Table 2.

Drugs/approaches targeting STAT3 activation in GB.

Drug/Approach	Target	STAT3 Inhibition	GB Effect	Reference
Sorafenib	JAK1/2	Upstream kinase inhibition	Reduce cell proliferation, increase apoptosis of GB cells	[18,19]
AG490	JAK2	Upstream kinase inhibition	Decrease migration and angiogenesis of GB cells	[18,19]
G6	JAK2	Upstream kinase inhibition	Increase apoptosis, reduces invasion	[64]
G5-7	JAK2	Upstream kinase inhibition	Reduce cell growth, decreases angiogenesis	[18,19]
SAR317461	JAK2	Upstream kinase inhibition	Induces autophagy	[65]
WP1066	JAK2	Upstream kinase inhibition	Induction of cytokines release (IL-2, IL-4, IL-12, and IL-15) that stimulate T cell effector function to overcome immunosuppression	[66]
Oleanolic acid	STAT3	Blocks STAT3 phosphorylation	Suppresses the M2 polarization of TAMs by reducing IL-10 secretion	[67]
Embelin	STAT3	Blocks STAT3 phosphorylation by increasing SHP2 activity	Limits IL-6/STAT3 activation and the Th17 immune response in GBs	[68]
Quercetin	STAT3	Blocks STAT3 phosphorylation	Inhibitor of the IL-6/STAT3 signaling pathway in GB cells	[69]
CpG oligodeoxynucleotides (ODN)containing conjugates of STAT3 inhibitors with synthetic TLR9 agonists	STAT3	Block of STAT3 phosphorylation	Reduce the tolerogenic effects of TME in vivo	[70,71]