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.

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

MY33-3 (1 μM; pretreated for 5 min) blocks Ethanol-induced activation of TrkA and ALK in SH-SY5Y cells[1]. MY33-3 (0.1-10 μM; 24 h) limits LPS-induced nitrites production and iNos increases in BV2 microglial cells[2]. Cell Viability Assay[1]Cell Line: SH-SY5Y cells Concentration: 1 μM Incubation Time: Pretreated for 5 min and co-treated for 15 min Result: Decreased the Ethanol-induced activation of TrkA and ALK. None of the treatments significantly changed total TrkA or total ALK protein levels.

MY33-3 (60 mg/kg; p.o. on days 3 and 4) reduces ethanol consumption when comparing day 2 with day 3. MY33-3 reduces preference for the ethanol solution on day 3[1]. MY33-3 (i.p.) reverses the Sevoflurane-induced decrease in the discrimination index and impaired motor learning ability[3]. Animal Model: Male C57BL/6J mice (8-10 weeks of age) are received two-bottle drinking in the dark (DID) procedure using 20% ethanol[1]Dosage: 60 mg/kg Administration: P.o. 1 hour before the drinking session in the DID test on days 3 and 4 Result: Reduced ethanol consumption when comparing day 2 with day 3. Showed a reduced preference for the ethanol solution. Not affected total fluid consumption.