Version July 2025
Esophageal squamous cell carcinoma, unresectable or metastatic, with PD-L1 expression (≥1) (first-line treatment): Note: Select patients for treatment based on the presence of PD-L1 in tumor specimens.
IV: 150 mg once every 2 weeks or 200 mg once every 3 weeks or 300 mg once every 4 weeks; in combination with cisplatin or oxaliplatin (platinum may be discontinued after 6 cycles) and either fluorouracil, capecitabine, or paclitaxel; continue until disease progression or unacceptable toxicity (Ref).
Esophageal squamous cell carcinoma, unresectable or metastatic (previously treated): IV: 150 mg once every 2 weeks or 200 mg once every 3 weeks or 300 mg once every 4 weeks; continue until disease progression or unacceptable toxicity (Ref).
Gastric or gastroesophageal junction adenocarcinoma, unresectable or metastatic, HER2 negative, with PD-L1 expression (≥1) (first-line treatment): Note: Select patients for treatment based on the presence of PD-L1 in tumor specimens.
IV: 150 mg once every 2 weeks or 200 mg once every 3 weeks or 300 mg once every 4 weeks; in combination with either capecitabine and oxaliplatin (CAPOX) or cisplatin and fluorouracil for up to 6 cycles, followed by tislelizumab (as a single agent or in combination with optional capecitabine maintenance [CAPOX arm only]); continue until disease progression or unacceptable toxicity (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Kidney impairment prior to treatment initiation:
Note: Kidney function estimated using Cockcroft-Gault equation.
CrCl ≥30 mL/minute: There are no dosage adjustments provided in the manufacturer’s labeling; however, there are no clinically significant differences in tislelizumab pharmacokinetics.
CrCl 15 to 29 mL/minute: There are no dosage adjustments provided in the manufacturer’s labeling (effect on tislelizumab pharmacokinetics is unknown).
End-stage kidney disease (CrCl <15 mL/minute): There are no dosage adjustments provided in the manufacturer’s labeling (effect on tislelizumab pharmacokinetics is unknown).
Kidney toxicity during treatment:
Note: If tislelizumab treatment interruption or discontinuation is required, administer systemic corticosteroids (prednisone 1 to 2 mg/kg/day [or equivalent]) or other appropriate therapy for immune-mediated adverse reactions until improvement to grade 1 or lower, then follow with a corticosteroid taper and continue to taper over at least 1 month. Prednisone tapering recommendations when used for immune-mediated adverse reactions associated with immune checkpoint inhibitor therapy may be found in the Prednisone monograph. Consider administration of other systemic immunosuppressants if immune-mediated adverse reaction is not controlled with corticosteroid therapy.
Immune-mediated nephritis with kidney dysfunction:
Grade 2 or grade 3 serum creatinine elevation: Withhold tislelizumab; resume tislelizumab after complete or partial (to grade 0 or 1) resolution after corticosteroid taper. Permanently discontinue tislelizumab if no complete or partial resolution within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation.
Grade 4 serum creatinine elevation: Permanently discontinue tislelizumab.
Hepatic impairment prior to treatment initiation:
Mild to moderate impairment (total bilirubin ≤3 times ULN and any AST): There are no dosage adjustments provided in the manufacturer’s labeling; however, there are no clinically significant differences in tislelizumab pharmacokinetics.
Severe impairment (total bilirubin >3 times ULN and any AST): There are no dosage adjustments provided in the manufacturer’s labeling (effect on tislelizumab pharmacokinetics is unknown).
Acute hepatotoxicity during treatment:
Note: If tislelizumab treatment interruption or discontinuation is required, administer systemic corticosteroids (prednisone 1 to 2 mg/kg/day [or equivalent]) or other appropriate therapy for immune-mediated adverse reactions until improvement to grade 1 or lower, then follow with a corticosteroid taper and continue to taper over at least 1 month. Prednisone tapering recommendations when used for immune-mediated adverse reactions associated with immune checkpoint inhibitor therapy may be found in the Prednisone monograph. Consider administration of other systemic immunosuppressants if immune-mediated adverse reaction is not controlled with corticosteroid therapy. Permanently discontinue tislelizumab if no complete or partial resolution within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation.
Immune-mediated hepatitis without tumor involvement of the liver:
AST or ALT >3 up to 8 times ULN or total bilirubin >1.5 up to 3 times ULN: Withhold tislelizumab treatment. Resume tislelizumab treatment after complete or partial resolution (to grade 0 or 1) of hepatitis after corticosteroid taper.
AST or ALT >8 times ULN or total bilirubin >3 times ULN: Permanently discontinue tislelizumab.
Immune-mediated hepatitis with tumor involvement of the liver: Note: If AST and ALT are ≤ ULN at baseline, follow recommendations for hepatitis without tumor involvement of the liver.
If baseline AST or ALT >1 up to 3 times ULN and increases to >5 up to 10 times ULN or baseline AST or ALT >3 up to 5 times ULN and increases to >8 up to 10 times ULN: Withhold tislelizumab treatment. Resume tislelizumab treatment with complete or partial resolution (to grade 0 or 1) of hepatitis after corticosteroid taper.
AST or ALT increases to >10 times ULN or total bilirubin increases to >3 times ULN: Permanently discontinue tislelizumab.
Addit ional recommendations:
Grade 2 immune-mediated hepatitis: Withhold immune checkpoint inhibitor (ICI); if no improvement within 3 to 5 days after ICI is withheld, consider initiation of corticosteroids (prednisone 0.5 to 1 mg/kg/day or equivalent) (Ref).
Grade 3 or 4 immune-mediated hepatitis: Withhold ICI; initiate corticosteroids (methylprednisolone 1 to 2 mg/kg or equivalent) (Ref). Based on data from a retrospective cohort study in patients with grade 3 or 4 immune-mediated hepatitis, initial treatment with methylprednisolone 1 mg/kg/day demonstrated similar time to ALT normalization (compared with higher methylprednisolone doses), while reducing the potential for corticosteroid-related complications (Ref).
American Society of Clinical Oncology guidelines for appropriate systemic therapy dosing in adults with cancer with a BMI ≥30 kg/m2: The dosing in the approved prescribing information should be followed in all patients, regardless of obesity status. If a patient with a BMI ≥30 kg/m2 experiences high-grade toxicity from systemic anticancer therapy, the same dosage modification recommendations should be followed for all patients, regardless of obesity status (Ref).
Note: No dosage reductions of tislelizumab are recommended. Other concomitant anticancer therapies may also require treatment interruption, dosage reduction, and/or discontinuation.
Immune-mediated adverse reactions (general information): In cases of suspected immune-mediated adverse reactions, initiate appropriate workup to exclude alternative etiologies (eg, infection). Institute medical management promptly, including specialty consultation when appropriate. Withhold tislelizumab for severe (grade 3) immune-mediated adverse reactions. Permanently discontinue tislelizumab for life-threatening (grade 4) immune-mediated adverse reactions, recurrent severe (grade 3) immune-mediated reactions that require systemic immunosuppressive treatment, or inability to reduce corticosteroid dose to prednisone ≤10 mg/day (or equivalent) within 12 weeks of initiating corticosteroids. If tislelizumab treatment interruption or discontinuation is required, administer systemic corticosteroids (1 to 2 mg/kg/day prednisone [or equivalent]) until improvement to ≤ grade 1; upon improvement to ≤ grade 1, initiate corticosteroid taper and continue to taper over at least 1 month. Consider administration of other systemic immunosuppressants if immune-mediated adverse reaction is not controlled with corticosteroid therapy. Systemic corticosteroids may not be necessary for certain adverse reactions. Hormone-replacement therapy may be required for endocrinopathies (if clinically indicated). See table for additional dosage modification guidance.
Additional management recommendations: Consider withholding checkpoint inhibitor therapy for most grade 2 toxicities and resume when symptoms and/or lab values resolve to ≤ grade 1; systemic corticosteroids (initial dose of 0.5 to 1 mg/kg/day prednisone [or equivalent]) may be administered if indicated for grade 2 toxicities (Ref). Refer to guideline for further information regarding management of immune-mediated adverse reactions associated with immune checkpoint inhibitor therapy.
|
Adverse reaction |
Severity |
Tislelizumab dosage modification |
|---|---|---|
|
a SJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysis; DRESS = drug rash with eosinophilia and systemic symptoms. | ||
|
b Prednisone tapering recommendations when used for immune-mediated adverse reactions associated with immune checkpoint inhibitor therapy may be found in the Prednisone monograph. | ||
|
Immune-mediated adverse reactions | ||
|
Cardiovascular toxicity: myocarditis |
Grade 2, 3, or 4 |
Permanently discontinue tislelizumab. |
|
Dermatologic toxicity |
Mild or moderate nonexfoliative rash |
May be managed with topical emollients and/or topical corticosteroids. |
|
Exfoliative dermatologic conditions: grade 3 or suspected SJS, TEN, or DRESS |
Withhold tislelizumab; resume tislelizumab after complete or partial (to grade 0 or 1) resolution after corticosteroid taper.b Permanently discontinue tislelizumab if no complete or partial resolution within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation. | |
|
Grade 4 or confirmed SJS, TEN, or DRESS |
Permanently discontinue tislelizumab. | |
|
Endocrinopathies |
Grade 3 or 4 |
Withhold tislelizumab until clinically stable or permanently discontinue depending on severity. |
|
Adrenal insufficiency, ≥ grade 2 |
Withhold tislelizumab (depending on the severity). Initiate symptomatic management (including hormone replacement as clinically indicated). | |
|
Diabetes, type 1 |
Withhold or permanently discontinue tislelizumab (depending on the severity). Initiate insulin therapy as clinically indicated. | |
|
Hypophysitis |
Withhold or discontinue tislelizumab (depending on the severity). Initiate hormone-replacement therapy as clinically indicated. | |
|
Hyperthyroidism/Thyroiditis |
Withhold or permanently discontinue tislelizumab (depending on the severity). Initiate medical management as clinically indicated. | |
|
Hypothyroidism |
Withhold or permanently discontinue tislelizumab (depending on the severity). Initiate thyroid hormone-replacement therapy as clinically indicated. | |
|
GI toxicity: colitis |
Grade 2 or 3 |
Withhold tislelizumab; resume tislelizumab after complete or partial (to grade 0 or 1) resolution after corticosteroid taper.b Permanently discontinue tislelizumab if no complete or partial response within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation. |
|
Grade 4 |
Permanently discontinue tislelizumab. | |
|
Neurologic toxicity |
Grade 2 |
Withhold tislelizumab; resume tislelizumab after complete or partial (to grade 0 or 1) resolution after corticosteroid taper.b Permanently discontinue tislelizumab if no complete or partial response within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation. |
|
Grade 3 or 4 |
Permanently discontinue tislelizumab. | |
|
Ocular disorders: Vogt-Koyanagi-Harada-like syndrome |
Any |
May require systemic corticosteroids to reduce the risk of permanent vision loss. |
|
Pulmonary toxicity: pneumonitis |
Grade 2 |
Withhold tislelizumab; resume tislelizumab after complete or partial (to grade 0 or 1) resolution after corticosteroid taper.b Permanently discontinue tislelizumab if no complete or partial response within 12 weeks of initiating corticosteroids, or if unable to reduce prednisone to ≤10 mg/day (or equivalent) within 12 weeks of corticosteroid initiation. |
|
Recurrent grade 2 |
Permanently discontinue tislelizumab. | |
|
Grade 3 or 4 |
Permanently discontinue tislelizumab. | |
|
Other adverse reactions | ||
|
Infusion-related reactions |
Grade 1 |
Slow tislelizumab infusion rate by 50%. |
|
Grade 2 |
Interrupt tislelizumab infusion; resume tislelizumab infusion at 50% of the previous rate if resolved or decreased to grade 1. | |
|
Grade 3 or 4 |
Stop infusion and permanently discontinue tislelizumab. | |
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in adults.
>10%:
Dermatologic: Skin rash (13%)
Endocrine & metabolic: Decreased serum albumin (33%), decreased serum phosphate (15%), decreased serum potassium (13%), decreased serum sodium (34%), hypothyroidism (13%), increased serum glucose (46%), weight loss (23%)
Gastrointestinal: Abdominal pain (11%), constipation (15%), decreased appetite (16%), diarrhea (13%; grades 3/4: 1%), dysphagia (11%), nausea (14%; grades 3/4: <1%), vomiting (11%; grades 3/4: <1%)
Hematologic & oncologic: Anemia (31%; grades 3/4: 6%), decreased platelet count (11%; grades 3/4: 1%), hemorrhage (12%; grades 3/4: 2%), lymphocytopenia (43%; grades 3/4: 11%)
Hepatic: Increased serum alanine aminotransferase (23%), increased serum alkaline phosphatase (32%), increased serum aspartate aminotransferase (27%), increased serum bilirubin (11%)
Immunologic: Antibody development (15%; neutralizing: 3%)
Nervous system: Fatigue (28%)
Neuromuscular & skeletal: Increased creatine phosphokinase in blood specimen (13%), musculoskeletal pain (24%)
Respiratory: Cough (22%), pneumonia (16%)
Miscellaneous: Fever (16%)
1% to 10%:
Endocrine & metabolic: Decreased serum glucose (10%)
Gastrointestinal: Esophageal obstruction (serious: ≥2%)
Hematologic & oncologic: Decreased white blood cell count (10%; grades 3/4: <1%)
Respiratory: Pneumonitis (serious: ≥2%)
Frequency not defined:
Cardiovascular: Myocarditis, pericarditis
Dermatologic: Dermatologic disorder
Endocrine & metabolic: Adrenocortical insufficiency, diabetes mellitus, hyperthyroidism, hypophysitis, pituitary insufficiency, thyroiditis
Gastrointestinal: Colitis
Hepatic: Hepatitis
Hypersensitivity: Infusion-related reaction
Immunologic: Sjögren disease
Nervous system: Encephalitis, myasthenia gravis
Neuromuscular & skeletal: Arthritis, myositis, polymyalgia rheumatica
Renal: Nephritis (with renal dysfunction)
Postmarketing: Dermatologic: Exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis
There are no contraindications listed in the manufacturer's labeling.
Concerns related to adverse effects:
• Adverse reactions (immune-mediated): PD-1/PD-L1 blockers (including tislelizumab) remove immune response inhibition, thus potentially breaking peripheral tolerance and inducing immune-mediated adverse reactions. Severe and fatal immune-mediated adverse reactions may occur in any organ system or tissue. Reactions generally occur during treatment (may occur at any time after tislelizumab initiation); reactions may also occur after tislelizumab discontinuation. Early identification and management of immune-mediated adverse reactions are necessary to ensure safe use of tislelizumab. If suspected immune-mediated reactions occur, initiate appropriate workup to exclude alternative causes (including infection).
• Dermatologic toxicity: Tislelizumab may cause immune-mediated rash or dermatitis; grade 2 to 4 events have been reported. Severe cutaneous adverse reactions, including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis have been observed with tislelizumab; drug rash with eosinophilia and systemic symptoms has occurred with other anti-PD-L1/PD-1 monoclonal antibodies; some cases were fatal. Systemic corticosteroids were required in some patients with immune-mediated dermatologic adverse reactions treated with tislelizumab, including high-dose corticosteroids. Dermatologic adverse reactions led to treatment interruption or permanent discontinuation in a small percentage of patients. Immune-mediated dermatologic adverse reactions resolved in approximately two-thirds of patients. A majority of these patients were able to reinitiate treatment with tislelizumab following interruption for dermatologic toxicity with a small percentage experiencing recurrence of symptoms.
• Endocrinopathies: Tislelizumab is associated with immune-mediated endocrinopathies (which can be fatal).
– Adrenal insufficiency: Tislelizumab may cause adrenal insufficiency; grades 2, 3, and 4 events have been reported. Adrenal insufficiency did not lead to permanent treatment discontinuation. Treatment interruption and systemic corticosteroids (including high-dose corticosteroids) were required in most patients with adrenal insufficiency; adrenal insufficiency resolved in one-fourth of patients. In patients requiring treatment interruption for adrenal insufficiency, approximately three-fourths were able to reinitiate treatment (after symptom improvement) without evidence of recurrence.
– Diabetes mellitus: Type 1 diabetes mellitus has been reported with PD-1 and PD-L1 blocking antibodies (including tislelizumab). Grade 2 to 4 diabetes mellitus events occurred. Treatment interruption and discontinuation was required rarely; two-thirds of patients who developed diabetes received insulin therapy. Diabetes mellitus resolved in approximately one-fourth of patients. All patients requiring treatment interruption for diabetes mellitus were able to reinitiate treatment (after symptom improvement) without evidence of recurrence.
– Hypophysitis: Tislelizumab may rarely cause immune-mediated hypophysitis. Hypophysitis may present with acute mass effect–associated symptoms such as headache, photophobia, or visual field defects. Hypophysitis may cause hypopituitarism. Hypophysitis/hypopituitarism (including grade 2 events) occurred rarely; patients were managed with systemic corticosteroids and treatment interruption without resolution. Upon treatment reinitiation following interruption, there was no evidence of recurrence of hypophysitis/hypopituitarism.
– Thyroid disorders: Tislelizumab may cause immune-mediated thyroid disorders. Hyperthyroidism occurred in a small percentage of patients, including rare grade 2 and 3 events. Discontinuation and treatment interruption were required in only a small number of patients. Systemic corticosteroids were occasionally required. Hyperthyroidism resolved in a majority of patients. Three-fourths of patients reinitiated treatment following interruption (after symptom improvement) without evidence of recurrence of hyperthyroidism. Hypothyroidism has also occurred, including grades 2 and 4 events. Hypothyroidism may follow hyperthyroidism. Discontinuation due to hypothyroidism was not required, although treatment interruption was required in a small number of patients. Systemic corticosteroids were required in a small percentage of patients with hypothyroidism; approximately two-thirds of patients required hormone-replacement therapy, with approximately one-half requiring long-term thyroid hormone replacement. Hypothyroidism resolved in approximately one-third of patients. A majority of patients reinitiated treatment following interruption (after symptom improvement without evidence of recurrence of hypothyroidism. Thyroiditis occurred rarely, including grade 2 events; systemic corticosteroids and treatment interruption were rarely necessary for thyroiditis, and thyroiditis resolved in nearly one-half of patients. Upon treatment reinitiation following interruption, there was no evidence of recurrence of thyroiditis. Thyroiditis can present with or without endocrinopathy.
• GI adverse reactions: Tislelizumab may cause immune-mediated colitis, which can be fatal. Immune-mediated colitis occurred in a small percentage of patients, including grade 2 and 3 events. Colitis led to permanent discontinuation or treatment interruption in a small number of patients. Systemic corticosteroids were required in three-fourths of patients with colitis; one-half of patients received high-dose corticosteroids and some patients required additional alternative immunosuppressive therapy. Colitis resolved in most patients. Some patients requiring treatment interruption for colitis reinitiated tislelizumab without recurrence of colitis. Cytomegalovirus infection/reactivation has been reported in patients with corticosteroid-refractory immune-mediated colitis who received anti-PD-L1/PD-1 monoclonal antibodies. Pancreatitis (including increased serum amylase and lipase levels), gastritis, and duodenitis have also been reported.
• Hepatitis: Tislelizumab may cause immune-mediated hepatitis, which may be fatal. Immune-mediated hepatitis occurred in a small percentage of patients, including grade 2 and higher events (some fatal). Hepatitis led to permanent discontinuation or treatment interruption in a small percentage of patients. Systemic corticosteroids were required in three-fourths of patients with hepatitis; approximately one-half of patients required high-dose systemic corticosteroids and some patients required additional immunosuppression. Hepatitis resolved in almost three-fourths of patients. Recurrence was not observed in patients who reinitiated tislelizumab (following symptom improvement).
• Infusion-related reactions: Severe or life-threatening infusion-related reactions have occurred (rarely) in patients receiving tislelizumab.
• Kidney toxicity: Tislelizumab may cause immune-mediated nephritis with kidney dysfunction, which can be fatal. Grades 2 and 3 events have occurred in a small number of patients. Nephritis led to treatment interruption or permanent discontinuation rarely. Systemic corticosteroids were required in one-half of patients with nephritis (including high-dose corticosteroids). Nephritis resolved in one-third of patients. Two-thirds of patients requiring treatment interruption for nephritis reinitiated tislelizumab after symptom improvement; recurrence was reported in some patients.
• Ocular disorders: Ocular events, including uveitis, iritis, and other ocular inflammatory toxicities have been reported; some cases may be associated with retinal detachment. Various grades of visual impairment (including blindness) may occur. If uveitis occurs in combination with other immune-mediated adverse reactions, consider a Vogt-Koyanagi-Harada-like syndrome.
• Pneumonitis: Tislelizumab may cause immune-mediated pneumonitis, which may be fatal. In patients who received other anti-PD-L1/PD-1 monoclonal antibodies, the incidence of pneumonitis was higher in patients who received prior thoracic radiation. Immune-mediated pneumonitis occurred in a small percentage of tislelizumab-treated patients; grade 2 and higher (some fatal) events have been observed. Pneumonitis led to permanent discontinuation or treatment interruption in a small percentage of patients. Systemic corticosteroids were required in approximately three-fourths of patients with pneumonitis; two-thirds of patients received high-dose corticosteroids. Pneumonitis resolved in one-half of patients. Of the patients who reinitiated tislelizumab (following symptom improvement), some experienced recurrence of pneumonitis.
• Other immune-mediated toxicities: Other clinically significant immune-mediated adverse reactions have been reported rarely with tislelizumab or with other anti-PD-L1/PD-1 monoclonal antibodies (some have been severe or fatal). Events have included meningitis, encephalitis, myelitis and demyelination, myasthenic syndrome/myasthenia gravis (including exacerbation), Guillain-Barre syndrome, nerve paresis, autoimmune neuropathy, myocarditis, pericarditis, vasculitis, myositis/polymyositis, rhabdomyolysis (and associated sequelae including kidney failure), arthritis, polymyalgia rheumatica, encephalitis, myasthenia gravis, Sjögren's syndrome, hypoparathyroidism, hemolytic anemia, aplastic anemia, hemophagocytic lymphohistiocytosis, systemic inflammatory response syndrome, histiocytic necrotizing lymphadenitis (Kikuchi lymphadenitis), sarcoidosis, immune thrombocytopenia (formerly known as immune thrombocytopenic purpura), solid organ transplant rejection, and other transplant (including corneal graft) rejection.
Disease-related concerns:
• Hematopoietic cell transplant: Fatal and other serious complications may occur in patients who receive allogeneic hematopoietic cell transplant (HCT) before or after treatment with an anti-PD-L1/PD-1 monoclonal antibody. Transplant-related complications included hyperacute graft-versus-host disease (GVHD), acute or chronic GVHD, hepatic veno-occlusive disease (also known as sinusoidal obstruction syndrome) after reduced-intensity conditioning, and steroid-requiring febrile syndrome (with no identified infectious etiology). These complications may occur despite intervening therapy between PD-L1/PD-1 blockade and HCT. Manage early signs/symptoms of transplant-related complications promptly. Assess the risks/benefits of treatment with an anti-PD-L1/PD-1 monoclonal antibody prior to or after an allogeneic HCT.
• Myasthenia gravis: Checkpoint inhibitors may worsen or precipitate new myasthenia gravis (MG), especially within the first 16 weeks of treatment; use with caution. Patients with well-controlled MG may be considered for checkpoint inhibitor therapy if MG treatment is maintained (or reinitiated in patients whose MG is in remission), combination therapy (eg, anti-CTLA-4 with anti-PD-a/PD-L1 monoclonal antibodies) is avoided, and respiratory and bulbar function are closely followed. In patients who develop overt MG during checkpoint inhibitor therapy, early aggressive treatment with plasma exchange or IVIG in combination with high-dose corticosteroids may be required (AAN [Narayanaswami 2021]).
Other warnings/precautions:
• Appropriate use: Select patients for first-line treatment of unresectable or metastatic HER2-negative gastric/gastroesophageal junction adenocarcinoma or for first-line treatment of unresectable or metastatic esophageal squamous cell carcinoma based on PD-L1 expression (≥1) in tumor specimens.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous [preservative free]:
Tevimbra: Tislelizumab-jsgr 100 mg/10 mL (10 mL)
No
Solution (Tevimbra Intravenous)
100 mg/10 mL (per mL): $655.68
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IV: For 150 mg and 200 mg doses, infuse the initial dose over 60 minutes; if tolerated, may infuse subsequent doses over 30 minutes. For 300 mg doses, infuse the initial dose over 90 minutes; if tolerated, may infuse the second dose over 60 minutes and subsequent doses over 30 minutes (if second dose is tolerated). Infuse through an IV line with a sterile, nonpyrogenic, low-protein binding, 0.2 or 0.22 micron inline or add-on filter. Do not infuse other medications through the same IV line. Do not administer as IV push or bolus. Flush IV line following completion of the infusion.
Interrupt or slow the infusion for grade 1 or grade 2 infusion-related reactions; permanently discontinue tislelizumab for grade 3 or 4 infusion-related reactions.
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Tevimbra: https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/761380s000lbl.pdf#page=26
Esophageal squamous cell carcinoma, unresectable or metastatic:
First-line treatment (in combination with platinum-containing chemotherapy) of unresectable or metastatic esophageal squamous cell carcinoma in adults whose tumors express PD-L1 (≥1).
Treatment (as a single agent) of unresectable or metastatic esophageal squamous cell carcinoma in adults after prior systemic chemotherapy that did not include a PD-1/PD-L1 inhibitor.
Gastric or gastroesophageal junction adenocarcinoma, unresectable or metastatic, HER2 negative, with PD-L1 expression: First-line treatment (in combination with platinum and fluoropyrimidine-based chemotherapy) of unresectable or metastatic HER2-negative gastric or gastroesophageal junction adenocarcinoma in adults whose tumors express PD-L1 (≥1).
Tislelizumab may be confused with atezolizumab, cosibelimab, pembrolizumab, tafasitamab, tarlatamab, teclistamab, tisotumab vedotin, teplizumab, tezepelumab, tocilizumab, toripalimab, tremelimumab.
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (chemotherapeutic agent, parenteral and oral) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care, Community/Ambulatory Care, and Long-Term Care Settings).
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acetaminophen: May decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor
Antibiotics: May decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor
Corticosteroids (Systemic): May decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Management: Carefully consider the need for corticosteroids, at doses of a prednisone-equivalent of 10 mg or more per day, during the initiation of immune checkpoint inhibitor therapy. Use of corticosteroids to treat immune related adverse events is still recommended Risk D: Consider Therapy Modification
Efgartigimod Alfa: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Inhibitors of the Proton Pump (PPIs and PCABs): May decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor
Ketoconazole (Systemic): Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies) may increase hepatotoxic effects of Ketoconazole (Systemic). Risk C: Monitor
Nipocalimab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Opioid Agonists: Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies) may decrease therapeutic effects of Opioid Agonists. Opioid Agonists may decrease therapeutic effects of Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies). Risk C: Monitor
Rozanolixizumab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Vitamin K Antagonists: Immune Checkpoint Inhibitors (Anti-PD-1, -PD-L1, and -CTLA4 Therapies) may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor
Verify pregnancy status prior to treatment initiation in patients who could become pregnant. Patients who could become pregnant should use effective contraception during therapy and for 4 months after the last tislelizumab dose.
Tislelizumab is Fc-engineered humanized monoclonal antibody (IgG4) that may cross the placenta. Human IgG crosses the placenta. Fetal exposure is dependent upon the IgG subclass, maternal serum concentrations, placental integrity, newborn birth weight, and gestational age, generally increasing as pregnancy progresses. The lowest exposure would be expected during the period of organogenesis and the highest during the third trimester (Clements 2020; Palmeira 2012; Pentsuk 2009).
Based on the mechanism of action, in utero exposure to tislelizumab may disrupt maternal tolerance to the fetus, increasing the risk of abortion or stillbirth. Based on animal data, maternal use of a PD-1/PD-L1 inhibitor may also result in immune-mediated disorders in the newborn.
The European Society for Medical Oncology (ESMO) has published guidelines for diagnosis, treatment, and follow-up of cancer during pregnancy. The guidelines recommend referral to a facility with expertise in cancer during pregnancy and encourage a multidisciplinary team (obstetrician, neonatologist, oncology team) approach (ESMO [Peccatori 2013]).
A long-term observational research study is collecting information about the diagnosis and treatment of cancer during pregnancy. For additional information about the pregnancy and cancer registry or to become a participant, contact Cooper Health (877-635-4499).
It is not known if tislelizumab is present in breast milk.
Tislelizumab is Fc-engineered humanized monoclonal antibody (IgG4). Human IgG is present in breast milk; concentrations are dependent upon IgG subclass and postpartum age (Anderson 2021).
Due to the potential for serious adverse reactions in the breastfed infant, breastfeeding is not recommended by the manufacturer during treatment and for 4 months after the last tislelizumab dose.
PD-L1 expression in tumor specimens (for first-line treatment of unresectable or metastatic HER2-negative gastric/gastroesophageal junction adenocarcinoma or first-line treatment of unresectable or metastatic esophageal squamous cell carcinoma). Monitor hepatic function (AST, ALT, and total bilirubin; at baseline and periodically during treatment); kidney function (serum creatinine; at baseline and periodically during treatment); thyroid function (at baseline, periodically during treatment and as clinically indicated); monitor blood glucose (for hyperglycemia). Verify pregnancy status (prior to therapy in patients who could become pregnant). Monitor closely for signs/symptoms of immune-mediated adverse reactions, including adrenal insufficiency, diarrhea/colitis (consider initiating or repeating infectious workup in patients with corticosteroid-refractory immune-mediated colitis to exclude alternative causes), dermatologic toxicity, diabetes mellitus, hypophysitis/hypopituitarism, neurologic toxicity, ocular disorders, thyroid disorders, pneumonitis, and other immune-mediated adverse reactions. Monitor for signs/symptoms of infusion-related reactions. If received/receiving hematopoietic stem cell transplant, monitor closely for early signs/symptoms of transplant-related complications.
The American Society of Clinical Oncology hepatitis B virus (HBV) screening and management provisional clinical opinion (ASCO [Hwang 2020]) recommends HBV screening with hepatitis B surface antigen, hepatitis B core antibody, total Ig or IgG, and antibody to hepatitis B surface antigen prior to beginning (or at the beginning of) systemic anticancer therapy; do not delay treatment for screening/results. Detection of chronic or past HBV infection requires a risk assessment to determine antiviral prophylaxis requirements, monitoring, and follow-up.
Cardiovascular monitoring: Comprehensive assessment prior to treatment including a history and physical examination, screening for cardiovascular disease risk factors such as hypertension, diabetes, dyslipidemia, obesity, and smoking (ASCO [Armenian 2017]). Obtain baseline ECG, natriuretic peptides, and troponins in all patients; obtain a baseline echocardiogram in high-risk patients; consider serial ECGs and cardiac troponins prior to doses 2, 3, and 4, and if normal, reduce to every 3 doses until completion of therapy; cardiovascular risk assessment every 6 to 12 months in high-risk patients who require long-term (>12 months) therapy, consider cardiovascular risk assessment every 6 to 12 months in all patients requiring long-term therapy (ESC [Lyon 2022]). Refer to a cardiologist when clinically indicated.
Additional suggested monitoring (ASCO [Schneider 2021):
Prior to therapy: CBC with differential, serum chemistries, creatine kinase, comprehensive clinical assessment including performance status, weight, BMI, heart rate, BP, and oxygen saturation; consider chest x-ray, ECG, and CT scan; assess history of autoimmune conditions, organ-specific disease, endocrinopathies, neuropathy, and infectious disease; assess bowel habits, respiratory symptoms, skin (for rash), arthralgias, and neurologic symptoms.
During therapy: Assess BP, weight, heart rate, and oxygen saturation; assess for infections, screen for hyperglycemia/diabetes (polyuria, polydipsia, weight loss); eye exam (including intraocular pressure after 6 weeks), CBC with differential, serum chemistries, and creatine kinase; monitor bone mineral density (with long-term therapy).
Tislelizumab is a recombinant humanized IgG4 kappa monoclonal antibody that inhibits programmed death-1 (PD-1) activity by binding to PD-1 and blocking the interactions with the ligands PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of immune response, including anti-tumor response. PD-1 ligand upregulation may occur in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Blocking PD-1 activity has resulted in decreased tumor growth in animal models.
Distribution: Vd: 6.42 L.
Half-life elimination: 24 days.
Excretion: Clearance: 0.153 L/day.
