Thymoglobulin® Anti-thymocyte Globulin (Rabbit) Injection

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 death^2-4
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 Rejection^1,7

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

Important Safety Information for Thymoglobulin [Anti-thymocyte Globulin (Rabbit)]:

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 that contraindicate any additional immunosuppression.

WARNINGS AND PRECAUTIONS

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.
Hypersensitivity and Infusion-Related Reactions: Severe hypersensitivity and infusion-related reactions, including fatal anaphylaxis and severe cytokine release syndrome (CRS), have been reported with the use of Thymoglobulin. 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-related reactions. Slowing the infusion rate may minimize the risk of infusion-related reactions.
If a hypersensitivity or infusion-related reaction occurs, terminate the infusion immediately and provide supportive treatment according to clinical practice.
Cytopenias: Cytopenias including anemia, neutropenia, and thrombocytopenia have occurred with Thymoglobulin administration. Monitor blood counts after Thymoglobulin administration. Adjust dose accordingly to reverse cytopenias.
Infection: Thymoglobulin is routinely used in combination with other immunosuppressive agents. Infections (bacterial, fungal, viral and protozoal), reactivation of infection (particularly cytomegalovirus [CMV]) and sepsis have been reported after Thymoglobulin administration in combination with multiple immunosuppressive agents. These infections can be fatal.
Monitor patients carefully and administer appropriate anti-infective treatment when indicated.
Malignancy: Malignancies with fatal outcomes have been reported in patients treated with Thymoglobulin. Use of immunosuppressive agents, including Thymoglobulin, may increase the risk of malignancies, including lymphoma or lymphoproliferative disorders.
Immunizations: 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.
Laboratory Tests: Thymoglobulin may interfere with rabbit antibody–based immunoassays and with cross-match or panel-reactive antibody cytotoxicity assays. Thymoglobulin has not been shown to interfere with any routine clinical laboratory tests that do not use immunoglobulins.

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.

The following postmarketing adverse reactions have been reported:

Hepatobiliary Disorders: Hepatic dysfunction including transient reversible elevations in aminotransferases without any clinical signs or symptoms, hepatic failure, hyperbilirubinemia.
Blood and Lymphatic System Disorders: Febrile neutropenia, coagulopathy without clinical signs or symptoms of bleeding, disseminated intravascular coagulopathy, anemia including hemolytic anemia, thrombotic microangiopathy.
Immune System Disorders: Hypersensitivity reactions including anaphylaxis, CRS.

OVERDOSAGE

Thymoglobulin overdosage may result in leukopenia (including lymphopenia and neutropenia) and/ or thrombocytopenia, which can be managed with dose reduction.

INDICATION

Thymoglobulin^®(anti-thymocyte globulin (rabbit)) is indicated for the prophylaxis and treatment of acute rejection in adult and pediatric patients receiving a kidney transplant in conjunction with concomitant immunosuppression.

Click here for full Prescribing Information.

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Important Safety Information

INDICATION

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.

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

Thymoglobulin May Suppress the Immune Response through Multiple Pathways1