Table 6.

Targeted compounds focused on monocyte–macrophage axis in renal diseases in various stages of clinical trials [17,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55].

Level of Target in the Monocyte–Macrophage Activation in Renal Disease Pathogenesis	Compounds in Clinical Trials
Recruitment of circulating monocytes in blood to injured site in renal parenchyma	CCR2 antagonist (phase III in diabetic kidney disease) [33] CCL2, CCL5, CXCL16 and CCL21 inhibition [33,34,35,36] CCR2, CXCR6, CCR7 and CX3CR1 inhibition [35,36,37,38,39,40] C3aR and C5aR inhibition [41,42,43] SYK inhibition (phase II in IgA Nephropathy) [44]
Monocyte proliferation	CSF1R inhibitor [45]
Inhibition of monocyte to M1 macrophage transition and proliferation of M1 macrophages	JNK inhibitor [46] SYK inhibition (phase II in IgA Nephropathy [44,47]
M1 macrophage to M2 macrophage transition	JAK-STAT inhibitor (phase II in Diabetic kidney disease) [48,49] IL-4R and IL-13R [48,49] Galectin 3 inhibitor (phase IIa in Diabetic kidney disease) [50,51,52]
M2 macrophage to myofibroblast transition	Src inhibitor [53] JAK-STAT inhibitor [54] Smad3 inhibitor [55] Asiatic acid and naringenin [38]

Abbreviations used: CCR—chemokine receptor, CCL—chemokine ligands, CXCL—CXC family of chemokine ligands, C3R and C5R—complement C3 and C5 receptors, SYK—novel spleen tyrosine kinase inhibitors, CSF1R—colony stimulating factor 1 receptor, JNK inhibitor–C-Jun N-terminal kinase inhibitor, JAK-STAT—Janus kinase/signal transducers and activators of transcription, IL—interleukins, SRC inhibitor—SRC family of tyrosine protein kinase inhibitor, Smad3—a family of smad proteins derived from the fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad (mothers against decapentaplegic) proteins to transduce signals.