Description
AP39 is a triphenylphosphonium derivatised anethole dithiolethione and mitochondria-targeting hydrogen sulfide (H 2 S) donor. AP39 increases intracellular H 2 S levels. AP39 exerts cytoprotective effects and maintains mitochondrial DNA integrity under oxidative stress conditions. AP39 protects against myocardial reperfusion injury in mice model and has the potential for Alzheimer's disease research. In VitroAP39 (25,100 nM; for 24 h) results in increase in cell viability in APP/PS1 neurons and has no effect on cell viability in WT neurons. AP39 (100 nM) increases the levels of OPA1 and Mfn1 but not Mfn2. Moreover, AP39 decreases the levels of Fis1 but not Drp1. AP39 (25-250 nM; 2 h) induces a concentration-dependent increase in H 2 S generation and in the fluorescence of the H 2 S-detecting dye AzMC. AP39 (100 nM) significantly increases the basal respiratory rate and the OCR-linked maximal respiratory capacity of the APP/PS1 neurons. AP39 significantly increases the ATP production in WT and APP/PS1 neurons. AP39 significantly protects against mtDNA damage in APP/PS1 neurons by partially restoring mtDNA integrity. AP39 consists of a mitochondria-targeting motif, triphenylphosphonium (TPP + ), coupled to a H 2 S-donating moiety (dithiolethione) by an aliphatic linker.\nAP39 (100 nM) reduces intracellular oxidative stress and in the meantime it consequently sustaines the cell viability, mitochondrial respiration and mitochondrial DNA integrity. These effects tend to be stimulatory at lower concentrations (30 and 100 nM), but tend to diminish or convert into inhibitory effects at a higher concentration (300 nM). MCE has not independently confirmed the accuracy of these methods. They are for reference only.In VivoAP39 (100 nM/kg/day; ip; for 6 weeks) ameliorates the learning and memory deficits of APP/PS1 mice. AP39 (25-250 nM/kg/day; ip; for 6 weeks) induces a dose-dependent increase in H 2 S generation in the cortex and hippocampus of WT and APP/PS1 mice. AP39 (0.01, 0.1, 1 µmol/kg; iv; bolus 10 min before reperfusion) dose‐dependently reduces infarct size anaesthetized by thiobutabarbital (200 mg/kg, i.p) in male Sprague Dawley rats, 300-350 g (9-11 weeks). MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: 12-month-old WT or APP/PS1 mice Dosage: 100 nM/kg Administration: IP; daily; for 6 weeks Result: Reversed the spatial learning and memory deficits of the aged AD model mice. Alleviated brain atrophy and ventricle asymmetryand inhibited Aβ plaque deposition in the brains in AD model mice.Form:Solid