REZUROCK targets both the inflammatory and the fibrotic processes of cGVHD1-3

REZUROCK IS AN IMMUNOMODULATOR THAT SELECTIVELY INHIBITS THE ROCK2 PATHWAY1-3

MECHANISMS OF CHRONIC INFLAMMATION IN cGVHD2,4-7

A depiction of inflamed tissue with an overabundance of blue cells

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

A depiction of inflamed tissue with few pink cells

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

SELECTIVE INHIBITION OF ROCK2 BY REZUROCK2,4,5

A depiction of less-inflamed tissue with fewer blue cells

Decreases activation of STAT3, triggering the significant downregulation of both Th17 and Tfh cells, leading to the downregulation of pro-inflammatory cytokines.2,5

A depiction of less-inflamed tissue with an abundance of pink cells

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

MECHANISMS OF FIBROSIS IN cGVHD8,9

A depiction of tissue with an overabundance of collagen deposits

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

 

SELECTIVE INHIBITION OF ROCK2 BY REZUROCK3,8

A depiction of fewer collagen deposits

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

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    MECHANISMS OF CHRONIC INFLAMMATION IN cGVHD2,4-7

    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

    a depiction of inflamed tissue with an  overabundance of blue cells and an arrow  pointing up indicating an increase in proinflammatory cells
    Blue icon with white text that states pro-inflammatory cells
    White arrow pointing up icon

    SELECTIVE INHIBITION OF ROCK2 BY REZUROCK2,4,5

    Decreases activation of STAT3, triggering the significant downregulation of both Th17 and Tfh cells, leading to the downregulation of pro-inflammatory cytokines.2,5

    A depiction of inflamed tissue with an overabundance of blue cells
    Blue icon with white text that states pro-inflammatory cells
    White arrow pointing down icon

    MECHANISMS OF CHRONIC INFLAMMATION IN cGVHD2,4-7

    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

    A depiction of inflamed tissue with few pink cells
    Blue icon with white text that states treg cells
    White arrow pointing down icon

    SELECTIVE INHIBITION OF ROCK2 BY REZUROCK2,4,5

    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

    A depiction of less-inflamed tissue with an abundance of pink cells
    Blue icon with white text that states treg cells
    White arrow pointing up icon

    MECHANISMS OF FIBROSIS IN cGVHD8,9

    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

    A depiction of tissue with an overabundance of collagen deposits
    Blue icon with white text that states fibrotic processes
    White arrow pointing up icon

    SELECTIVE INHIBITION OF ROCK2 BY REZUROCK3,8

    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

    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

    A depiction of fewer collagen deposits
    Blue icon with white text that states fibrotic processes
    White arrow pointing down icon

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

See the results with a DUAL INHIBITOR OF
INFLAMMATION AND FIBROSIS.1-3

BMT, bone marrow transplant; cGVHD, chronic graft-versus-host disease; JAK2, Janus kinase 2; LPA, lysophosphatidic acid; MOA, mechanism of action; MRTF, myocardin-related transcription factor; ROCK2, rho-associated coiled-coil–containing protein kinase-2; STAT3, signal transducer and activator of transcription factor 3; STAT5, signal transducer and activator of transcription factor 5; Tfh, follicular helper T [cell]; TGF-β, transforming growth factor-beta; Th17, type 17 helper T [cell]; Treg, regulatory T [cell].

References: 1. REZUROCK. Package insert. Kadmon Pharmaceuticals, LLC. 2. Zanin-Zhorov A, Weiss JM, Nyuydzefe MS, et al. Selective oral ROCK2 inhibitor down-regulates IL-21 and IL-17 secretion in human T cells via STAT3-dependent mechanism. Proc Natl Acad Sci USA. 2014;111(47):16814-16819. doi:10.1073/pnas.1414189111 3. Flynn R, Paz K, Du J, et al. Targeted Rho-associated kinase 2 inhibition suppresses murine and human chronic GVHD through a Stat3-dependent mechanism. Blood. 2016;127(17):2144-2154. doi:10.1182/blood-2015-10-678706 4. Chen W, Nyuydzefe MS, Weiss JM, Zhang J, Waksal SD, Zanin-Zhorov A. ROCK2, but not ROCK1 interacts with phosphorylated STAT3 and co-occupies TH17/TFH gene promoters in TH17-activated human T cells. Sci Rep. 2018;8(1):16636. doi:10.1038/s41598-018-35109-9 5. Weiss JM, Chen W, Nyuydzefe MS, et al. ROCK2 signaling is required to induce a subset of T follicular helper cells through opposing effects on STATs in autoimmune settings. Sci Signal. 2016;9(437):ra73. doi:10.1126/scisignal.aad8953 6. Zeiser R, Blazar BR. Pathophysiology of chronic graft-versus-host disease and therapeutic targets. N Engl J Med. 2017;377(26):2565-2579. doi:10.1056/NEJMra1703472 7. Matsuoka K-I, Kim HT, McDonough S, et al. Altered regulatory T cell homeostasis in patients with CD4+ lymphopenia following allogeneic hematopoietic stem cell transplantation. J Clin Invest. 2010;120(5):1479-1493. doi:10.1172/JC141072 8. Riches DWH, Backos DS, Redente EF. ROCK and Rho: promising therapeutic targets to ameliorate pulmonary fibrosis. Am J Pathol. 2015;185(4):909-912. doi:10.1016/j.ajpath.2015.01.005 9. Knipe RS, Tager AM, Liao JK. The Rho kinases: critical mediators of multiple profibrotic processes and rational targets for new therapies for pulmonary fibrosis. Pharmacol Rev. 2015;67(1):103-117. doi:10.1124/pr.114.009381

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