3-TYP 是一种选择性的 SIRT3 抑制剂，IC₅₀ 值为 16 nM, 比对 SIRT1 和 SIRT2 的选择性强，IC₅₀ 值分别为 88 nM 和 92 nM。

3-TYP is a selective SIRT3 inhibitor, with an IC 50 of 16 nM, more potent over SIRT1 (IC 50 =88 nM), SIRT2 (IC 50 =92 nM).

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SIRT3 16 nM (IC50) SIRT1 88 nM (IC50

3-TYP inhibits melatonin-enhanced SIRT3 activity but does not affect SIRT3 protein expression. 3-TYP pretreatment reverses the protective effects of melatonin on cadmium (Cd)-induced mitochondrial-derived O2 production and autophagic cell death. 3-TYP significantly attenuates melatonin-induced increases in deacetylated-SOD2 expression and SOD2 activity in HepG2 cells exposed to Cd. has not independently confirmed the accuracy of these methods. They are for reference only.

3-TYP (50 mg/kg, i.p.) does not significantly influence the LVEF, LVFS, infarct size, serum LDH levels, apoptosis, and oxidative stress compared with those of the Sham group. Moreover, 3-TYP has little effect on gp91phox, Nrf2, NQO 1, Bax, Bcl-2, Caspase-3, and cleaved Caspase-3 expression levels, compared with the Sham group. 3-TYP significantly decreases SIRT3 activity and increases the acetylation of SOD2 compared with that in the control group, without influencing SIRT3 expression. 3-TYP attenuates the cardioprotective effects of melatonin by decreasing the LVEF and LVFS after 24 hour of reperfusion. 3-TYP also increases the infarct size, serum LDH levels, and apoptotic ratio compared with those in the IR+Mel group. has not independently confirmed the accuracy of these methods. They are for reference only.

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[1]. Pi H, et al. SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin. Autophagy. 2015;11(7):1037-51.
[2]. Zhai M, et al. Melatonin ameliorates myocardial ischemia reperfusion injury through SIRT3-dependent regulation of oxidative stress and apoptosis. J Pineal Res. 2017 Sep;63(2).

In Vitro: DMSO : 125 mg/mL (855.29 mM; Need ultrasonic)Ethanol : 16.67 mg/mL (114.06 mM; Need ultrasonic)H₂O : 1 mg/mL (6.84 mM; ultrasonic and warming and heat to 60°C)