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. Author manuscript; available in PMC: 2022 Aug 1.
Published in final edited form as: Free Radic Biol Med. 2021 May 16;171:219–231. doi: 10.1016/j.freeradbiomed.2021.05.023

Table 6:

MC65 Cells

Compound -tet
No treatment 14.2 ± 2.7%
Ferrostatin (10 μM) 77.5 ± 7.2%****
Liproxstatin (1 μM) 97.2 ± 5.9%****
Deferiprone (100 μM) 95.8 ± 2.5%****
MitoQ (10 nM) 39.4 ± 5.1%*
Clorgyline (10 μM) 82.1 ± 1.1%****
968 (5 μM) 64.6 ± 1.8%****
GSK2795039 (10 μM) 98.0 ± 1.3%****
GKT137831 (10 μM) 106.8 ± 16%****
PD146176 (2.5 μM) 91.4 ± 7.1%****
Troglitazone (1 μM) 89.1 ± 5.7%****
Idebenone(1 μM) 77.1 ± 2.1%****
CoCl2 (100 μM) 88.4 ± 2.0%****
LY83583 (1 μM) 80.3 ± 2.4%****
Apomorphine (5 μM) 96.3 ± 24.5%****
BI-6C9 (5 μM) 112.8 ± 13.4%****
Bafilomycin (100 nm) 4.9 ± 6.1%
Scriptaid (250 nm) 64.1 ± 8.3%****
Nullscript (250 nm) 1.7 ± 2.7%
Flt3 inhibitor (1 μM) 101.3 ± 9.5%****

The oxytosis/ferroptosis inhibitors that were effective against glutamate, erastin and RSL3 as shown in Table 1 were tested for their ability to protect human MC65 cells against intracellular Aβ toxicity. Initially, the same inhibitor concentrations that were effective in the HT22 cells were tested. If no protection or toxicity was seen, then a range of concentrations was tested. The most effective concentrations are reported here. The values presented are the average of a minimum of three independent experiments with all treatments done in duplicate.

*

p<0.05;

****

p<0.0001 versus -tet alone.