jor birth defectsand miscarriage in clinically recognizedpregnancies is 2% to 4% and 15% to 20%, respectively.
Data
Animal Data
An enhanced pre- and post-natal developmental toxicity study was conducted in cynomolgusmonkeys. Pregnant cynomolgus monkeys were administered weekly subcutaneous doses ofrisankizumab-rzaa of 5 or 50 mg/kg from gestation day 20 to parturition and the cynomolgusmonkeys (mother and infants) were monitored for 6 months after delivery. No maternal toxicitywas noted in this study. There were no treatment-related effects on growth and development,malformations, developmental immunotoxicology or neurobehavioral development. However, adose-dependent increase in fetal/infant loss was noted in the risankizumab-rzaa-treated groups(32% and 43% in the 5 mg/kg and 50 mg/kg groups, respectively) compared to the vehiclecontrol group (19%). The increased fetal/infant loss in the 50 mg/kg group was considered to berelated to risankizumab-rzaa treatment. The no observed adverse effect level (NOAEL) formaternal toxicity was identified as 50 mg/kg (20 times the MRHD, based on mg/kg comparison)and the NOAEL for developmental toxicity was identified as 5 mg/kg (2 times the MRHD, basedon mg/kg comparison). In the infants, mean serum concentrations increased in a dose-dependentmanner and were approximately 17-86% of the respective maternal concentrations. Followingdelivery, most adult female cynomolgus monkeys and all infants from the risankizumabrzaa-treatedgroups had measurable serum concentrations of risankizumab-rzaa up to 91 dayspostpartum. Serum concentrations were below detectable levels at 180 days postpartum.
8.2 Lactation
Risk Summary
There are no data on the presence of risankizumab-rzaa in human milk, the effects on thebreastfed infant, or the effects on milk production. Maternal IgG is known to be present inhuman milk. The developmental and health benefits of breastfeeding should be considered alongwith the mother's clinical need for SKYRIZI and any potential adverse effects on the breastfedinfant from SKYRIZI or from the underlying maternal condition.
8.4 Pediatric Use
The safety and efficacy of SKYRIZI in pediatric patients less than 18 years of age have not yetbeen established.
8.5 Geriatric Use
Of the 2234 subjects with plaque psoriasis exposed to SKYRIZI, 243 subjects were 65 years orolder and 24 subjects were 75 years or older. No overall differences in risankizumab-rzaaexposure, safety or effectiveness were observed between older and younger subjects whoreceived SKYRIZI. However, the number of subjects aged 65 years and older was not sufficientto determine whether they respond differently from younger subjects.
10 OVERDOSAGE
In the event of overdosage, monitor the patient for any signs or symptoms of adverse reactionsand administer appropriate symptomatic treatment immediately.
11 DESCRIPTION
Risankizumab-rzaa, an interleukin-23 antagonist, is a humanized immunoglobulin G1 (IgG1)monoclonal antibody. Risankizumab-rzaa is produced in a mammalian cell line usingrecombinant DNA technology.
SKYRIZI (risankizumab-rzaa) injection is a sterile, preservative-free, colorless to slightlyyellow, and clear to slightly opalescent solution for subcutaneous use.
Each prefilled syringe delivers 0.83 mL containing 75 mg risankizumab-rzaa, disodium succinatehexahydrate (0.88 mg), polysorbate 20 (0.17 mg), sorbitol (34 mg), succinic acid (0.049 mg),an |
