Table 1.

Glycolysis inhibitors and their anti-inflammatory activity.

Inhibitor	Intracellular Target	Biological Action	Refs.
BAY-876	GLUTs	↓ CD4+ T cells ↓ macrophages	[103]
CD-5	GLUTs	↓ CD4+ T cells ↓ Th1 and TH17 polarization ↑ Treg differentiation	[104,105]
2-DG	Hexokinase	↓ Macrophages polarization (asthma model and chitin-induced inflammation) ↓ Peritoneal macrophages (adjuvant arthritis model) ↓ IL-6 signaling pathway (bowel disease and rheumatoid arthritis models) ↓ LPS-induced pulmonary inflammation	[33,34,35,42]
WP1122	Hexokinase	↓ Glycolysis (cancer models)	[69,70]
BrPA	Hexokinase	↓ Th17 cells ↓ DCs activation ↑ Treg differentiation (rheumatoid arthritis model)	[102]
PFK15	PFK1	↓ T cells metabolic reprogramming (type 1 diabetes model) ↓ LPS-induced DCs cells ↑ Immunosuppressive T cells (CIA model) ↓ CD45+ cells, chemokines (IBD model)	[77,78,79]
3PO	PFK1	↓ LPS-stimulated activation of human alveolar epithelial cells ↓ Pro-inflammatory cytokines, ROS (sepsis-induced lung injury model) ↓ TLR2-induced NF-κB, STAT3 activation, pro-inflammatory cytokines (rheumatoid arthritis model) ↓ Atherosclerotic macrophages ↓ Synovia inflammation	[84,85,86,87,88]
Koningic acid	GAPDH	↓ LPS-stimulated macrophages ↓ M1 macrophages polarization ↓ Pro-inflammatory cytokines (HIV-infected macrophages)	[107,108]
4-OI	GAPDH	↓ LPS-stimulated macrophages and IL-1β secretion ↓ CD4+ and CD8+ T cells	[71,72,73]
DCA	PDK	↓ CIA-induced arthritis ↓ Sepsis-induced inflammation ↓ Atherosclerosis ↓ Colitis	[93,94,95,96]

↑—upregulation, ↓—downregulation.