ROCK2 interacts with and phosphorylates STAT3, leading to the formation of the JAK2-STAT3 complex and the upregulation of Th17 and Tfh cells.2,4,5
ROCK2 interacts with and phosphorylates STAT3, leading to the formation of the JAK2-STAT3 complex and the upregulation of Th17 and Tfh cells.2,4,5
Decreases activation of STAT3, triggering the significant downregulation of both Th17 and Tfh cells, leading to the downregulation of pro-inflammatory cytokines.2,5
Decreases activation of STAT3, triggering the significant downregulation of both Th17 and Tfh cells, leading to the downregulation of pro-inflammatory cytokines.2,5
Thymic injury induced by high-dose chemotherapy and irradiation during a BMT inhibits the production of Treg cells and allows autoreactive and alloreactive T cells to escape regulation and contribute to chronic inflammation.6,7
Thymic injury induced by high-dose chemotherapy and irradiation during a BMT inhibits the production of Treg cells and allows autoreactive and alloreactive T cells to escape regulation and contribute to chronic inflammation.6,7
Increases phosphorylation of STAT5,
causing the upregulation of Treg cells.4 This has an immunomodulatory effect on STAT3 and STAT5 phosphorylation that reduces inflammation.2,5
Increases phosphorylation of STAT5,
causing the upregulation of Treg cells.4 This has an immunomodulatory effect on STAT3 and STAT5 phosphorylation that reduces inflammation.2,5
Macrophages activate profibrotic mediators, such as LPA and TGF-β, to subsequently activate ROCK2,8,9 which polymerizes G-actin to F-actin.8 This frees the transcription factor MRTF and leads to transcription of profibrotic genes.8
The process results in changes to the cellular structure, increasing tissue stiffness.8
Macrophages activate profibrotic mediators, such as LPA and TGF-β, to subsequently activate ROCK2,8,9 which polymerizes G-actin to F-actin.8 This frees the transcription factor MRTF and leads to transcription of profibrotic genes.8
The process results in changes to the cellular structure, increasing tissue stiffness.8
Prevents the polymerization of G-actin to F-actin as well as MRTF changes to profibrotic gene expression.3
This results in the downregulation of fibrosis, as evidenced by decreased collagen deposition around the bronchioles and the delayed progression of scleroderma in animal cGVHD models.3
Prevents the polymerization of G-actin to F-actin as well as MRTF changes to profibrotic gene expression.3
This results in the downregulation of fibrosis, as evidenced by decreased collagen deposition around the bronchioles and the delayed progression of scleroderma in animal cGVHD models.3
The mechanism of action of belumosudil in cGVHD is not fully understood.
REZUROCK is an innovative treatment designed to restore immune homeostasis and to downregulate the fibrotic processes of cGVHD.1-3