6J mice (8-10 weeks old) undergoing a two-bottle drinking in the dark (DID) procedure with 20% ethanol. This comparison highlights a significant reduction in ethanol intake from day 2 to day 3 and a diminished preference for the ethanol solution by day 3, without impacting the overall fluid consumption. Furthermore, MY33-3 (administered intraperitoneally (i.p.)) counteracts the decline in discrimination index and the deterioration of motor learning abilities induced by Sevoflurane, illustrating its potential in reversing cognitive impairments associated with substance exposure.