TECENTRIQ
Clinical safety rating: caution
Comprehensive clinical and safety monograph for TECENTRIQ (TECENTRIQ).
Atezolizumab is a humanized monoclonal IgG1 antibody that binds to PD-L1, blocking its interaction with PD-1 and CD80 receptors, thereby reversing PD-L1-mediated inhibition of T-cell activation and restoring anti-tumor immune responses.
| Metabolism | Atezolizumab is a monoclonal antibody that undergoes catabolic degradation via general protein degradation pathways; no specific metabolic enzymes or pathways have been identified. |
| Excretion | Tecentriq (atezolizumab) is a monoclonal antibody; elimination occurs via intracellular catabolism into amino acids. No renal or biliary/fecal excretion of intact drug. 0% unchanged in urine or feces. |
| Half-life | Terminal elimination half-life is approximately 27 days (range: 20–35 days). This long half-life supports every-3-week dosing and reflects slow clearance typical of IgG1 antibodies. |
| Protein binding | Not specifically studied; as a monoclonal antibody, atezolizumab is not subject to conventional protein binding. Endogenous IgG binding to FcRn may influence half-life. |
| Volume of Distribution | Volume of distribution at steady state is approximately 6.9 L (range 4.8–10.3 L), equivalent to about 0.1 L/kg. Small Vd indicates limited extravascular distribution, consistent with a large protein. |
| Bioavailability | Atezolizumab is administered intravenously; bioavailability is 100% by IV route. No oral or other routes are relevant. |
| Onset of Action | Onset of clinical effect is variable; for cancer immunotherapy, tumor response may be observed after 2–3 months of treatment. No immediate onset. |
| Duration of Action | Pharmacodynamic effects persist for months due to prolonged receptor occupancy. Duration of response varies; median duration of response in clinical trials is around 29–30 months (for some indications). |
| Action Class | Programmed Cell Death 1 (PD-1) Checkpoint Inhibitors |
800 mg intravenously every 2 weeks; or 1200 mg intravenously every 3 weeks; or 1680 mg intravenously every 4 weeks.
| Dosage form | INJECTABLE |
| Renal impairment | No dose adjustment required for mild to moderate renal impairment (GFR 30-89 mL/min). Insufficient data for severe renal impairment (GFR <30 mL/min). |
| Liver impairment | No dose adjustment required for mild hepatic impairment (Child-Pugh A). Not recommended in moderate or severe hepatic impairment (Child-Pugh B or C) due to lack of data. |
| Pediatric use | Safety and efficacy not established in pediatric patients. |
| Geriatric use | No specific dose adjustment necessary; elderly patients may have increased incidence of immune-related adverse events. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for TECENTRIQ (TECENTRIQ).
| Breastfeeding | No data are available on the presence of atezolizumab in human milk, its effects on the breastfed infant, or its effects on milk production. Human IgG is known to be excreted in human milk, but the extent of absorption of intact antibodies from breast milk into neonatal circulation is likely low. However, because of the potential for serious adverse reactions in nursing infants, women are advised not to breastfeed during treatment and for at least 5 months after the last dose. The milk-to-plasma ratio (M/P) is unknown. |
| Teratogenic Risk | Atezolizumab (TECENTRIQ) is an immune checkpoint inhibitor. Based on its mechanism of action (PD-L1 blockade), it can cause fetal harm when administered to a pregnant woman. There are no adequate and well-controlled studies in pregnant women. In animal models, inhibition of PD-L1 signaling has been shown to disrupt immune tolerance and increase the risk of fetal loss, stillbirth, and preterm birth. Ignoring the developmental window, if exposure occurs during the first trimester, there is a theoretical risk of altered immune system development. During the second and third trimesters, PD-L1 inhibition may increase the risk of immune-mediated fetal injury. Human IgG antibodies cross the placenta increasingly as pregnancy progresses, with the largest transfer in the third trimester. Therefore, the risk of fetal harm is highest in the second and third trimesters, but potential risks exist throughout pregnancy. Pregnancy should be avoided during treatment and for at least 5 months after the last dose. |
■ FDA Black Box Warning
Immune-Mediated Adverse Reactions: Severe and fatal immune-mediated adverse reactions, including pneumonitis, colitis, hepatitis, endocrinopathies, nephritis, skin adverse reactions, and myocarditis, can occur. Infusion-Related Reactions: Severe or life-threatening infusion-related reactions have been reported. Complications of allogeneic hematopoietic stem cell transplantation (HSCT): Fatal and other serious complications may occur in patients who receive allogeneic HSCT before or after PD-1/PD-L1 blockade.
| Serious Effects |
None known.
| Precautions | Immune-mediated adverse reactions (pneumonitis, colitis, hepatitis, endocrinopathies, nephritis, skin reactions, myocarditis, other), infusion-related reactions, complications of allogeneic HSCT, embryo-fetal toxicity, increased mortality in patients with multiple myeloma when combined with lenalidomide and dexamethasone, increased incidence of infections, increased hepatotoxicity in patients with pre-existing autoimmune disease. |
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| Fetal Monitoring | Monitor pregnant women for potential adverse effects including fetal growth restriction, preterm labor, and immune-mediated fetal injury (e.g., pneumonitis, hepatitis, dermatitis). Perform serial ultrasound assessments to monitor fetal growth and amniotic fluid volume. Consider monitoring for maternal thyroid dysfunction, as immune checkpoint inhibitors can cause immune-mediated thyroiditis. No specific fetal heart rate monitoring is recommended, but assess for signs of fetal distress as clinically indicated. Postnatally, monitor the infant for signs of immune-mediated disorders. |
| Fertility Effects | No human data on the effect of atezolizumab on fertility. In animal studies with mice, administration of anti-PD-L1 antibody resulted in altered immune function in offspring, but no direct fertility studies have been conducted. Based on the mechanism, potential effects on male and female fertility cannot be excluded. Atezolizumab may cause hormonal changes secondary to immune-mediated endocrinopathies (e.g., hypophysitis, adrenal insufficiency) that could impair fertility. Patients should be counseled about the potential risk to reproductive capacity. |