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Graphic with the text 'Thymoglobulin® [Anti‑thymocyte Globulin (Rabbit)'] with antibody symbol icon on a blue background with kidney line patterns behind a man and a small disclaimer 'Not an actual patient'.

About Thymoglobulin® [Anti-thymocyte Globulin (Rabbit)]

Thymoglobulin May Suppress the Immune Response through Multiple Pathways1

The mechanism of action by which Thymoglobulin suppresses the immune response is not fully understood, but may include1:

  • T-cell clearance from the circulation
  • Modulation of T-cell activation, homing, and cytotoxic activities

See How it Works

View a full depiction of the mechanisms of acute rejection and how Thymoglobulin may help with prevention or treatment.

Click here for full Prescribing Information.

Thymoglobulin includes antibodies against T-cell markers such as CD2, CD3, CD4, CD8, CD11a, CD18, CD25, CD44, CD45, HLA-DR, HLA Class I heavy chains, and β2 micro-globulin.1

Graphic showing four blue spheres representing T cells from left to right. Each T cell has differently colored Y-shaped antibodies attached. The first T cell has CD2, HLA class I heavy chain, and β2-micro-globulin attached. The second T cell has HLA-DR, CD44, and CD8 attached, with “Thymoglobulin” written above it. The third T cell has CD4, CD45, and CD25 attached. The fourth T cell has CD11a, CD18, and CD3 attached.

Potential Mechanisms of Action of Thymoglobulin

T-Cell Clearance From the Circulation

Thymoglobulin may deplete T cells through 3 different mechanisms:

  • Apoptosis via activation-induced cell death2-4
  • Antibody-dependent cell-mediated cytotoxicity4
  • Complement-dependent cytotoxicity4

The clinical significance of these mechanisms is unknown.

Graphic showing three immune cell killing mechanisms from left to right. On the left, a T cell labeled “Thymoglobulin” interacts with another via FasL and Fas, causing apoptosis via activation-induced cell death. In the center, an activated NK cell kills a target coated with antibodies in antibody-dependent cell-mediated cytotoxicity. On the right, antibodies on a target activate C1q and the complement system, while an effector cell directly kills the target, labeled complement-dependent cytotoxicity.

Modulation of T-Cell Activation, Homing, and Cytotoxic Activities

Thymoglobulin may modulate immunosuppression through the following mechanisms:

  • Downmodulation of the expression of several molecules that control T-cell activation (ie, TCR/CD3, CD4, CD8, CD25, CD45,
    HLA class I, HLA-DR)1,5
  • Binding to selectins and integrin families (CD11a, CD18), thereby preventing T-cell homing5
  • Prevention of cytotoxic activities1,5,6

The clinical significance of these mechanisms is unknown.

Graphic showing three mechanisms of T cell modulation from left to right. On the left, a T cell with TCR/CD3, CD45, and CD8 engages HLA class I on an antigen-presenting cell (APC), labeled "Modulation of T-cell activation." In the center, a T cell’s integrins CD11a and CD18 interact with endothelial cells, labeled "Modulation of homing." On the right, a T cell with TCR/CD3 and HLA class I releases perforin/granzymes toward a target cell, labeled "Modulation of cytotoxic activities."

Thymoglobulin Is the Only Polyclonal T-Cell–Depleting Agent That Is FDA Approved for Prevention of Acute Rejection1,7

Line graph showing mean T-cell counts after Thymoglobulin treatment (1.5 mg/kg/day). The x-axis shows days 0 to 14, and the y-axis shows mean T cells/mm³ (0–500). A blue dotted line represents CD3 T cells and a navy dotted line represents CD2 T cells. Both start between 300-400/mm³, drop sharply in the first two days, and remain low through day 14.
  • Based on data collected from 12 patients in the phase 3 trial, T-cell depletion is usually observed within a day from initiating Thymoglobulin therapy.1

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Important Safety Information

WARNING: IMMUNOSUPPRESSION. Thymoglobulin should only be used by physicians experienced in immunosuppressive therapy in transplantation.
  • Contraindications. Thymoglobulin is contraindicated in patients with a history of allergy or anaphylaxis to rabbit proteins or to any product excipients, or who have active acute or chronic infections which contraindicate any additional immunosuppression.
  • Management of Immunosuppression. To prevent over-immunosuppression, physicians may wish to decrease the dose of the maintenance immunosuppression regimen during the period of Thymoglobulin use. Dosing for Thymoglobulin is different from dosing for other ATG products, because protein composition and concentrations vary depending on the source of ATG. Thymoglobulin should be used under strict medical supervision in a hospital setting, and patients should be carefully monitored during the infusion.
  • Immune Mediated Reactions. Serious immune-mediated reactions, including anaphylaxis or severe cytokine release syndrome (CRS), have been reported with the use of Thymoglobulin. Fatal anaphylaxis has been reported. If an anaphylactic reaction occurs, the infusion should be terminated immediately.
  • Infusion-Associated Reactions. Cases consistent with cytokine release syndrome (CRS) have been reported with rapid infusion rates. CRS is attributed to the release of cytokines by activated monocytes and lymphocytes. Severe acute CRS can cause serious cardiorespiratory events and/or death. Close compliance with the recommended dosage and infusion time may reduce the incidence and severity of infusion-associated reactions (IARs). Slowing the infusion rate may minimize many of these IARs. Reactions at the infusion site may include pain, swelling, and redness of the skin.
  • Hematologic Effects. Low counts of platelets and white blood cells (including low counts of lymphocytes and neutrophils) have been identified and are reversible following dose adjustments. Total white blood cell and platelet counts should be monitored.
  • Infection and Malignancy. Infections, reactivation of infection, febrile neutropenia, sepsis, malignancies including lymphoproliferative disorders (LPD) and other lymphomas as well as solid tumors have been reported after Thymoglobulin administration in combination with multiple immunosuppressive agents. These events can be fatal.
  • Immunization. The safety of immunization with attenuated live vaccines following Thymoglobulin therapy has not been studied; therefore, immunization with attenuated live vaccines is not recommended for patients who have recently received Thymoglobulin.
  • Overdosage. Thymoglobulin overdosage may result in leukopenia (including lymphopenia and neutropenia) and/ or thrombocytopenia, which can be managed with dose reduction.
  • Adverse Reactions. The most common adverse reactions and laboratory abnormalities (incidence >5% higher than comparator) are urinary tract infection, abdominal pain, hypertension, nausea, shortness of breath, fever, headache, anxiety, chills, increased potassium levels in the blood, and low counts of platelets and white blood cells.
  • During post-marketing surveillance, arthralgia/myalgia, lymphadenopathy, proteinuria, and decreased oxygen saturation tend to occur 5 to 15 days after Thymoglobulin infusion and are consistent with serum sickness. Symptoms are manageable with corticosteroid treatment.

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Important Safety Information

Abbreviations: CD, cluster of differentiation; FDA, Food and Drug Administration; FasL, Fas ligand; HLA, human leukocyte antigen; HLA-DR, human leukocyte antigen-D related; NK, natural killer cells; TCR, T-cell receptor.

References:

1. Thymoglobulin [prescribing information]. Cambridge, MA: Genzyme Corporation; 2026.
2. Woodside KJ, Hu M, Gugliuzza KK, Hunter GC, Daller JA. T-lymphocyte apoptosis is increased by non-interleukin-2-dependent induction in human mixed lymphocyte cultures. Transplantation Proc. 2005;37(4):1949-1952.
3. Bonnefoy-Berard N, Genestier L, Preville X, Revillard JP. TNFα and CD95-L contribute to apoptosis of activated lymphocytes triggered by ATGs. Transplantation Proc. 1999;31(1-2):775-777.
4. Genestier L, Fournel S, Flacher M, Assossou O, Revillard JP, Bonnefoy-Berard N. Induction of Fas (Apo-1, CD95)-mediated apoptosis of activated lymphocytes by polyclonal antithymocyte globulins. Blood. 1998;91(7):2360-2368.
5. Mueller TF. Mechanisms of action of Thymoglobulin. Transplantation. 2007;84(11S):S5-S10.
6. Krepsova E, Tycova I, Sekerkova A, et al. Effect of induction therapy on the expression of molecular markers associated with rejection and tolerance. BMC Nephrol. 2015;16:146.
7. Atgam [prescribing information]. New York, NY: Pfizer Inc; 2023.

Thymoglobulin and Sanofi are registered trademarks of Sanofi or an affiliate. MAT-US-2600057-v1.0-03/2026

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