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    Afimkibart

    Other names: RG6631; RO7790121

    Modality: Anti-TL1A monoclonal antibody

    Disease State: Atopic Dermatitis (AD), Inflammatory Bowel Disease (IBD), Rheumatoid Arthritis (RA), and Metabolic Dysfunction-associated Steatohepatitis (MASH)

    Atopic Dermatitis Inflammatory Bowel Disease Rheumatoid Arthritis

    Summary

    Afimkibart is an investigational monoclonal antibody, targeting the tumor necrosis factor-like ligand 1A (TL1A) protein, being evaluated as a potential treatment for inflammatory and fibrotic disease.1

    Clinical Trials

    Atopic dermatitis
    NCT ID Study Phase Enrollment Status Study Title
    NCT07223697 Phase II Recruiting A Long Term Extension Study to Evaluate the Safety and Efficacy of Afimkibart (RO7790121) in Participants With Atopic Dermatitis View details
    NCT06863961 Phase II Active, not recruiting A Study to Assess the Efficacy and Safety of Afimkibart (RO7790121) in Participants With Moderate to Severe Atopic Dermatitis View details

    Proposed Mechanism of Action

    Afimkibart is being investigated in the treatment of inflammatory bowel disease (IBD), atopic dermatitis (AD), rheumatoid arthritis (RA) and metabolic dysfunction-associated steatohepatitis (MASH) as a potential first-in-class agent that targets both inflammatory and fibrotic pathways by inhibiting TL1A, a regulator of immune pathways and cytokine expression, without general immunosuppression.2,3,5,6 TL1A may have a role in the inflammation of AD and inhibiting TL1A may potentially benefit patients who have moderate to severe disease.3,4 TL1A binds its receptor, death receptor 3 (DR3) and amplifies inflammatory response. Early clinical studies with afimkibart demonstrated downregulated tissue T helper 1 (Th1) and T helper 17 (Th17) cells and showed first-in-human impact on fibrotic pathways.5,6

    TL1A (TNF-like ligand 1A) is a key cytokine that amplifies inflammation

    DR3, death receptor 3; GM-CSF, Granulocyte-macrophage colony-stimulating factor; IFN, interferon; IL, interleukin; ILC, innate lymphoid cell; Mo, monocyte; Th, T helper; TL1A, tumor necrosis factor-like ligand 1A; TNF, tumor necrosis factor

    1. Solitano V, Jairath V, Ungaro F, et al. TL1A inhibition for inflammatory bowel disease treatment: from inflammation to fibrosis. Med. 2024;5(5):386-400. doi:10.1016/​j.medj.2024.03.010 2. Migone TS, Zhang J, Luo X, et al. TL1A is a TNF-like ligand for DR3 and TR6/DcR3 and functions as a T cell costimulator. Immunity. 2002;16(3):479-492. doi:10.1016/​s1074-7613(02)00283-2 3. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:583. doi:10.3389/​fimmu.2019.00583 4. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1a therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446. doi:10.1093/​ibd/​izab193 5. Bamias G, Menghini P, Pizarro TT, et al. Targeting TL1A and DR3: the new frontier of anti-cytokine therapy in IBD. Gut. 2025;74(4):652-668. doi:10.1136/​gutjnl-2024-332504 6. Xu WD, Li R, Huang AF. Role of TL1A in inflammatory autoimmune diseases: a comprehensive review. Front Immunol. 2022;13:891328. doi:10.3389/​fimmu.2022.891328 7. Kobayashi T, Siegmund B, Le Berre C, et al. Ulcerative colitis. Nat Rev Dis Primers. 2020;6(1):74. doi:10.1038/​s41572-020-0205-x 8. Pappu BP, Borodovsky A, Zheng TS, et al. TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease. J Exp Med. 2008;205(5):1049-1062. doi:10.1084/​jem.20071364 9. Wang S, Kozai M, Hiraishi M, et al. Roles of tumor necrosis factor-like ligand 1A in γ T-cell activation and psoriasis pathogenesis. Front Immunol. 2024;15:1340467. doi:10.3389/​fimmu.2024.1340467

    TL1A, a member of the tumor necrosis factor (TNF) superfamily, is a cytokine that has been identified as a potential therapeutic target for IBD, AD, RA and MASH.1 It has been shown to amplify proinflammatory pathways and expression is upregulated in inflamed tissues.3-5,7

    • TL1A is expressed mainly on antigen-presenting cells (APCs) under inflammatory conditions and binds to its functional receptor DR3, which is primarily expressed on lymphocytes. The interaction between TL1A and DR3 modulates the immune response.8
    1. Genentech. Our Pipeline: Afimkibart. Genentech. Accessed September 20, 2025. https://www.gene.com/​medical-professionals/​pipeline#afimkibart-anti-tl1a-atopic-dermatitis
    2. A study to assess the efficacy and safety of RO7790121 in participants with moderate to severe atopic dermatitis. ClinicalTrials.gov identifier: NCT06863961. Accessed September 20, 2025. https://clinicaltrials.gov/​study/​NCT06863961
    3. Xu WD, Li R, Huang AF. Role of TL1A in inflammatory autoimmune diseases: a comprehensive review. Front Immunol. 2022;13:891328. doi:10.3389/​fimmu.2022.891328
    4. Hisamoto T, Suga H, Yoshizaki-Ogawa A, Sato S, Yoshizaki A. Increased serum levels of tumor necrosis factor-like ligand 1a in atopic dermatitis. Int J Mol Sci. 2023;24(3):1813. doi:10.3390/​ijms24031813
    5. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1A therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446. doi:10.1093/​ibd/​izab193
    6. Takedatsu H, Michelsen KS, Wei B, et al. TL1A (TNFSF15) regulates the development of chronic colitis by modulating both T-helper 1 and T-helper 17 activation. Gastroenterology. 2008;135(2):552-567. doi:10.1053/​j.gastro.2008.04.037
    7. Moy AP, Murali M, Kroshinsky D, et al. Immunologic overlap of helper T-cell subtypes 17 and 22 in erythrodermic psoriasis and atopic dermatitis. JAMA Dermatol. 2015;151(7):753-760. doi:10.1001/​jamadermatol.2015.2
    8. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:421466. doi:10.3389/​fimmu.2019.00583

    Summary

    Afimkibart is an investigational monoclonal antibody that targets both inflammatory and fibrotic pathways by inhibiting the tumor necrosis factor-like cytokine 1A (TL1A), a cytokine that amplifies inflammatory response and modulates fibrotic pathways in IBD.1

    Clinical Trials

    IBD
    NCT ID Study Phase Enrollment Status Study Title
    NCT05910528 Phase II Active, not recruiting Afimkibart (RO7790121) for the Treatment of Moderate to Severe Active Crohn's Disease View details
    NCT07298421 Phase III Recruiting A Study to Assess the Pharmacokinetics, Effectiveness and Safety of Afimkibart for Induction and Maintenance Therapy in Children With Moderately to Severely Active Crohn's Disease View details
    NCT07158242 Phase III Recruiting A Study to Evaluate the Pharmacokinetics, Safety and Efficacy of Afimkibart (RO7790121) in Children With Moderately to Severely Active Ulcerative Colitis View details
    NCT06819891 Phase III Recruiting A Study to Assess the Efficacy and Safety of Induction Therapy With Afimkibart (RO7790121) in Participants With Moderately to Severely Active Crohn's Disease View details
    NCT06819878 Phase III Recruiting A Study to Assess the Efficacy and Safety of Induction and Maintenance Therapy With Afimkibart (RO7790121) in Participants With Moderately to Severely Active Crohn's Disease View details
    NCT06588855 Phase III Recruiting A Study to Assess the Efficacy and Safety of Induction Therapy With Afimkibart (Also Known as RO7790121) in Participants With Moderately to Severely Active Ulcerative Colitis View details
    NCT06589986 Phase III Active, not recruiting A Study to Assess the Efficacy and Safety of Afimkibart (Also Known as RO7790121) for Induction and Maintenance Therapy in Participants With Moderately to Severely Active Ulcerative Colitis View details

    Proposed Mechanism of Action

    Afimkibart is an investigational molecule being evaluated as an agent designed to target both inflammatory and fibrotic pathways by inhibiting tumor necrosis factor-like cytokine 1A (TL1A), a cytokine that is involved in the pathogenesis of inflammatory bowel disease (IBD). By binding to death domain receptor 3 (DR3), TL1A amplifies the inflammatory response and activates fibrotic pathways in IBD patients. Early clinical studies with afimkibart demonstrated downregulated tissue T helper 1 (Th1) and T helper 17 (Th17) cells and showed first-in-human impact on inflammatory and fibrotic pathways.1

    TL1A in IBD

    DR3= death receptor 3; GM-CSF= granulocyte-macrophage colony-stimulating factor; IFN= interferon; IL= interleukin; ILC= innate lymphoid cell; Mo= monocyte; Th= T helper cell; TL1A= tumour necrosis factor-like ligand 1A; TNF= tumour necrosis factor.

    1. Solitano V, Jairath V, Ungaro F, et al. TL1A inhibition for inflammatory bowel disease treatment: from inflammation to fibrosis. Med. 2024;5(5):386-400. doi:10.1016/​j.medj.2024.03.010 2. Migone TS, Zhang J, Luo X, et al. TL1A is a TNF-like ligand for DR3 and TR6/DcR3 and functions as a T cell costimulator. Immunity. 2002;16(3):479-492. doi:10.1016/​s1074-7613(02)00283-2 3. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:583. doi:10.3389/​fimmu.2019.00583 4. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1a therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446. doi:10.1093/​ibd/​izab193 5. Bamias G, Menghini P, Pizarro TT, et al. Targeting TL1A and DR3: the new frontier of anti-cytokine therapy in IBD. Gut. 2025;74(4):652-668. doi:10.1136/​gutjnl-2024-332504 6. Xu WD, Li R, Huang AF. Role of TL1A in inflammatory autoimmune diseases: a comprehensive review. Front Immunol. 2022;13:891328. doi:10.3389/​fimmu.2022.891328 7. Kobayashi T, Siegmund B, Le Berre C, et al. Ulcerative colitis. Nat Rev Dis Primers. 2020;6(1):74. doi:10.1038/​s41572-020-0205-x 8. Pappu BP, Borodovsky A, Zheng TS, et al. TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease. J Exp Med. 2008;205(5):1049-1062. doi:10.1084/​jem.20071364 9. Wang S, Kozai M, Hiraishi M, et al. Roles of tumor necrosis factor-like ligand 1A in γ T-cell activation and psoriasis pathogenesis. Front Immunol. 2024;15:1340467. doi:10.3389/​fimmu.2024.1340467

    TL1A, a member of the tumor necrosis factor (TNF) superfamily, is a cytokine that is involved in the pathogenesis of IBD and has been identified as a potential therapeutic target. It has been shown to amplify proinflammatory pathways and its expression is upregulated in inflamed intestinal tissues.2-4

    • TL1A is expressed mainly on antigen-presenting cells (APCs) under inflammatory conditions and binds to its functional receptor DR3, which is primarily expressed on lymphocytes. The interaction between TL1A and DR3 modulates the immune response, particularly at the mucosal surfaces.5

    TL1A has been found to play an important role in the development of intestinal fibrosis, as demonstrated in animal studies. Sustained TL1A expression in colitis mouse models leads to small and large intestinal fibrostenosis and treatment with neutralizing TL1A antibody (Ab) reversed colonic fibrosis. Hence, the TL1A-DR3 antagonism may be a therapeutic opportunity for targeting inflammation and fibrosis in IBD and potentially other inflammatory/fibrotic conditions.4

    1. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1A therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446.
    2. Barrett R, Zhang X, Koon HW, et al. Constitutive TL1A expression under colitogenic conditions modulates the severity and location of gut mucosal inflammation and induces fibrostenosis. Am J Pathol. 2012;180(2):636-649.
    3. Takedatsu H, Michelsen KS, Wei B, et al. TL1A (TNFSF15) regulates the development of chronic colitis by modulating both T-helper 1 and T-helper 17 activation. Gastroenterology. 2008;135(2):552-567.
    4. Shih DQ, Zheng L, Zhang X, et al. Inhibition of a novel fibrogenic factor Tl1a reverses established colonic fibrosis. Mucosal Immunol. 2014;7(6):1492-1503.
    5. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:421466.

    Summary

    Afimkibart is an investigational monoclonal antibody, targeting the tumor necrosis factor-like ligand 1A (TL1A) protein, being evaluated as a potential treatment for inflammatory and fibrotic disease.1

    Clinical Trials

    Rheumatoid arthritis
    NCT ID Study Phase Enrollment Status Study Title
    NCT07137598 Phase II Recruiting A Study to Assess the Efficacy and Safety of RO7790121 in Participants With Moderate to Severe Rheumatoid Arthritis Who Have Not Responded to or Who Cannot Tolerate Tumor Necrosis Factor (TNF) and/or Janus Kinase (JAK Inhibitors) View details
    NCT07620392 Phase II Recruiting An Extension Study to Assess Long-Term Safety and Efficacy of Afimkibart in Participants With Rheumatoid Arthritis View details

    Proposed Mechanism of Action

    Afimkibart is being investigated in the treatment of inflammatory bowel disease (IBD), atopic dermatitis (AD), rheumatoid arthritis (RA) and metabolic dysfunction-associated steatohepatitis (MASH) as a potential first-in-class agent designed to target inflammatory and fibrotic pathways by inhibiting TL1A, a regulator of immune pathways and cytokine expression, without general immunosuppression.1-5

    TL1A binds its receptor, death receptor 3 (DR3) and amplifies inflammatory response. Early clinical studies with Afimkibart demonstrated downregulated tissue T helper 1 (Th1) and T helper 17 (Th17) cells and showed first-in-human impact on fibrotic pathways.3,4

    TL1A (TNF-like ligand 1A) is a key cytokine that amplifies inflammation

    DR3, death receptor 3; GM-CSF, Granulocyte-macrophage colony-stimulating factor; IFN, interferon; IL, interleukin; ILC, innate lymphoid cell; Mo, monocyte; Th, T helper; TL1A, tumor necrosis factor-like ligand 1A; TNF, tumor necrosis factor

    1. Solitano V, Jairath V, Ungaro F, et al. TL1A inhibition for inflammatory bowel disease treatment: from inflammation to fibrosis. Med. 2024;5(5):386-400. doi:10.1016/​j.medj.2024.03.010 2. Migone TS, Zhang J, Luo X, et al. TL1A is a TNF-like ligand for DR3 and TR6/DcR3 and functions as a T cell costimulator. Immunity. 2002;16(3):479-492. doi:10.1016/​s1074-7613(02)00283-2 3. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:583. doi:10.3389/​fimmu.2019.00583 4. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1a therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446. doi:10.1093/​ibd/​izab193 5. Bamias G, Menghini P, Pizarro TT, et al. Targeting TL1A and DR3: the new frontier of anti-cytokine therapy in IBD. Gut. 2025;74(4):652-668. doi:10.1136/​gutjnl-2024-332504 6. Xu WD, Li R, Huang AF. Role of TL1A in inflammatory autoimmune diseases: a comprehensive review. Front Immunol. 2022;13:891328. doi:10.3389/​fimmu.2022.891328 7. Kobayashi T, Siegmund B, Le Berre C, et al. Ulcerative colitis. Nat Rev Dis Primers. 2020;6(1):74. doi:10.1038/​s41572-020-0205-x 8. Pappu BP, Borodovsky A, Zheng TS, et al. TL1A-DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease. J Exp Med. 2008;205(5):1049-1062. doi:10.1084/​jem.20071364 9. Wang S, Kozai M, Hiraishi M, et al. Roles of tumor necrosis factor-like ligand 1A in γ T-cell activation and psoriasis pathogenesis. Front Immunol. 2024;15:1340467. doi:10.3389/​fimmu.2024.1340467

    TL1A, a member of the tumor necrosis factor (TNF) superfamily, is a cytokine that has been identified as a potential therapeutic target for IBD, AD, RA and MASH.1 It has been shown to amplify proinflammatory pathways and expression is upregulated in inflamed tissues.3, 5-7

    • TL1A is expressed mainly on antigen-presenting cells (APCs) under inflammatory conditions and binds to its functional receptor DR3, which is primarily expressed on lymphocytes. The interaction between TL1A and DR3 modulates the immune response.8
    1. Genentech. Our Pipeline: Afimkibart. Genentech. Accessed September 20, 2025. https://www.gene.com/​medical-professionals/​pipeline#afimkibart-anti-tl1a-rheumatoid-arthritis
    2. A study to assess the efficacy and safety of RO7790121 in participants with moderate to severe rheumatoid arthritis who have not responded to or who cannot tolerate tumor necrosis factor (TNF) and/or janus kinase (JAK inhibitors). ClinicalTrials.gov identifier: NCT07137598. Accessed August 25, 2025. https://clinicaltrials.gov/​study/​NCT07137598
    3. Hassan-Zahraee M, Ye Z, Xi L, et al. Antitumor necrosis factor-like ligand 1A therapy targets tissue inflammation and fibrosis pathways and reduces gut pathobionts in ulcerative colitis. Inflamm Bowel Dis. 2022;28(3):434-446. doi:10.1093/​ibd/​izab193
    4. Takedatsu H, Michelsen KS, Wei B, et al. TL1A (TNFSF15) regulates the development of chronic colitis by modulating both T-helper 1 and T-helper 17 activation. Gastroenterology. 2008;135(2):552-567.
    5. Xu WD, Li R, Huang AF. Role of TL1A in inflammatory autoimmune diseases: a comprehensive review. Front Immunol. 2022;13:891328. doi:10.3389/​fimmu.2022.891328
    6. Hisamoto T, Suga H, Yoshizaki-Ogawa A, Sato S, Yoshizaki A. Increased serum levels of tumor necrosis factor-like ligand 1a in atopic dermatitis. Int J Mol Sci. 2023;24(3):1813. doi:10.3390/​ijms24031813
    7. Moy AP, Murali M, Kroshinsky D, et al. Immunologic overlap of helper T-cell subtypes 17 and 22 in erythrodermic psoriasis and atopic dermatitis. JAMA Dermatol. 2015;151(7):753-760. doi:10.1001/​jamadermatol.2015.2
    8. Valatas V, Kolios G, Bamias G. TL1A (TNFSF15) and DR3 (TNFRSF25): a co-stimulatory system of cytokines with diverse functions in gut mucosal immunity. Front Immunol. 2019;10:421466. doi:10.3389/​fimmu.2019.00583

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    TOP

    • AD
      Atopic dermatitis

    • APC
      Antigen-presenting cells

    • DR3
      Death receptor 3

    • GM-CSF
      Granulocyte-macrophage colony-stimulating factor

    • IBD
      Inflammatory bowel disease

    • IFN
      Interferon

    • IL
      Interleukin

    • ILC
      Innate lymphoid cell

    • MASH
      Metabolic dysfunction-associated steatohepatitis

    • Mo
      Monocyte

    • RA
      Rheumatoid arthritis

    • Th1
      T helper 1

    • Th17
      T helper 17

    • Th
      T helper

    • TL1A
      Tumor necrosis factor-like ligand 1A

    • TNF
      Tumor necrosis factor

    • Ab
      Antibody

    • APCs
      antigen-presenting cells

    • TCR
      T-cell receptor

    • TL1A
      tumor necrosis factor-like cytokine 1A

    • JAK
      Janus kinase

    +