Table 1.

Compounds targeting ER stress signaling and used in different experimental settings.

Disorder	Chemical compound	UPR branch/target	Effects	References
ALS	Sephin1	Inhibition of stress-induced phosphatase p-eIF2α is increased	Neuroprotection	Das et al., 2015
Excitotoxicity Brain ischemia	Salubrinal	Inhibits GADD34 p-eIF2α increased	Neuroprotection	Sokka et al., 2007; Anuncibay-Soto et al., 2016
PD	Salubrinal	p-eIF2α increased	Neuroprotection in α.synuclein mouse model	Colla et al., 2012
Drug abuse	ISRIB	Increase in the eIF2B guanine nucletide exchange factor	Increase p-eIF2α translation and Induction of LTP by cocaine	Placzek et al., 2016
Prion disease	GSK2606414	PERK inhibitor p-eIF2α reduced	Increase in synaptic proteins and reduced neurodegeneration	Moreno et al., 2013
Inflammation arthritis	4μ8C	IRE1 pathway/ inhibits XBP-1 splicing	reduced cytokines improvement of model of rheumatoid arthritis	Qiu et al., 2013
Multiple myelom	MKC-3946	inhibits XBP-1 splicing	Growth inhibition	Mimura et al., 2012
Pancreatic cancer cell	STF-083010	IRE1 inhibition	Growth retardation
Tumor cells	Irestin	IRE1-RNase inhibitor, blocks XBP1 effects	Tumor cell survival reduced
Hepatocellular carcinoma	GSK2656157 or 4μ8C +oprozomib	PERK inhibitor IRE inhibitor Proteasome inhibitor	Antitumor effects	Vandewynckel et al., 2016
Cultured cells	Compound 147	ATF6 activators	Reduced secretion of misfolded protein protein	Plate et al., 2016b
Osteosarcoma cells	Ceapins	ATF6 inhibitor	Sensitizes cells to ER stress	Gallagher et al., 2016

Summary of small molecules and compounds used to experimentally address ER stress pathways in different disorders. The list gives a glimpse into reported activities in this rapidly progressing field. For more details please see the main text.