- Actemra 20 mg
- Actemra injection
- Actemra 4 mg
- Actemra dosage
- Actemra drug
- Actemra action
- Actemra 50 mg
- Actemra side effects
- Actemra effects of
- Actemra adverse effects
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What else should I know about tocilizumab?
Injection: 20 mg/mlHow should I keep tocilizumab stored?
Tocilizumab should be stored refrigerated at 2 to 8 C (36 to 46 F).
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FDA prescribing information for Actemra
Drug Abuse and Dependence
No studies on the potential for Actemra to cause dependence have been performed. However, there is no evidence from the available data that Actemra treatment results in dependence.
Tocilizumab is a recombinant humanized anti-human interleukin 6 (IL-6) receptor monoclonal antibody of the immunoglobulin IgG1κ (gamma 1, kappa) subclass with a typical H2L2 polypeptide structure. Each light chain and heavy chain consists of 214 and 448 amino acids, respectively. The four polypeptide chains are linked intra- and inter-molecularly by disulfide bonds. Actemra has a molecular weight of approximately 148 kDa. The antibody is produced in mammalian (Chinese hamster ovary) cells.
Actemra (tocilizumab) injection is supplied as a sterile, preservative-free solution for further dilution prior to intravenous infusion at a concentration of 20 mg/mL. Actemra is a clear, colorless to pale yellow liquid, with a pH of about 6.5. Single-dose vials are available for intravenous administration containing 80 mg/4 mL, 200 mg/10 mL, or 400 mg/20 mL of Actemra. Injectable solutions of Actemra are formulated in an aqueous solution containing disodium phosphate dodecahydrate and sodium dihydrogen phosphate dehydrate (as a 15 mmol per L phosphate buffer), polysorbate 80 (0.5 mg per mL), and sucrose (50 mg per mL).
Actemra (tocilizumab) injection is supplied as a sterile, clear, colorless to slightly yellowish, preservative-free liquid solution for subcutaneous administration with a pH of approximately 6.0. It is supplied in a 1 mL ready-to-use, single-use prefilled syringe (PFS) with a needle safety device. Each prefilled syringe delivers 0.9 mL (162 mg) of Actemra, in a histidine buffered solution composed of Actemra (180 mg/mL), polysorbate 80, L-histidine and L-histidine monohydrochloride, L-arginine and L-arginine hydrochloride, L-methionine, and water for injection.
Actemra - Clinical Pharmacology
Mechanism of Action
Tocilizumab binds to both soluble and membrane-bound IL-6 receptors (sIL-6R and mIL-6R), and has been shown to inhibit IL-6-mediated signaling through these receptors. IL-6 is a pleiotropic pro-inflammatory cytokine produced by a variety of cell types including T- and B-cells, lymphocytes, monocytes and fibroblasts. IL-6 has been shown to be involved in diverse physiological processes such as T-cell activation, induction of immunoglobulin secretion, initiation of hepatic acute phase protein synthesis, and stimulation of hematopoietic precursor cell proliferation and differentiation. IL-6 is also produced by synovial and endothelial cells leading to local production of IL-6 in joints affected by inflammatory processes such as rheumatoid arthritis.
In clinical studies in RA patients with the 4 mg per kg and 8 mg per kg IV doses or the 162 mg weekly and every other weekly SC doses of Actemra, decreases in levels of C-reactive protein (CRP) to within normal ranges were seen as early as week 2. Changes in pharmacodynamic parameters were observed (i.e., decreases in rheumatoid factor, erythrocyte sedimentation rate (ESR), serum amyloid A and increases in hemoglobin) with doses, however the greatest improvements were observed with 8 mg per kg Actemra. Pharmacodynamic changes were also observed to occur after Actemra administration in GCA, PJIA, and SJIA patients (decreases in CRP, ESR, and increases in hemoglobin). The relationship between these pharmacodynamic findings and clinical efficacy is not known.
In healthy subjects administered Actemra in doses from 2 to 28 mg per kg intravenously and 81 to 162 mg subcutaneously, absolute neutrophil counts decreased to the nadir 3 to 5 days following Actemra administration. Thereafter, neutrophils recovered towards baseline in a dose dependent manner. Rheumatoid arthritis and GCA patients demonstrated a similar pattern of absolute neutrophil counts following Actemra administration [see Warnings and Precautions (5.3)].
Rheumatoid ArthritisIntravenous Administration
The pharmacokinetics characterized in healthy subjects and RA patients suggested that PK is similar between the two populations. The clearance (CL) of tocilizumab decreased with increased doses. At the 10 mg per kg single dose in RA patients, mean CL was 0.29 ± 0.10 mL per hr per kg and mean apparent terminal t1/2 was 151 ± 59 hours (6.3 days).
The pharmacokinetics of tocilizumab were determined using a population pharmacokinetic analysis of 1793 rheumatoid arthritis patients treated with Actemra 4 and 8 mg per kg every 4 weeks for 24 weeks.
The pharmacokinetic parameters of tocilizumab did not change with time. A more than dose-proportional increase in area under the curve (AUC) and trough concentration (Cmin) was observed for doses of 4 and 8 mg per kg every 4 weeks. Maximum concentration (Cmax) increased dose-proportionally. At steady-state, estimated AUC and Cmin were 2.7 and 6.5-fold higher at 8 mg per kg as compared to 4 mg per kg, respectively. In a long-term study with dosing for 104 weeks, observed Cmin was sustained over time.
For doses of Actemra 4 mg per kg given every 4 weeks, the estimated mean (± SD) steady-state AUC, Cmin and Cmax of tocilizumab were 13000 ± 5800 mcg∙h per mL, 1.49 ± 2.13 mcg per mL, and 88.3 ± 41.4 mcg per mL, respectively. The accumulation ratios for AUC and Cmax were 1.11 and 1.02, respectively. The accumulation ratio was higher for Cmin (1.96). Steady-state was reached following the first administration for Cmax and AUC, respectively, and after 16 weeks Cmin. For doses of Actemra 8 mg per kg given every 4 weeks, the estimated mean (± SD) steady-state AUC, Cmin and Cmax of tocilizumab were 35000 ± 15500 mcg∙h per mL, 9.74 ± 10.5 mcg per mL, and 183 ± 85.6 mcg per mL, respectively. The accumulation ratios for AUC and Cmax were 1.22 and 1.06, respectively. The accumulation ratio was higher for Cmin (2.35). Steady-state was reached following the first administration and after 8 and 20 weeks for Cmax, AUC, and Cmin, respectively. Tocilizumab AUC, Cmin and Cmax increased with increase of body weight. At body weight at or above 100 kg, the estimated mean (± SD) steady-state AUC, Cmin and Cmax of tocilizumab were 55500 ± 14100 mcg∙h per mL, 19.0 ± 12.0 mcg per mL, and 269 ± 57 mcg per mL, respectively, which are higher than mean exposure values for the patient population. Therefore, Actemra doses exceeding 800 mg per infusion are not recommended [see Dosage and Administration (2.1)].
Rheumatoid ArthritisSubcutaneous Administration
The pharmacokinetics of tocilizumab was characterized using a population pharmacokinetic analysis using a database composed of 1759 rheumatoid arthritis patients treated with 162 mg SC every week, 162 mg SC every other week, and 8 mg/kg every 4 weeks for 24 weeks.
The pharmacokinetic parameters of tocilizumab did not change with time. For the 162 mg every week dose, the estimated mean (±SD) steady-state AUC1week, Cmin and Cmax of tocilizumab were 8200 ± 3600 mcg∙h/mL, 44.6 ± 20.6 mcg/mL, and 50.9 ± 21.8 mcg/mL, respectively. The accumulation ratios for AUC, Cmin, and Cmax were 6.83, 6.37, and 5.47, respectively. Steady state was reached after 12 weeks for AUC, Cmin, and Cmax.
For the 162 mg every other week dose, the estimated mean (±SD) steady-state AUC2week, Cmin, and Cmax of tocilizumab were 3200 ± 2700 mcg∙h/mL, 5.6 ± 7.0 mcg/mL, and 12.3 ± 8.7 mcg/mL, respectively. The accumulation ratios for AUC, Cmin, and Cmax were 2.67, 5.6, and 2.12, respectively. Steady state was reached after 12 weeks for AUC and Cmin, and after 10 weeks for Cmax.
Giant Cell Arteritis – Subcutaneous Administration
The pharmacokinetics of tocilizumab in GCA patients was determined using a population pharmacokinetic analysis on a dataset composed of 149 GCA patients treated with 162 mg SC every week or with 162 mg SC every other week.
For the 162 mg every week dose, the estimated mean (±SD) steady-state Cavg, Cmin and Cmax of tocilizumab were 71.3 ± 30.1 mcg/mL, 68.1± 29.5 mcg/mL, and 73 ± 30.4 mcg/mL, respectively. The accumulation ratios for Cavg or AUCtau, Cmin, and Cmax were 10.9, 9.6, and 8.9, respectively. Steady state was reached after 17 weeks.
For the 162 mg every other week dose, the estimated mean (±SD) steady-state Cavg, Cmin, and Cmax of tocilizumab were 16.2 ± 11.8 mcg/mL, 11.1 ± 10.3 mcg/mL, and 19.3 ± 12.8 mcg/mL, respectively. The accumulation ratios for Cavg or AUCtau, Cmin, and Cmax were 2.8, 5.6, and 2.3 respectively. Steady-state was reached after 14 weeks.
Polyarticular Juvenile Idiopathic ArthritisIntravenous Administration
The pharmacokinetics of tocilizumab was determined using a population pharmacokinetic analysis on a database composed of 188 patients with polyarticular juvenile idiopathic arthritis.
For doses of 8 mg/kg tocilizumab (patients with a body weight at or above 30 kg) given every 4 weeks, the estimated mean (± SD) AUC4weeks, Cmax and Cmin of tocilizumab were 29500 ± 8660 mcg∙hr/mL, 182 ± 37 mcg/mL and 7.49 ± 8.2 mcg/mL, respectively.
For doses of 10 mg/kg tocilizumab (patients with a body weight less than 30 kg) given every 4 weeks, the estimated mean (± SD) AUC4weeks, Cmax and Cmin of tocilizumab were 23200 ± 6100 mcg∙hr/mL, 175 ± 32 mcg/mL and 2.35 ± 3.59 mcg/mL, respectively.
The accumulation ratios were 1.05 and 1.16 for AUC4weeks, and 1.43 and 2.22 for Cmin for 10 mg/kg (BW less than 30 kg) and 8 mg/kg (BW at or above 30 kg) doses, respectively. No accumulation for Cmax was observed.
Systemic Juvenile Idiopathic ArthritisIntravenous Administration
The pharmacokinetics of tocilizumab were determined using a population pharmacokinetic analysis on a database composed of 75 patients with SJIA treated with 8 mg per kg (patients with a body weight at or above 30 kg) or 12 mg per kg (patients with a body weight less than 30 kg), given every 2 weeks. The estimated mean (± SD) AUC2weeks, Cmax and Cmin of tocilizumab were 32200 ± 9960 mcg∙hr per mL, 245 ± 57.2 mcg per mL and 57.5 ± 23.3 mcg per mL, respectively. The accumulation ratio for Cmin (week 12 over week 2) was 3.2 ± 1.3. Steady state was reached on or after week 12. Mean estimated tocilizumab exposure parameters were similar between the two dose groups defined by body weight.
Following SC dosing in RA and GCA patients, the absorption half-life was around 4 days. The bioavailability for the SC formulation was 0.8.
In RA patients the median values of Tmax were 2.8 days after the tocilizumab every week dose and 4.7 days after the tocilizumab every other week dose.
In GCA patients, the median values of Tmax were 3 days after the tocilizumab every week dose and 4.5 days after the tocilizumab every other week dose.
Following intravenous dosing, tocilizumab undergoes biphasic elimination from the circulation. In rheumatoid arthritis patients the central volume of distribution was 3.5 L and the peripheral volume of distribution was 2.9 L, resulting in a volume of distribution at steady state of 6.4 L.
In GCA patients, the central volume of distribution was 4.09 L, the peripheral volume of distribution was 3.37 L resulting in a volume of distribution at steady state of 7.46 L.
In pediatric patients with PJIA, the central volume of distribution was 1.98 L, the peripheral volume of distribution was 2.1 L, resulting in a volume of distribution at steady state of 4.08 L.
In pediatric patients with SJIA, the central volume of distribution was 0.94 L, the peripheral volume of distribution was 1.60 L resulting in a volume of distribution at steady state of 2.54 L.
Actemra is eliminated by a combination of linear clearance and nonlinear elimination. The concentration-dependent nonlinear elimination plays a major role at low tocilizumab concentrations. Once the nonlinear pathway is saturated, at higher tocilizumab concentrations, clearance is mainly determined by the linear clearance. The saturation of the nonlinear elimination leads to an increase in exposure that is more than dose-proportional. The pharmacokinetic parameters of Actemra do not change with time.
Population pharmacokinetic analyses in any patient population tested so far indicate no relationship between apparent clearance and the presence of anti-drug antibodies.
The linear clearance in the population pharmacokinetic analysis was estimated to be 12.5 mL per h in RA patients, 6.7 mL per h in GCA patients, 5.8 mL per h in pediatric patients with PJIA, and 7.1 mL per h in pediatric patients with SJIA.
Due to the dependence of total clearance on Actemra serum concentrations, the half-life of Actemra is also concentration-dependent and varies depending on the serum concentration level.
For IV administration in RA patients, the concentration-dependent apparent t1/2 is up to 11 days for 4 mg per kg and up to 13 days for 8 mg per kg every 4 weeks in patients with RA at steady-state. For SC administration in RA patients, the concentration-dependent apparent t1/2 is up to 13 days for 162 mg every week and 5 days for 162 mg every other week in patients with RA at steady-state.
In GCA patients at steady state, the effective t1/2 of tocilizumab varied between 18.3 and 18.9 days for 162 mg SC every week dosing regimen and between 4.2 and 7.9 days for 162 mg SC every other week dosing regimen.
The t1/2 of tocilizumab in children with PJIA is up to 16 days for the two body weight categories (8 mg/kg for body weight at or above 30 kg or 10 mg/kg for body weight below 30 kg) during a dosing interval at steady state.
The t1/2 of tocilizumab in pediatric patients with SJIA is up to 23 days for the two body weight categories at week 12.
Pharmacokinetics in Special Populations
Population pharmacokinetic analyses in adult rheumatoid arthritis patients and GCA patients showed that age, gender and race did not affect the pharmacokinetics of tocilizumab. Linear clearance was found to increase with body size. In RA patients, the body weight-based dose (8 mg per kg) resulted in approximately 86% higher exposure in patients who are greater than 100 kg in comparison to patients who are less than 60 kg. There was an inverse relationship between tocilizumab exposure and body weight for flat dose SC regimens.
In GCA patients, higher exposure was observed in patients with lower body weight. For the 162 mg every week dosing regimen, the steady-state Cavg was 51% higher in patients with body weight less than 60 kg compared to patients weighing between 60 to 100 kg. For the 162 mg every other week regimen, the steady-state Cavg was 129% higher in patients with body weight less than 60 kg compared to patients weighing between 60 to 100 kg. There is limited data for patients above 100 kg (n=7).
No formal study of the effect of hepatic impairment on the pharmacokinetics of tocilizumab was conducted.
No formal study of the effect of renal impairment on the pharmacokinetics of tocilizumab was conducted.
Most of the RA and GCA patients in the population pharmacokinetic analysis had normal renal function or mild renal impairment. Mild renal impairment (estimated creatinine clearance less than 80 mL per min and at or above 50 mL per min based on Cockcroft-Gault formula) did not impact the pharmacokinetics of tocilizumab.
Approximately one-third of the patients in the GCA clinical trial had moderate renal impairment at baseline (estimated creatinine clearance of 30-59 mL/min). No impact on tocilizumab exposure was noted in these patients.
No dose adjustment is required in patients with mild or moderate renal impairment.
In vitro data suggested that IL-6 reduced mRNA expression for several CYP450 isoenzymes including CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, and this reduced expression was reversed by co-incubation with tocilizumab at clinically relevant concentrations. Accordingly, inhibition of IL-6 signaling in RA patients treated with tocilizumab may restore CYP450 activities to higher levels than those in the absence of tocilizumab leading to increased metabolism of drugs that are CYP450 substrates. Its effect on CYP2C8 or transporters (e.g., P-gp) is unknown. This is clinically relevant for CYP450 substrates with a narrow therapeutic index, where the dose is individually adjusted. Upon initiation of Actemra, in patients being treated with these types of medicinal products, therapeutic monitoring of the effect (e.g., warfarin) or drug concentration (e.g., cyclosporine or theophylline) should be performed and the individual dose of the medicinal product adjusted as needed. Caution should be exercised when Actemra is coadministered with drugs where decrease in effectiveness is undesirable, e.g., oral contraceptives (CYP3A4 substrates) [see Drug Interactions (7.2)].
Simvastatin is a CYP3A4 and OATP1B1 substrate. In 12 RA patients not treated with Actemra, receiving 40 mg simvastatin, exposures of simvastatin and its metabolite, simvastatin acid, was 4- to 10-fold and 2-fold higher, respectively, than the exposures observed in healthy subjects. One week following administration of a single infusion of Actemra (10 mg per kg), exposure of simvastatin and simvastatin acid decreased by 57% and 39%, respectively, to exposures that were similar or slightly higher than those observed in healthy subjects. Exposures of simvastatin and simvastatin acid increased upon withdrawal of Actemra in RA patients. Selection of a particular dose of simvastatin in RA patients should take into account the potentially lower exposures that may result after initiation of Actemra (due to normalization of CYP3A4) or higher exposures after discontinuation of Actemra.
Omeprazole is a CYP2C19 and CYP3A4 substrate. In RA patients receiving 10 mg omeprazole, exposure to omeprazole was approximately 2 fold higher than that observed in healthy subjects. In RA patients receiving 10 mg omeprazole, before and one week after Actemra infusion (8 mg per kg), the omeprazole AUCinf decreased by 12% for poor (N=5) and intermediate metabolizers (N=5) and by 28% for extensive metabolizers (N=8) and were slightly higher than those observed in healthy subjects.
Dextromethorphan is a CYP2D6 and CYP3A4 substrate. In 13 RA patients receiving 30 mg dextromethorphan, exposure to dextromethorphan was comparable to that in healthy subjects. However, exposure to its metabolite, dextrorphan (a CYP3A4 substrate), was a fraction of that observed in healthy subjects. One week following administration of a single infusion of Actemra (8 mg per kg), dextromethorphan exposure was decreased by approximately 5%. However, a larger decrease (29%) in dextrorphan levels was noted after Actemra infusion.
Carcinogenesis, Mutagenesis, Impairment of Fertility
No long-term animal studies have been performed to establish the carcinogenicity potential of tocilizumab. Literature indicates that the IL-6 pathway can mediate anti-tumor responses by promoting increased immune cell surveillance of the tumor microenvironment. However, available published evidence also supports that IL-6 signaling through the IL-6 receptor may be involved in pathways that lead to tumorigenesis. The malignancy risk in humans from an antibody that disrupts signaling through the IL-6 receptor, such as tocilizumab, is presently unknown.
Fertility and reproductive performance were unaffected in male and female mice that received a murine analogue of tocilizumab administered by the intravenous route at a dose of 50 mg/kg every three days.
Before receiving Actemra, tell your doctor about all of your medical conditions including if you:
- are allergic to Actemra or to any of its ingredients
- have an infection
- have liver problems
- have any stomach-area (abdominal) pain or been diagnosed with diverticulitis or ulcers in your stomach or intestines
- have had a reaction to Actemra or any of the ingredients in Actemra
- have or had a condition that affects your nervous system, such as multiple sclerosis
- have recently received or are scheduled to receive a vaccine. People who take Actemra should not receive live vaccines.
- plan to have surgery or a medical procedure
- have any other medical conditions
- are pregnant
- are breastfeeding
Actemra FDA Warning
WARNING: RISK OF SERIOUS INFECTIONS
Patients treated with Actemra are at increased risk for developing serious infections that may lead to hospitalization or death. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.
If a serious infection develops, interrupt Actemra until the infection is controlled.
Reported infections include:
- Active tuberculosis, which may present with pulmonary or extrapulmonary disease. Patients should be tested for latent tuberculosis before Actemra use and during therapy. Treatment for latent infection should be initiated prior to Actemra use.
- Invasive fungal infections, including candidiasis, aspergillosis, and pneumocystis. Patients with invasive fungal infections may present with disseminated, rather than localized, disease.
- Bacterial, viral and other infections due to opportunistic pathogens.
The risks and benefits of treatment with Actemra should be carefully considered prior to initiating therapy in patients with chronic or recurrent infection.
Patients should be closely monitored for the development of signs and symptoms of infection during and after treatment with Actemra, including the possible development of tuberculosis in patients who tested negative for latent tuberculosis infection prior to initiating therapy.
Black Box Warnings
Serious infections leading to hospitalization or death (ie, tuberculosis; bacterial, invasive fungal, viral, or other opportunistic infections) have occurred with use
Stop therapy if serious infection occurs; can restart if infection is controlled
Test for latent tuberculosis before initiating; if positive, initiate tuberculosis therapy before starting tocilizumab
Continue to monitor all patients for active tuberculosis during therapy
Risk for serious infections (see Black Box Warnings)
If a serious infection develops, interrupt therapy until infection controlled
Tocilizumab has not been studied in combination with biological DMARDs (eg, TNF antagonists, IL-1R antagonists, anti-CD20 monoclonal antibodies, selective costimulation modulators) and its use should be avoided in combination with these agents because of increased immunosuppression and risk of infection
Nonmelanoma skin cancers reported; periodic skin examination recommended
Caution if increased risk for GI perforation
May cause neutropenia, decreased platelets, elevated liver transaminases, and increased lipid parameters; monitor neutrophils, platelets, lipids, and liver function tests every 4-8 weeks
Anaphylaxis or serious hypersensitivity reactions have occurred, including fatalities, with or without concomitant arthritis therapies
Do not coadminister with live vaccines (eg, MMR, intranasal influenza); IL-6 inhibition may interfere with the normal immune response to new antigens, all patients, particularly those with PJIA and SJIA, should be current with their immunizations before initiating therapy
Pregnancy & Lactation
Pregnancy: Pregnancy exposure registry that monitors pregnancy outcomes in women exposed to during pregnancy; physicians are encouraged to register patients and pregnant women are encouraged to register themselves by calling 1-877-311-8972; the limited available data in pregnant women are not sufficient to determine whether there is a drug-associated risk for major birth defects and miscarriage; monoclonal antibodies are increasingly transported across placenta as pregnancy progresses, with largest amount transferred during third trimester; risks and benefits should be considered prior to administering live or live-attenuated vaccines to infants exposed to therapy in utero
Lactation: No information is available on presence of tocilizumab in human milk, the effects of drug on breastfed infant, or effects of drug on milk production; maternal immunoglobulin G (IgG) is present in human milk; if tocilizumab is transferred into human milk, effects of local exposure in gastrointestinal tract and potential limited systemic exposure in infant to tocilizumab are unknown; developmental and health benefits of breastfeeding should be considered along with mother’s clinical need for therapy and potential adverse effects on breastfed child from tocilizumab or from underlying maternal condition
A:Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.
B:May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.
C:Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.
D:Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.
X:Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.
NA:Information not available.
What is Actemra?
Actemra (tocilizumab) reduces the effects of a substance in the body that can cause inflammation.
Actemra is used to treat moderate to severe rheumatoid arthritis in adults. It is sometimes given together with other arthritis medicines.
Actemra is used to treat systemic juvenile idiopathic arthritis (or "Still disease") in children who are at least 2 years old. It is sometimes given together with methotrexate (Rheumatrex, Trexall).
Actemra is also used in adults to treat giant cell arteritis, or inflammation of the lining of your arteries (blood vessels that carry blood from your heart to other parts of your body).
Actemra is usually given after other medications have been tried without successful treatment of symptoms.
Tocilizumab Breastfeeding Warnings
A decision should be made to discontinue breastfeeding or discontinue the drug, taking into account the importance of the drug to the mother. Excreted into human milk: Unknown; however, endogenous immunoglobulins of the IgG isotype are excreted into human milk Excreted into animal milk: Yes Comments: -The effects in the nursing infant are unknown. -Little information is available on the clinical use of this drug during breastfeeding. Because it is a large protein molecule, the amount in milk is likely to be very low and absorption is unlikely because it is probably destroyed in the infant GI tract. Until more data become available, caution should be exercised if this drug is used during breastfeeding, especially while nursing a newborn or preterm infant.