MY33-3 is a potent and selective inhibitor of receptor protein tyrosine phosphatase (RPTP)β/ζ , with an IC 50 of ~0.1 μM. MY33-3 also inhibits PTP-1B ( IC 50 ~0.7 μM). MY33-3 can reduce ethanol consumption and alleviate Sevoflurane-induced neuroinflammation and cognitive dysfunction In Vitro MY33-3 (1 μM; pretreated for 5 min) blocks Ethanol-induced activation of TrkA and ALK in SH-SY5Y cells. MY33-3 (0.1-10 μM; 24 h) limits LPS-induced nitrites production and iNos increases in BV2 microglial cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell 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. In Vivo 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 . MY33-3 (i.p.) reverses the Sevoflurane-induced decrease in the discrimination index and impaired motor learning ability. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male C57BL/6J mice (8-10 weeks of age) are received two-bottle drinking in the dark (DID) procedure using 20% ethanol 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. Form:Solid IC50& Target:IC50: 0.1 μM (RPTPβ/ζ), 0.7 μM (PTP-1B)