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Risankizumab-rzaa, an interleukin-23 (IL-23) antagonist, is a humanized immunoglobulin G1 (IgG1) monoclonal antibody. Risankizumab-rzaa is produced by recombinant DNA technology in Chinese hamster ovary cells and has an approximate molecular weight of 149 kDa.
Each SKYRIZI prefilled syringe contains a sterile, preservative-free, colorless to slightly yellow, and clear to slightly opalescent solution. Each syringe delivers 90 mg of risankizumab-rzaa, and inactive ingredients polysorbate 20 (0.2 mg), sodium succinate (0.63 mg), sorbitol (41 mg), succinic acid (0.059 mg), and Water for Injection, USP. The pH is 6.2.
Each SKYRIZI prefilled pen or prefilled syringe contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each syringe and pen delivers 150 mg of risankizumab-rzaa and the inactive ingredients glacial acetic acid (0.054 mg), polysorbate 20 (0.2 mg), sodium acetate (0.75 mg), trehalose (63.33 mg), and Water for Injection, USP. The pH is 5.7.
Each SKYRIZI prefilled syringe contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each syringe delivers 180 mg of risankizumab-rzaa, and inactive ingredients glacial acetic acid (0.065 mg), polysorbate 20 (0.24 mg), sodium acetate (0.898 mg), trehalose (76.0 mg), and Water for Injection, USP. The pH is 5.7.
Each SKYRIZI prefilled cartridge contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each cartridge delivers 180 mg of risankizumab-rzaa, and the inactive ingredients glacial acetic acid (0.065 mg), polysorbate 20 (0.24 mg), sodium acetate (0.9 mg), trehalose (76 mg), and Water for Injection, USP. The pH is 5.7.
Each SKYRIZI prefilled cartridge contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each cartridge delivers 360 mg of risankizumab-rzaa, and the inactive ingredients glacial acetic acid (0.13 mg), polysorbate 20 (0.48 mg), sodium acetate (1.8 mg), trehalose (152 mg), and Water for Injection, USP. The pH is 5.7.
SKYRIZI (risankizumab-rzaa) injection 600 mg/10 mL (60 mg/mL) is a sterile, preservative- free, colorless to slightly yellow, and clear to slightly opalescent solution in a 10 mL single-dose vial.
Each 10 mL single-dose vial contains 600 mg of risankizumab-rzaa, and the inactive ingredients glacial acetic acid (0.54 mg), polysorbate 20 (2 mg), sodium acetate (7.5 mg), trehalose (633.3 mg), and Water for Injection, USP. The pH is 5.7.
SKYRIZI® is indicated for the treatment of moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy.
SKYRIZI is indicated for the treatment of active psoriatic arthritis in adults.
SKYRIZI is indicated for the treatment of moderately to severely active Crohn's disease in adults.
SKYRIZI is indicated for the treatment of moderately to severely active ulcerative colitis in adults.
The recommended dosage is 150 mg administered by subcutaneous injection at Week 0, Week 4, and every 12 weeks thereafter.
The recommended dosage is 150 mg administered by subcutaneous injection at Week 0, Week 4, and every 12 weeks thereafter.
SKYRIZI may be administered alone or in combination with non-biologic disease-modifying antirheumatic drugs (DMARDs).
The SKYRIZI “Instructions for Use” contains more detailed instructions on the preparation and administration of SKYRIZI [see Instructions for Use]. Instruct the patient to read the Instructions for Use before administration.
The recommended induction dosage of SKYRIZI is 600 mg administered by intravenous infusion over a period of at least one hour at Week 0, Week 4, and Week 8.
The recommended maintenance dosage of SKYRIZI is 180 mg or 360 mg administered by subcutaneous injection at Week 12, and every 8 weeks thereafter. Use the lowest effective dosage needed to maintain therapeutic response.
The recommended induction dosage of SKYRIZI is 1,200 mg administered by intravenous infusion over a period of at least two hours at Week 0, Week 4, and Week 8.
The recommended maintenance dosage of SKYRIZI is 180 mg or 360 mg administered by subcutaneous injection at Week 12, and every 8 weeks thereafter. Use the lowest effective dosage needed to maintain therapeutic response.
Table 1: Total Volume of Diluent Required for Intravenous Induction Dose
| Indication | Intravenous Induction Dose | Number of SKYRIZI 600 mg/10 mL Vials | Total Volume of 5% Dextrose or 0.9% Sodium Chloride Injection |
| Crohn’s disease | 600 mg | 1 | 100 mL, or 250 mL, or 500 mL |
| Ulcerative colitis | 1,200 mg | 2 | 250 mL, or 500 mL |
Using the single-dose 180 mg or 360 mg prefilled cartridge with On-Body Injector
The SKYRIZI “Instructions for Use” contains more detailed instructions on the preparation and administration of SKYRIZI [see Instructions for Use]. Instruct the patient to read the Instructions for Use before administration.
Using The 90 mg/mL or 180 mg/1.2 mL prefilled syringe:
The SKYRIZI “Instructions for Use” contains more detailed instructions on the preparation and administration of SKYRIZI [see Instructions for Use]. Instruct the patient to read the Instructions for Use before administration.
SKYRIZI Pen
SKYRIZI Prefilled Syringe
SKYRIZI Prefilled Cartridge with Supplied On-Body Injector
SKYRIZI Vial
SKYRIZI (risankizumab-rzaa) injection is supplied in the following strengths:
| Strength | Pack Size | NDC |
| Subcutaneous Injection | ||
| 150 mg/mL single-dose pen | Carton of 1 | 0074-2100-01 |
| 90 mg/mL single-dose prefilled syringe |
Carton of 2 | 0074-7040-02 |
| Carton of 4 | 0074-7042-04 | |
| 180 mg/1.2 mL (150 mg/mL) single- dose prefilled syringe |
Carton of 1 | 0074-8300-01 |
| Carton of 2 | 0074-8350-01 | |
| 150 mg/mL single-dose prefilled syringe |
Carton of 1 | 0074-1050-01 |
| 180 mg/1.2 mL (150 mg/mL) single- dose prefilled cartridge with on-body injector |
Kit | 0074-1065-01 |
| 360 mg/2.4 mL (150 mg/mL) single- dose prefilled cartridge with on-body injector |
Kit | 0074-1070-01 |
| Intravenous Infusion | ||
| 600 mg/10 mL (60 mg/mL) single- dose vial | Carton of 1 | 0074-5015-01 |
Subcutaneous Injection
SKYRIZI 150 mg/mL prefilled syringe or prefilled pen contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each prefilled syringe or prefilled pen consists of a 1 mL glass syringe with a fixed 27-gauge ½ inch needle with needle guard.
SKYRIZI 90 mg/mL prefilled syringe contains a sterile, preservative-free, colorless to slightly yellow and clear to slightly opalescent solution. Each prefilled syringe consists of a 1 mL glass syringe with a fixed 29-gauge ½ inch needle with needle guard.
SKYRIZI 180 mg/1.2 mL (150 mg/mL) prefilled syringe contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution. Each prefilled syringe consists of a 2.25 mL glass syringe with a fixed 27-gauge ½ inch needle with needle guard.
SKYRIZI 180 mg/1.2 mL (150 mg/mL) cyclic olefin polymer prefilled cartridge with a septum and cap contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution for use with supplied on-body injector administration device.
SKYRIZI 360 mg/2.4 mL (150 mg/mL) cyclic olefin polymer prefilled cartridge with a septum and cap contains a sterile, preservative-free, colorless to yellow, and clear to slightly opalescent solution for use with supplied on-body injector administration device.
Intravenous Infusion
SKYRIZI 600 mg/10 mL (60 mg/mL) vial contains a sterile and preservative-free, colorless to slightly yellow, and clear to slightly opalescent solution. Each glass vial is closed with a stopper and blue flip cap.
AbbVie Inc., North Chicago, IL 60064, U.S.A.
The following adverse reactions are discussed in other sections of labeling:
Because clinical trials are conducted under widely varying conditions, adverse drug reaction rates observed in the clinical trials of a drug cannot be directly compared with rates in the clinical trials of another drug and may not reflect the rates observed in practice.
A total of 2234 subjects were treated with SKYRIZI in clinical development trials in plaque psoriasis. Of these, 1208 subjects with psoriasis were exposed to SKYRIZI for at least one year.
Data from placebo- and active-controlled trials were pooled to evaluate the safety of SKYRIZI for up to 16 weeks. In total, 1306 subjects were evaluated in the SKYRIZI 150 mg group.
Table 2 summarizes the adverse drug reactions that occurred at a rate of at least 1% and at a higher rate in the SKYRIZI group than the placebo group during the 16-week controlled period of pooled clinical trials.
Table 2: Adverse Drug Reactions Occurring in ≥ 1% of Subjects with Plaque Psoriasis on SKYRIZI through Week 16
| Adverse Drug Reactions | SKYRIZI N = 1306 n (%) |
Placebo N = 300 n (%) |
| Upper respiratory infectionsa | 170 (13.0) | 29 (9.7) |
| Headacheb | 46 (3.5) | 6 (2.0) |
| Fatiguec | 33 (2.5) | 3 (1.0) |
| Injection site reactionsd | 19 (1.5) | 3 (1.0) |
| Tinea infectionse | 15 (1.1) | 1 (0.3) |
| a Includes: respiratory tract infection (viral, bacterial or unspecified), sinusitis (including acute), rhinitis, nasopharyngitis, pharyngitis (including viral), tonsillitis b Includes: headache, tension headache, sinus headache, cervicogenic headache c Includes: fatigue, asthenia d Includes: injection site bruising, erythema, extravasation, hematoma, hemorrhage, infection, inflammation, irritation, pain, pruritus, reaction, swelling, warmth e Includes: tinea pedis, tinea cruris, body tinea, tinea versicolor, tinea manuum, tinea infection, onychomycosis |
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Adverse drug reactions that occurred in < 1% but > 0.1% of subjects in the SKYRIZI group and at a higher rate than in the placebo group through Week 16 were folliculitis and urticaria.
In the first 16 weeks, infections occurred in 22.1% of the SKYRIZI group (90.8 events per 100 subject-years) compared with 14.7% of the placebo group (56.5 events per 100 subject-years) and did not lead to discontinuation of SKYRIZI. The rates of serious infections for the SKYRIZI group and the placebo group were ≤0.4%. Serious infections in the SKYRIZI group included cellulitis, osteomyelitis, sepsis, and herpes zoster. In Studies PsO-1 and PsO-2, through Week 52, the rate of infections (73.9 events per 100 subject-years) was similar to the rate observed during the first 16 weeks of treatment.
Through Week 52, no new adverse reactions were identified, and the rates of the adverse reactions were similar to those observed during the first 16 weeks of treatment. During this period, serious infections that led to study discontinuation included pneumonia.
The overall safety profile observed in subjects with psoriatic arthritis treated with SKYRIZI is generally consistent with the safety profile in subjects with plaque psoriasis. Additionally, in the Phase 3 placebo-controlled trials the incidence of hepatic events was higher in the SKYRIZI group (5.4%, 16.7 events per 100 patient years) compared to the placebo group (3.9%, 12.6 events per 100 patient years). Of these, the most common events that were reported more frequently in both the placebo group and the SKYRIZI group were ALT increased (placebo: n=12 (1.7%); SKYRIZI: n=16 (2.3%)), AST increased (placebo: n=9 (1.3%); SKYRIZI: n=13 (1.8%)), and GGT increased (placebo: n=5 (0.7%); SKYRIZI: n=8 (1.1%)). There were no serious hepatic events reported. The incidence of hypersensitivity reactions was higher in the SKYRIZI group (n=16, 2.3%) compared to the placebo group (n=9, 1.3%). In the Phase 3 placebo-controlled trials, hypersensitivity reactions reported at a higher rate in the SKYRIZI group included rash (placebo: n=4 (0.6%); SKYRIZI: n=5 (0.7%), allergic rhinitis (placebo: n=1 (0.1%); SKYRIZI: n=2 (0.3%), and facial swelling (placebo: n=0 (0.0%); SKYRIZI n=1 (0.1%). One case of anaphylaxis was reported in a subject who received SKYRIZI in the Phase 2 clinical trial.
SKYRIZI was studied up to 12 weeks in subjects with moderately to severely active Crohn’s disease in two randomized, double-blind, placebo-controlled induction studies (CD-1, CD-2) and a randomized, double-blind, placebo-controlled, dose-finding study (CD-4; NCT02031276). Long-term safety up to 52 weeks was evaluated in subjects who responded to induction therapy in a randomized, double-blind, placebo-controlled maintenance study (CD-3) [see Clinical Studies].
In the two induction studies (CD-1, CD-2) and the dose finding study (CD-4), 620 subjects received the SKYRIZI intravenous induction regimen at Weeks 0, 4 and 8. In the maintenance study (CD-3), 297 subjects who achieved clinical response, defined as a reduction in CDAI of at least 100 points from baseline after 12 weeks of induction treatment with intravenous SKYRIZI in studies CD-1 and CD-2, received a maintenance regimen of SKYRIZI either 180 mg or 360 mg subcutaneously at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks.
Adverse reactions reported in > 3% of subjects in induction studies and at a higher rate than placebo are shown in Table 3.
Table 3: Adverse Drug Reactions Reported in > 3% of Subjects with Crohn’s Disease Treated with SKYRIZI in Placebo-Controlled 12-Week Induction Studies (CD-1, CD-2, and CD-4)
| Adverse Drug Reactions | SKYRIZI 600 mg Intravenous Infusiona N = 620 n (%) |
Placebo N = 432 n (%) |
| Upper respiratory infectionsb | 66 (10.6) | 40 (9.3) |
| Headachec | 41 (6.6) | 24 (5.6) |
| Arthralgia | 31 (5.0) | 19 (4.4) |
| a SKYRIZI 600 mg as an intravenous infusion at Week 0, Week 4, and Week 8. b Includes: influenza like illness, nasopharyngitis, influenza, pharyngitis, upper respiratory tract infection, viral upper respiratory tract infection, COVID-19, nasal congestion, respiratory tract infection viral, viral pharyngitis, tonsillitis, upper respiratory tract inflammation c Includes: headache, tension headache |
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Adverse reactions reported in >3% of subjects in the maintenance study and at a higher rate than placebo are shown in Table 4.
Table 4: Adverse Reactions Reported in >3% of Subjects with Crohn’s Disease Treated with SKYRIZIa in Placebo-Controlled 52-Week Maintenance Study (CD-3)
| Adverse Drug Reactions | SKYRIZI 180 mg Subcutaneous Injection N = 155 n (%) |
SKYRIZI 360 mg Subcutaneous Injection N = 142 n (%) |
Placebo N = 143 n (%) |
| Arthralgia | 13 (8.4) | 13 (9.2) | 12 (8.4) |
| Abdominal painb | 9 (5.8) | 12 (8.5) | 6 (4.2) |
| Injection site reactionsc,d | 7 (4.5) | 8 (5.6) | 4 (2.8) |
| Anemia | 7 (4.5) | 7 (4.9) | 6 (4.2) |
| Pyrexia | 4 (2.6) | 7 (4.9) | 4 (2.8) |
| Back pain | 3 (1.9) | 6 (4.2) | 3 (2.1) |
| Arthropathy | 1 (0.6) | 5 (3.5) | 2 (1.4) |
| Urinary tract infection | 1 (0.6) | 5 (3.5) | 4 (2.8) |
| a SKYRIZI 180 mg or 360 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks b Includes: abdominal pain, abdominal pain upper, abdominal pain lower c Includes: injection site rash, injection site erythema, injection site swelling, injection site urticaria, injection site warmth, injection site pain, injection site hypersensitivity, injection site reaction d Some subjects had multiple occurrences of injection site reactions. In this table, injection site reactions are counted only once per subject for the rate calculations. |
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In the maintenance study (CD-3) through Week 52, the rate of infections was 32.3% (50.2 events per 100 subject-years) in subjects who received SKYRIZI 180 mg and 36.6% (60.8 events per 100 subject-years) in subjects who received SKYRIZI 360 mg compared to 36.4% (60.3 events per 100 subject-years) in subjects who received placebo after SKYRIZI induction. The rate of serious infections was 2.6% (2.7 events per 100 subject-years) in subjects who received SKYRIZI 180 mg and 5.6% (7.4 events per 100 subject-years) in subjects who received SKYRIZI 360 mg compared to 2.1% (2.4 events per 100 subject-years) in subjects who received placebo after SKYRIZI induction.
Elevations in lipid parameters (total cholesterol and low-density lipoprotein cholesterol [LDLC]) were first assessed at 4 weeks following initiation of SKYRIZI in the induction trials (CD-1, CD-2). Increases from baseline and increases relative to placebo were observed at Week 4 and remained stable to Week 12. Following SKYRIZI induction, mean total cholesterol increased by 9.4 mg/dL from baseline to a mean absolute value of 175.1 mg/dL at Week 12. Similarly, mean LDL-C increased by 6.6 mg/dL from baseline to a mean absolute value of 92.6 mg/dL at Week 12. Mean LDL-C increased by 3.1 mg/dL from baseline to a mean absolute value of 99.0 mg/dL at Week 52 with SKYRIZI 180 mg maintenance treatment and by 2.3 mg/dL from baseline to a mean absolute value of 102.2 mg/dL at Week 52 with SKYRIZI 360 mg maintenance treatment (CD-3).
SKYRIZI was studied up to 12 weeks in subjects with moderately to severely active ulcerative colitis in a randomized, double-blind, placebo-controlled induction study (UC-1) and a randomized, double-blind, placebo-controlled, dose-finding study (UC-3). Long-term safety up to 52 weeks was evaluated in subjects who responded to induction therapy in a randomized, double-blind, placebo-controlled maintenance study (UC-2) [see Clinical Studies].
In the induction studies (UC-1 and UC-3), 712 subjects received the SKYRIZI 1,200 mg intravenous induction regimen at Weeks 0, 4 and 8. In the maintenance study (UC-2), 347 subjects who achieved clinical response, defined as a decrease in mMS of ≥2 points and ≥30% from baseline and a decrease in RBS ≥1 from baseline or an absolute RBS ≤1, received a maintenance regimen of SKYRIZI either 180 mg or 360 mg subcutaneously at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks.
The adverse reaction reported in ≥3% subjects treated with SKYRIZI in the ulcerative colitis induction studies (UC-1 and UC-3) and at a higher rate than placebo was arthralgia (3% SKYRIZI vs 1% placebo).
Adverse reactions reported in ≥3% of subjects treated with SKYRIZI in the maintenance study (UC-2) and at a higher rate than placebo are shown in Table 5.
Table 5. Adverse Reactions Reported in ≥3% of Subjects with Ulcerative Colitis Treated
with SKYRIZIa in Placebo-Controlled 52-Week Maintenance Study (UC-2)
| Adverse Drug Reactions | SKYRIZI 180 mg Subcutaneous Injection N = 170 n (%) |
SKYRIZI 360 mg Subcutaneous Injection N = 177 n (%) |
Placebo N = 173 n (%) |
| Arthralgia | 9 (5.3) | 17 (9.6) | 8 (4.6) |
| Pyrexia | 8 (4.7) | 7 (4.0) | 6 (3.5) |
| Injection site reactionsb,c | 5 (2.9) | 5 (2.8) | 2 (1.2) |
| Rashd | 7 (4.1) | 1 (0.6) | 3 (1.7) |
|
a SKYRIZI 180 mg or 360 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks b Includes: application site pain, injection site erythema, injection site pain, injection site pruritus, injection site reaction c Some subjects had multiple occurrences of injection site reactions. In this table, injection site reactions are counted only once per subject for the rate calculations. d Includes: rash and rash macular |
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The rates of infections, serious infections, and lipid elevations in subjects with UC who received SKYRIZI compared to subjects who received placebo in the induction studies (UC-1 and UC-3) and maintenance study (UC-2) were similar to the rates in subjects with CD who received SKYRIZI compared to subjects who received placebo in the induction studies (CD-1, CD-2, and CD-4) and maintenance study (CD-3).
As with all therapeutic proteins, there is potential for immunogenicity. The detection of antibody formation is highly dependent on the sensitivity and specificity of the assay. Additionally, the observed incidence of antibody (including neutralizing antibody) positivity in an assay may be influenced by several factors including assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies in the studies described below with the incidence of antibodies in other studies or to other products, including other risankizumab products, may be misleading.
By Week 52, approximately 24% (263/1079) of subjects treated with SKYRIZI at the recommended dose developed antibodies to risankizumab-rzaa. Of the subjects who developed antibodies to risankizumab-rzaa, approximately 57% (14% of all subjects treated with SKYRIZI) had antibodies that were classified as neutralizing. Higher antibody titers in approximately 1% of subjects treated with SKYRIZI were associated with lower risankizumab-rzaa concentrations and reduced clinical response.
By Week 28, approximately 12.1% (79/652) of subjects treated with SKYRIZI at the recommended dose developed antibodies to risankizumab-rzaa. None of the subjects who developed antibodies to risankizumab-rzaa had antibodies that were classified as neutralizing. Antibodies to risankizumab-rzaa were not associated with changes in clinical response for psoriatic arthritis. A higher proportion of subjects with anti-drug antibodies experienced hypersensitivity reactions (6.3% (5/79)) and injection site reactions (2.5% (2/79)) compared to subjects without anti-drug antibodies (3.8% (22/574) with hypersensitivity reactions and 0.7% (4/574) with injection site reactions). None of these hypersensitivity and injection site reactions led to discontinuation of risankizumab-rzaa.
By Week 64, antibodies to risankizumab-rzaa developed in approximately 3.4% (2/58) of subjects treated with SKYRIZI induction followed by 360 mg maintenance regimen. No subjects (0/57) treated with SKYRIZI induction followed by 180 mg maintenance regimen developed antibodies to risankizumab-rzaa. None of the subjects who developed antibodies to risankizumab-rzaa had antibodies that were classified as neutralizing.
By Week 64, antibodies to risankizumab-rzaa developed in approximately 8.9% (8/90) or 4.4% (4/91) of subjects treated with SKYRIZI induction followed by the 180 mg or 360 mg maintenance regimen, respectively. Of the subjects who developed antibodies to risankizumabrzaa, 75% (6.7% of all subjects treated with SKYRIZI induction followed by the 180 mg maintenance regimen) or 50% (2.2% of all subjects treated with SKYRIZI induction followed by the 360 mg maintenance regimen), respectively, had antibodies that were classified as neutralizing.
The following adverse reactions have been reported during post-approval of SKYRIZI. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to SKYRIZI exposure:
No Information provided
Included as part of the PRECAUTIONS section.
Serious hypersensitivity reactions, including anaphylaxis, have been reported with use of SKYRIZI. If a serious hypersensitivity reaction occurs, discontinue SKYRIZI and initiate appropriate therapy immediately [see ADVERSE REACTIONS].
SKYRIZI may increase the risk of infections [see ADVERSE REACTIONS].
Treatment with SKYRIZI should not be initiated in patients with any clinically important active infection until the infection resolves or is adequately treated.
In patients with a chronic infection or a history of recurrent infection, consider the risks and benefits prior to prescribing SKYRIZI. Instruct patients to seek medical advice if signs or symptoms of clinically important infection occur. If a patient develops such an infection or is not responding to standard therapy, monitor the patient closely and do not administer SKYRIZI until the infection resolves.
Evaluate patients for tuberculosis (TB) infection prior to initiating treatment with SKYRIZI. Across the Phase 3 psoriasis clinical studies, of the 72 subjects with latent TB who were concurrently treated with SKYRIZI and appropriate TB prophylaxis during the studies, none developed active TB during the mean follow-up of 61 weeks on SKYRIZI. Two subjects taking isoniazid for treatment of latent TB discontinued treatment due to liver injury. Of the 31 subjects from the PsO-3 study with latent TB who did not receive prophylaxis during the study, none developed active TB during the mean follow-up of 55 weeks on SKYRIZI. Consider anti-TB therapy prior to initiating SKYRIZI in patients with a past history of latent or active TB in whom an adequate course of treatment cannot be confirmed. Monitor patients for signs and symptoms of active TB during and after SKYRIZI treatment. Do not administer SKYRIZI to patients with active TB.
A serious adverse reaction of drug-induced liver injury in conjunction with a rash that required hospitalization was reported in a patient with Crohn's disease (ALT 54x ULN, AST 30x ULN, and total bilirubin 2.2x ULN) following two 600 mg intravenous doses of SKYRIZI. The liver test abnormalities resolved following administration of steroids. SKYRIZI was subsequently discontinued.
For the treatment of Crohn's disease and ulcerative colitis, evaluate liver enzymes and bilirubin at baseline, and during induction at least up to 12 weeks of treatment. Monitor thereafter according to routine patient management.
Consider other treatment options in patients with evidence of liver cirrhosis. Prompt investigation of the cause of liver enzyme elevation is recommended to identify potential cases of drug-induced liver injury. Interrupt treatment if drug-induced liver injury is suspected, until this diagnosis is excluded. Instruct patients to seek immediate medical attention if they experience symptoms suggestive of hepatic dysfunction.
Avoid use of live vaccines in patients treated with SKYRIZI. Medications that interact with the immune system may increase the risk of infection following administration of live vaccines. Prior to initiating therapy with SKYRIZI, complete all age-appropriate vaccinations according to current immunization guidelines. No data are available on the response to live or inactive vaccines.
Advise the patient and/or caregiver to read the FDA-approved patient labeling (Medication Guide and Instructions for Use).
Advise patients to discontinue SKYRIZI and seek immediate medical attention if they experience any symptoms of serious hypersensitivity reactions [see Warnings and Precautions (5.1)].
Inform patients that SKYRIZI may lower the ability of their immune system to fight infections. Instruct patients of the importance of communicating any history of infections to the healthcare provider and contacting their healthcare provider if they develop any symptoms of an infection [see Warnings and Precautions (5.2)].
Inform patients that SKYRIZI may cause liver injury, especially during the initial 12 weeks of treatment. Instruct patients to seek immediate medical attention if they experience symptoms suggestive of liver dysfunction. (e.g., unexplained rash, nausea, vomiting, abdominal pain, fatigue, anorexia, or jaundice and/or dark urine) [see Warnings and Precautions (5.4)].
Advise patients that vaccination with live vaccines is not recommended during SKYRIZI treatment and immediately prior to or after SKYRIZI treatment. Medications that interact with the immune system may increase the risk of infection following administration of live vaccines. Instruct patients to inform the healthcare practitioner that they are taking SKYRIZI prior to a potential vaccination [see Warnings and Precautions (5.5)].
Instruct patients or caregivers to perform the first self-injected dose under the supervision and guidance of a qualified healthcare professional for training in preparation and administration of SKYRIZI, including choosing anatomical sites for administration, and proper subcutaneous injection technique [see Instructions for Use].
If using SKYRIZI 90 mg/mL, instruct patients or caregivers to administer two 90 mg single-dose syringes to achieve the full 180 mg maintenance dose or four 90 mg single-dose syringes to achieve the full 360 mg maintenance dose of SKYRIZI for Crohn’s disease or ulcerative colitis [see Instructions for Use].
If using SKYRIZI 180 mg/1.2 mL, instruct patients or caregivers to administer one 180 mg single-dose syringe to achieve the full 180 mg maintenance dose or two 180 mg single-dose syringes to achieve the full 360 mg maintenance dose of SKYRIZI for Crohn’s disease or ulcerative colitis [see Instructions for Use].
Instruct patients or caregivers in the technique of pen or syringe disposal [see Instructions forUse].
Advise patients that there is a pregnancy registry that monitors pregnancy outcomes in women exposed to SKYRIZI during pregnancy [see Use in Specific Populations (8.1)].
Carcinogenicity and mutagenicity studies have not been conducted with SKYRIZI.
No effects on male fertility parameters were observed in sexually mature male cynomolgus monkeys dosed weekly for 26 weeks with 50 mg/kg risankizumab-rzaa at 4 times the exposure (AUC) in humans administered the maximum recommended induction dose (1,200 mg) and 39 times the exposure in humans administered the maximum recommended maintenance dose (360 mg).
There is a pregnancy exposure registry that monitors outcomes in women who become pregnant while treated with SKYRIZI. Patients should be encouraged to enroll by calling 1-877-302-2161 or visiting https://glowpregnancyregistry.com.
Available pharmacovigilance and clinical trial data with risankizumab use in pregnant women are insufficient to establish a drug-associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. Although there are no data on risankizumab-rzaa, monoclonal antibodies can be actively transported across the placenta, and SKYRIZI may cause immunosuppression in the in utero-exposed infant. There are adverse pregnancy outcomes in women with inflammatory bowel disease (see Clinical Considerations).
In an enhanced pre- and post-natal developmental toxicity study, pregnant cynomolgus monkeys were administered subcutaneous doses of 5 or 50 mg/kg risankizumab-rzaa once weekly during the period of organogenesis up to parturition. Increased fetal/infant loss was noted in pregnant monkeys at the 50 mg/kg dose (see Data). The 50 mg/kg dose in pregnant monkeys resulted in approximately 5 times the exposure (AUC) in humans administered the maximum recommended induction dose (1,200 mg) and 32 times the exposure (AUC) to the maximum recommended maintenance dose (360 mg). No risankizumab-rzaa-related effects on functional or immunological development were observed in infant monkeys from birth through 6 months of age. The clinical significance of these findings for humans is unknown.
All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. The background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively.
Disease-Associated Maternal And Embryo/Fetal Risk
Published data suggest that the risk of adverse pregnancy outcomes in women with inflammatory bowel disease is associated with increased disease activity. Adverse pregnancy outcomes include preterm delivery (before 37 weeks of gestation), low birth weight (less than 2,500 g) infants, and small for gestational age at birth.
Fetal/Neonatal adverse reactions
Transport of endogenous IgG antibodies across the placenta increases as pregnancy progresses, and peaks during the third trimester. Because risankizumab may interfere with immune response to infections, risks and benefits should be considered prior to administering live vaccines to infants exposed to SKYRIZI in utero. There are insufficient data regarding infant serum levels of risankizumab at birth and the duration of persistence of risankizumab in infant serum after birth. Although a specific timeframe to delay live virus immunizations in infants exposed in utero is unknown, a minimum of 5 months after birth should be considered because of the half-life of the product.
Animal Data
An enhanced pre- and post-natal developmental toxicity study was conducted in cynomolgus monkeys. Pregnant cynomolgus monkeys were administered weekly subcutaneous doses of risankizumab-rzaa of 5 or 50 mg/kg from gestation day 20 to parturition, and the cynomolgus monkeys (mother and infants) were monitored for 6 months after delivery. No maternal toxicity was noted in this study. There were no treatment-related effects on growth and development, malformations, developmental immunotoxicology, or neurobehavioral development. However, a dose-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 with the vehicle control group (19%). The increased fetal/infant loss in the 50 mg/kg group was considered to be related to risankizumab-rzaa treatment. The no-observed adverse effect level (NOAEL) for maternal toxicity was identified as 50 mg/kg, and the NOAEL for developmental toxicity was identified as 5 mg/kg. The 5 mg/kg dose in pregnant monkeys resulted in approximately 0.6 times the exposure (AUC) in humans administered the maximum recommended induction dose (1,200 mg) and 5 times the exposure (AUC) in humans administered the maximum recommended maintenance dose (360 mg). In the infants, mean serum concentrations increased in a dose-dependent manner and were approximately 17%-86% of the respective maternal concentrations. Following delivery, most adult female cynomolgus monkeys and all infants from the risankizumab-rzaa-treated groups had measurable serum concentrations of risankizumab-rzaa up to 91 days postpartum. Serum concentrations were below detectable levels at 180 days postpartum.
There are no data on the presence of risankizumab-rzaa in human milk, the effects on the breastfed infant, or the effects on milk production. Endogenous maternal IgG and monoclonal antibodies are transferred in human milk. The effects of local gastrointestinal exposure and limited systemic exposure in the breastfed infant to risankizumab-rzaa are unknown. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for SKYRIZI and any potential adverse effects on the breastfed infant from SKYRIZI or from the underlying maternal condition.
The safety and effectiveness of SKYRIZI have not been established in pediatric patients.
Of the 6,862 subjects exposed to SKYRIZI, a total of 664 were 65 years or older (243 subjects with plaque psoriasis, 246 subjects with psoriatic arthritis, 72 subjects with Crohn's disease and 103 subjects with ulcerative colitis), and 71 subjects were 75 years or older.
Clinical studies of SKYRIZI, within each indication, did not include sufficient numbers of subjects 65 years of age and older to determine whether they respond differently from younger adult subjects.
No clinically meaningful differences in the pharmacokinetics of risankizumab-rzaa were observed based on age[see CLINICAL PHARMACOLOGY].
No information provided
SKYRIZI is contraindicated in patients with a history of serious hypersensitivity reaction to risankizumab-rzaa or any of the excipients [see Warnings and Precautions (5.1)].
Risankizumab-rzaa is a humanized IgG1 monoclonal antibody that selectively binds to the p19 subunit of human IL-23 cytokine and inhibits its interaction with the IL-23 receptor. IL-23 is a naturally occurring cytokine that is involved in inflammatory and immune responses.
Risankizumab-rzaa inhibits the release of pro-inflammatory cytokines and chemokines.
No formal pharmacodynamics studies have been conducted with risankizumab-rzaa.
Risankizumab-rzaa plasma concentrations, after single dose administration increased dose proportionally from 18 mg to 360 mg when administered subcutaneously (0.12 to 2.4 times the lowest recommended dose and 0.05 to 1 times the highest recommended dose) and from 200 mg to 1,800 mg when administered as an up to 3-hour intravenous infusion (0.2 to 3 times the recommended dose) in healthy subjects.
In subjects with plaque psoriasis treated with 150 mg subcutaneously at Weeks 0, 4, and every 12 weeks thereafter, steady-state peak concentration (Cmax) and trough concentration (Ctrough) are estimated to be 12 mcg/mL and 2 mcg/mL, respectively.
With the same subcutaneous dosing regimen, the pharmacokinetics of risankizumab-rzaa in subjects with psoriatic arthritis were similar to that in subjects with plaque psoriasis.
In subjects with Crohn]s disease treated with 600 mg intravenous induction dose at Weeks 0, 4, and 8, followed by 180 mg or 360 mg subcutaneous maintenance dose at Week 12 and every 8 weeks thereafter, the median Cmax and Ctrough are estimated to be 156 mcg/mL and 38.8 mcg/mL, respectively, during Weeks 8-12; and the steady state median Cmax and Ctrough are estimated to be 14.0 mcg/mL and 4.1 mcg/mL, respectively for 180 mg or 28.0 mcg/mL and 8.1 mcg/mL, respectively, for 360 mg, during Weeks 40-48.
In subjects with ulcerative colitis treated with 1,200 mg intravenous induction dose at Weeks 0, 4, and 8, followed by 180 mg or 360 mg subcutaneous maintenance dose at Week 12 and every 8 weeks thereafter, the median Cmax and Ctrough are estimated to be 350 and 87.7 mcg/mL, respectively, during the induction period (Weeks 8-12); and the steady state median Cmax and Ctrough are estimated to be 19.6 and 4.64 μg/mL, respectively, for 180 mg or 39.2 mcg/mL and 9.29 mcg/mL, respectively, for 360 mg, during the maintenance period (Weeks 40-48).
Based on population pharmacokinetic analyses, the pharmacokinetics of risankizumab-rzaa in subjects with ulcerative colitis was generally similar to that in subjects with Crohn]s disease.
The absolute bioavailability of risankizumab-rzaa was estimated to be 74 to 89% following subcutaneous injection. In healthy subjects, following administration of a single subcutaneous dose, Cmax was reached by 3 to 14 days.
The estimated steady-state volume of distribution (inter-subject CV%) was 11.2 L (34%) in subjects with plaque psoriasis, and 7.68 L (64%) in subjects with Crohn's disease.
The estimated systemic clearance (inter-subject CV%) was 0.31 L/day (24%) and 0.30 L/day (34%) and terminal elimination half-life was approximately 28 days and 21 days in subjects with plaque psoriasis and Crohn's disease, respectively.
Metabolism
The metabolic pathway of risankizumab-rzaa has not been characterized. As a humanized IgG1 monoclonal antibody, risankizumab-rzaa is expected to be degraded into small peptides and amino acids via catabolic pathways in a manner similar to endogenous IgG.
Risankizumab-rzaa exposures (Ctrough) in geriatric patients (≥65 years) are comparable to those in younger adult patients within each indication. No studies have been conducted to determine the effect of renal or hepatic impairment on the pharmacokinetics of risankizumab-rzaa.
Risankizumab-rzaa clearance and volume of distribution increase and plasma concentrations decrease as body weight increases; however, no dose adjustment is recommended based on body weight.
No clinically significant changes in exposure of caffeine (CYP1A2 substrate), warfarin (CYP2C9 substrate), omeprazole (CYP2C19 substrate), metoprolol (CYP2D6 substrate), or midazolam (CYP3A substrate) were observed when used concomitantly with risankizumab-rzaa in subjects with plaque psoriasis (risankizumab-rzaa 150 mg administered subcutaneously at Weeks 0, 4, 8, and 12) and subjects with Crohn's disease or ulcerative colitis (risankizumab-rzaa 1,800 mg administered intravenously at Weeks 0, 4, and 8, i.e., 3 times and 1.5 times the recommended dose for Crohn's disease and ulcerative colitis, respectively).
Four multicenter, randomized, double-blind studies [PsO-1 (NCT02684370), PsO-2 (NCT02684357), PsO-3 (NCT02672852), and PsO-4 (NCT02694523)] enrolled 2,109 subjects 18 years of age and older with moderate to severe plaque psoriasis who had a body surface area (BSA) involvement of ≥10%, a static Physician's Global Assessment (sPGA) score of ≥3 (“moderate”) in the overall assessment (plaque thickness/induration, erythema, and scaling) of psoriasis on a severity scale of 0 to 4, and a Psoriasis Area and Severity Index (PASI) score ≥12.
Overall, subjects had a median baseline PASI score of 17.8 and a median BSA of 20%. Baseline sPGA score was 4 (“severe”) in 19% of subjects. A total of 10% of study subjects had a history of diagnosed psoriatic arthritis.
Across all studies, 38% of subjects had received prior phototherapy, 48% had received prior nonbiologic systemic therapy, and 42% had received prior biologic therapy for the treatment of psoriasis.
In studies PsO-1 and PsO-2, 997 subjects were enrolled (including 598 subjects randomized to the SKYRIZI 150 mg group, 200 subjects randomized to the placebo group, and 199 to the biologic active control group). Subjects received treatment at Weeks 0, 4, and every 12 weeks thereafter.
Both studies assessed the responses at Week 16 compared with placebo for the two co-primary endpoints:
Secondary endpoints included the proportion of subjects who achieved PASI 100, sPGA 0, and Psoriasis Symptom Scale (PSS) 0 at Week 16.
The results are presented in Table 6.
Table 6: Efficacy Results at Week 16 in Adults with Plaque Psoriasis in PsO-1 and PsO-2
| PsO-1 | PsO-2 | |||
| SKYRIZI (N=304) n (%) |
Placebo (N=102) n (%) |
SKYRIZI (N=294) n (%) |
Placebo (N=98) n (%) | |
| sPGA 0 or 1 (“clear or almost clear”)a | 267 (88) | 8 (8) | 246 (84) | 5 (5) |
| PASI 90a | 229 (75) | 5 (5) | 220 (75) | 2 (2) |
| sPGA 0 (“clear”) | 112 (37) | 2 (2) | 150 (51) | 3 (3) |
| PASI 100 | 109 (36) | 0 (0) | 149 (51) | 2 (2) |
| a Co-primary endpoints | ||||
Examination of age, gender, race, body weight, baseline PASI score and previous treatment with systemic or biologic agents did not identify differences in response to SKYRIZI among these subgroups at Week 16.
In PsO-1 and PsO-2 at Week 52, subjects receiving SKYRIZI achieved sPGA 0 (58% and 60%, respectively), PASI 90 (82% and 81%, respectively), and PASI 100 (56% and 60%, respectively).
Patient Reported Outcomes
Improvements in signs and symptoms related to pain, redness, itching and burning at Week 16 compared to placebo were observed in both studies as assessed by the PSS. In PsO-1 and PsO-2, about 30% of the subjects who received SKYRIZI achieved PSS 0 (“none”) at Week 16 compared to 1% of the subjects who received placebo.
Study PsO-3 enrolled 507 subjects (407 randomized to SKYRIZI 150 mg and 100 to placebo). Subjects received treatment at Weeks 0, 4, and every 12 weeks thereafter.
At Week 16, SKYRIZI was superior to placebo on the co-primary endpoints of sPGA 0 or 1 (84% SKYRIZI and 7% placebo) and PASI 90 (73% SKYRIZI and 2% placebo). The respective response rates for SKYRIZI and placebo at Week 16 were: sPGA 0 (46% SKYRIZI and 1% placebo); PASI 100 (47% SKYRIZI and 1% placebo); and PASI 75 (89% SKYRIZI and 8% placebo).
In PsO-1 and PsO-2, among the subjects who received SKYRIZI and had PASI 100 at Week 16, 80% (206/258) of the subjects who continued on SKYRIZI had PASI 100 at Week 52. For PASI 90 responders at Week 16, 88% (398/450) of the subjects had PASI 90 at Week 52.
In PsO-3, subjects who were originally on SKYRIZI and had sPGA 0 or 1 at Week 28 were rerandomized to continue SKYRIZI every 12 weeks or withdrawal of therapy. At Week 52, 87% (97/111) of the subjects re-randomized to continue treatment with SKYRIZI had sPGA 0 or 1 compared to 61% (138/225) who were re-randomized to withdrawal of SKYRIZI.
The safety and efficacy of SKYRIZI were assessed in 1407 subjects in 2 randomized, doubleblind, placebo-controlled studies (964 in PsA-1 [NCT03675308] and 443 in PsA-2 [NCT03671148]) in subjects 18 years and older with active psoriatic arthritis (PsA).
Subjects in these studies had a diagnosis of PsA for at least 6 months based on the Classification Criteria for Psoriatic Arthritis (CASPAR), a median duration of PsA of 4.9 years at baseline, ≥ 5 tender joints and ≥ 5 swollen joints, and active plaque psoriasis or psoriatic nail disease at baseline. Regarding baseline clinical presentation, 55.9% of subjects had ≥3% BSA with active plaque psoriasis; 63.4% and 27.9% of subjects had enthesitis and dactylitis, respectively. In PsA- 1 where psoriatic nail disease was further assessed, 67.3% had psoriatic nail disease.
In PsA-1, all subjects had a previous inadequate response or intolerance to non-biologic DMARD therapy and were biologic naive. In PsA-2, 53.5% of subjects had a previous inadequate response or intolerance to non-biologic DMARD therapy, and 46.5% of subjects had a previous inadequate response or intolerance to biologic therapy.
In both studies, subjects were randomized to receive SKYRIZI 150 mg or placebo at Weeks 0, 4, and 16. Starting from Week 28, all subjects received SKYRIZI every 12 weeks. Both studies included a long-term extension for up to an additional 204 weeks. Regarding use of concomitant medications, 59.6% of subjects were receiving concomitant methotrexate (MTX), 11.6% were receiving concomitant non-biologic DMARDs other than MTX, and 28.9% were receiving SKYRIZI monotherapy.
For both studies, the primary endpoint was the proportion of subjects who achieved an American College of Rheumatology (ACR) 20 response at Week 24.
In both studies, treatment with SKYRIZI resulted in significant improvement in measures of disease activity compared with placebo at Week 24. See Tables 7 and 8 for key efficacy results.
In both studies, similar responses were seen regardless of concomitant non-biologic DMARD use, number of prior non-biologic DMARDs, age, gender, race, and BMI. In PsA-2, responses were seen regardless of prior biologic therapy.
Table 7: Efficacy Results in Study PsA-1
| Endpoint | Placebo N=481 Response Rate |
SKYRIZI N=483 Response Rate |
Difference from Placebo (95% CI) |
| ACR20 Response* | |||
| Week 16 | 33.4% | 56.3%a | 23.1% (16.8, 29.4) |
| Week 24 | 33.5% | 57.3%a | 24.0% (18.0, 30.0) |
| ACR50 Response* | |||
| Week 16 | 11.1% | 26.4% | 15.4% (10.6, 20.2) |
| Week 24 | 11.3% | 33.4 % | 22.2% (17.3, 27.2) |
| ACR70 Response* | |||
| Week 16 | 2.7% | 11.8% | 9.2% (6.1, 12.4) |
| Week 24 | 4.7% | 15.3% | 10.5% (6.9, 14.2) |
| a multiplicity-controlled p≤0.001, SKYRIZI vs. placebo comparison. *A Subject was considered as a non-responder after initiation of rescue medication or concomitant medications for PsA that could meaningfully impact efficacy assessment. |
|||
Table 8: Efficacy Results in Study PsA-2
| Endpoint | Placebo N=219 Response Rate |
SKYRIZI N=224 Response Rate |
Difference from Placebo (95% CI) |
| ACR20 Response* | |||
| Week 16 | 25.3% | 48.3% a | 22.6% (13.9, 31.2) |
| Week 24 | 26.5% | 51.3% a | 24.5% (15.9, 33.0) |
| ACR50 Response* | |||
| Week 16 | 6.8% | 20.3% | 13.5% (7.3, 19.7) |
| Week 24 | 9.3% | 26.3% | 16.6% (9.7, 23.6) |
| ACR70 Response* | |||
| Week 16 | 3.4% | 11.2% | 7.8% (3.0, 12.6) |
| Week 24 | 5.9% | 12.0% | 6.0% (0.8, 11.3) |
| a multiplicity-controlled p≤0.001, SKYRIZI vs. placebo comparison. *A Subject was considered as a non-responder after initiation of rescue medication or concomitant medications for PsA that could meaningfully impact efficacy assessment. |
|||
The percent of subjects achieving ACR20 responses in study PsA-1 through Week 24 is shown in Figure 1.
Figure 1: Percent of Subjects Achieving ACR20 Responses in Study PsA-1 through Week 24
 |
The results of the components of the ACR response criteria for both studies are shown in Table 9.
Table 9: Mean Change from Baseline in ACR Components
| PsA-1 | PsA-2 | |||
| Placebo (N=481) Mean (SD) |
SKYRIZI (N=483) Mean (SD) |
Placebo (N=219) Mean (SD) |
SKYRIZI (N=224) Mean (SD) |
|
| Number of Swollen Joints (0-66) | ||||
| Baseline | 12.2 (8.0) | 12.1 (7.8) | 13.6 (9.0) | 13.0 (8.7) |
| Mean change at Week 16 | -5.5 (7.0) | -7.7 (7.2) | -5.4 (8.5) | -8.0 (7.4) |
| Mean change at Week 24 | -6.7 (7.2) | -8.7 (7.2) | -6.5 (7.8) | -9.1 (7.6) |
| Number of Tender Joints (0-68) | ||||
| Baseline | 20.5 (12.8) | 20.8 (14.0) | 22.3 (13.8) | 22.8 (14.9) |
| Mean change at Week 16 | -6.3 (11.1) | -10.7 (11.4) | -6.0 (13.1) | -11.3 (13.0) |
| Mean change at Week 24 | -7.9 (10.7) | -12.0 (12.3) | -8.3 (11.3) | -13.0 (12.5) |
| Patient’s Assessment of Pain a | ||||
| Baseline | 57.1 (22.6) | 57.1 (22.6) | 57.0 (23.1) | 55.0 (23.5) |
| Mean change at Week 16 | -8.6 (23.7) | -18.4 (26.3) | -5.7 (22.7) | -14.4 (26.4) |
| Mean change at Week 24 | -10.9 (25.4) | -21.4 (26.5) | -8.7 (25.3) | -15.3 (26.5) |
| Patient’s Global Assessment a | ||||
| Baseline | 57.4 (22.1) | 57.9 (21.7) | 56.2 (23.0) | 56.2 (21.8) |
| Mean change at Week 16 | -10.2 (23.9) | -19.4 (25.7) | -4.9 (23.6) | -17.0 (27.1) |
| Mean change at Week 24 | -11.1 (25.1) | -22.6 (26.9) | -8.7 (25.4) | -17.7 (27.7) |
| Physician Global Assessment a | ||||
| Baseline | 62.4 (17.0) | 61.3 (17.6) | 60.7 (16.4) | 63.0 (17.0) |
| Mean change at Week 16 | -18.3 (22.5) | -31.1 (23.4) | -19.0 (23.3) | -32.7 (24.7) |
| Mean change at Week 24 | -22.2 (22.8) | -34.8 (23.2) | -21.3 (25.2) | -35.5 (25.6) |
| Health Assessment Questionnaire - Disability Index (HAQ-DI) b | ||||
| Baseline | 1.2 (0.7) | 1.2 (0.7) | 1.1 (0.6) | 1.1 (0.6) |
| Mean change at Week 16 | -0.1 (0.5) | -0.3 (0.5) | -0.1 (0.5) | -0.2 (0.5) |
| Mean change at Week 24 | -0.1 (0.5) | -0.3 (0.5) | -0.1 (0.4) | -0.2 (0.5) |
| High sensitivity C-reactive protein (hs-CRP) mg/L | ||||
| Baseline | 11.3 (14.1) | 11.9 (15.9) | 8.2 (17.1) | 7.4 (10.9) |
| Mean change at Week 16 | -0.3 (14.7) | -4.8 (14.2) | -0.1 (6.8) | -2.1 (7.5) |
| Mean change at Week 24 | -0.2 (11.7) | -4.3 (12.8) | -0.5 (14.5) | -1.8 (13.4) |
| SD= Standard Deviation. a Assessment based on Visual Analog Scale (100 mm) with the left end indicating “no pain” (for patient's assessment of pain), “very well” (for patient global assessment), or “no arthritis activity” (for physician global assessment) and the right end indicating “the worst possible pain” (for patient assessment of pain), “poor” (for patient global assessment), or “extremely active arthritis” (for physician global assessment). b Disability Index of the Health Assessment Questionnaire; 0 = no difficulty to 3 = inability to perform, measures the patient's ability to perform the following: dressing, arising, eating, walking, hygiene, reaching, gripping, and activities of daily living. |
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Treatment with SKYRIZI resulted in improvement in dactylitis and enthesitis in subjects with pre-existing dactylitis or enthesitis.
In patients with coexistent plaque psoriasis receiving SKYRIZI, the skin lesions of psoriasis improved with treatment, relative to placebo, as measured by the Psoriasis Area Severity Index (PASI 90) at Week 24.
In both studies, patients treated with SKYRIZI showed statistically significant improvement from baseline in physical function compared with placebo as assessed by HAQ-DI at Week 24 (Table 7). The mean difference (95% CI) from placebo in HAQ-DI change from baseline at Week 24 was -0.20 (-0.26, -0.14) in study PsA-1 and -0.16 (-0.26, -0.07) in study PsA-2.
In both studies, a greater proportion of subjects achieved a reduction of at least 0.35 in HAQ-DI score from baseline in the SKYRIZI group compared with placebo at Week 24.
In both studies, general health status was assessed by the 36-Item Short Form Health Survey (SF- 36 V2). Fatigue was assessed by Functional Assessment of Chronic Illness Therapy Fatigue Scale (FACIT-Fatigue).
In both studies at Week 24, subjects treated with SKYRIZI showed improvements in the SF-36 physical component summary scores compared with subjects who received placebo. There were also numerical improvements in subjects treated with SKYRIZI in physical functioning, role physical, bodily pain, general health, vitality, social functioning, mental health, role emotional domain scores and mental component summary scores in both studies at week 24 compared to placebo. In both studies at Week 24, subjects treated with SKYRIZI showed improvements in FACIT-Fatigue scores compared with subjects who received placebo.
In two 12-week induction studies (CD-1; NCT03105128 and CD-2; NCT03104413), subjects with moderately to severely active Crohn's disease were randomized to receive SKYRIZI 600 mg, SKYRIZI 1,200 mg, or placebo as an intravenous infusion at Week 0, Week 4, and Week 8. Moderately to severely active CD was defined as a Crohn's Disease Activity Index (CDAI) of 220 to 450 and Simple Endoscopic Score for Crohn's disease (SES-CD) ≥6 (or ≥4 for isolated ileal disease). Subjects with inadequate response, loss of response, or intolerance to oral aminosalicylates, corticosteroids, immunosuppressants, and/or biologic therapy were enrolled.
At baseline, the median CDAI was 307 (range: 76 – 634) and 307 (range: 72-651), and the median SES-CD was 12 (range: 4-45) and 13 (range 4-40), in CD-1 and CD-2, respectively. In CD-1, 58% (491/850) of subjects had failed or were intolerant to treatment with one or more biologic therapies (prior biologic failure). All subjects in CD-2 had prior biologic failure. At baseline, 30% and 34% of patients were receiving corticosteroids, 24% and 23% of patients were receiving immunomodulators (azathioprine, 6-mercaptopurine, methotrexate), and 31% and 19% of patients were receiving aminosalicylates in CD-1 and CD-2, respectively. In CD-1 and CD-2 combined, the median age was 36 years (ranging from 16 to 80 years), 81% (1145/1419) of subjects were white, and 53% (753/1419) were male.
In CD-1 and CD-2, the co-primary endpoints were clinical remission and endoscopic response at Week 12. Secondary endpoints included clinical response and endoscopic remission (see Table 10 and Table 11). The SKYRIZI 1,200 mg dosage did not demonstrate additional treatment benefit over the 600 mg dosage and is not a recommended regimen [see DOSAGE AND ADMINISTRATION].
Table 10: Proportion of Subjects Meeting Efficacy Endpoints at Week 12 — Study CD-1
| Endpoint | Placebo | SKYRIZI 600 mg Intravenous Infusiona | Treatment Difference b (95% CI) |
| Clinical Remissionc,d | |||
| Total Population | N=175 25% | N=336 45% | 21% e (12%, 29%) |
| Prior biologic failuref | N=97 26% | N=195 42% | |
| Without prior biologic failure | N=78 23% | N=141 49% | |
| Endoscopic Responsec,g | |||
| Total Population | N=175 12% | N=336 40% | 28% e (21%, 35%) |
| Prior biologic failuref | N=97 11% | N=195 33% | |
| Without prior biologic failure | N=78 13% | N=141 50% | |
| Clinical Responseh | |||
| Total Population | N=175 37% | N=336 60% | 23% e (14%, 32%) |
| Prior biologic failuref | N=97 34% | N=195 58% | |
| Without prior biologic failure | N=78 40% | N=141 62% | |
| Endoscopic Remissioni | |||
| Total Population | N=175 9% | N=336 24% | 15% e (9%, 21%) |
| Prior biologic failuref | N=97 5% | N=195 18% | |
| Without prior biologic failure | N=78 14% | N=141 32% | |
| a SKYRIZI 600 mg as an intravenous infusion at Week 0, Week 4, and Week 8 b Adjusted treatment difference (95% CI) based on Cochran-Mantel-Haenszel method adjusted for randomization stratification factors c Co-primary endpoints d CDAI <150 e p <0.001 f Prior biologic failure includes inadequate response, loss of response, or intolerance to one or more biologic treatments for CD g A decrease in SES-CD > 50% from baseline, or a decrease of at least 2 points for subjects with a baseline score of 4 and isolated ileal disease, based on central reading h A reduction of CDAI ≥ 100 points from baseline i SES-CD ≤ 4 and at least a 2-point reduction from baseline, with no individual subscore greater than 1, based on central reading |
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Table 11: Proportion of Subjects Meeting Efficacy Endpoints at Week 12 — Study CD-2a
| Endpoint | Placebo N=187 | SKYRIZI 600 mg Intravenous Infusionb N=191 |
Treatment Differencec (95% CI) |
| Clinical Remissiond,e | 20% | 42% | 22% f (13%, 31%) |
| Endoscopic Response d,g | 11% | 29% | 18% f (10%, 25%) |
| Clinical Responseh | 30% | 60% | 29% f (20%, 39%) |
| Endoscopic Remissioni | 4% | 19% | 15% f (9%, 21%) |
| a All subjects enrolled in CD-2 had prior biologic failure. Prior biologic failure includes inadequate response, loss of response, or intolerance to one or more biologic treatments for CD b SKYRIZI 600 mg as an intravenous infusion at Week 0, Week 4, and Week 8 c Adjusted treatment difference (95% CI) based on Cochran-Mantel-Haenszel method adjusted for randomization stratification factors d Co-primary endpoints e CDAI score <150 f p < 0.001 g A decrease in SES-CD > 50% from baseline, or a decrease of at least 2 points for subjects with a baseline score of 4 and isolated ileal disease, based on central reading h A reduction of CDAI ≥ 100 points from baseline i SES-CD ≤ 4 and at least a 2-point reduction versus from baseline, with and no individual subscore greater than 1, based on central reading |
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Onset of clinical response and clinical remission based on CDAI occurred as early as Week 4 in a greater proportion of subjects treated with the SKYRIZI 600 mg induction regimen compared to placebo.
Reductions in stool frequency and abdominal pain were observed in a greater proportion of subjects treated with the SKYRIZI 600 mg induction regimen compared to placebo at Week 12.
The maintenance study CD-3 evaluated 382 subjects who achieved clinical response defined as a reduction in CDAI of at least 100 points from baseline after 12 weeks of induction treatment with intravenous SKYRIZI in studies CD-1 and CD-2. Subjects were randomized to receive a maintenance regimen of SKYRIZI 180 mg or SKYRIZI 360 mg or placebo at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks.
The co-primary endpoints in CD-3 were clinical remission and endoscopic response at Week 52 (see Table 12).
Table 12: Proportion of Subjects Meeting Efficacy Endpoints at Week 52 — Study CD-3
| Endpoint | Placeboa | SKYRIZI 180 mg Subcutaneous Injectionb | SKYRIZI 360 mg Subcutaneous Injectionc | Treatment Difference vs Placebod (95% CI) | |
| SKYRIZI 180 mg | SKYRIZI 360 mg | ||||
| Clinical Remissione,f | |||||
| Total Population | N=130 | N=135 | N=117 | 17%g | 14%g |
| 46% | 61% | 57% | (6%, 28%) | (3%, 26%) | |
| Prior biologic failureh | N=99 | N=95 | N=83 | ||
| 40% | 56% | 51% | |||
| Without prior biologic failure | N=31 | N=40 | N=34 | ||
| 65% | 75% | 71% | |||
| Endoscopic Responsee,i | |||||
| Total Population | N=130 | N=135 | N=117 | 30%g | 31%g |
| 22% | 50% | 48% | (20%, 39%) | (21%, 41%) | |
| Prior biologic failureh | N=99 | N=95 | N=83 | ||
| 21% | 44% | 44% | |||
| Without prior biologic failure | N=31 | N=40 | N=34 | ||
| 23% | 65% | 59% | |||
| a The placebo group consisted of patients who were in response to SKYRIZI and were randomized to receive placebo at the start of maintenance therapy. b SKYRIZI 180 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks c SKYRIZI 360 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks d Adjusted treatment difference and 95% CI computed using Cochran-Mantel-Haenszel method adjusted for randomization stratification factors e Co-primary endpoints f CDAI <150 g p <0.05 h Prior biologic failure includes inadequate response, loss of response, or intolerance to one or more biologic treatments for CD i A decrease in SES-CD > 50% from baseline, or a decrease of at least 2 points for subjects with a baseline score of 4 and isolated ileal disease, based on central reading |
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Endoscopic remission was observed at Week 52 in 33% (44/135) of subjects treated with the SKYRIZI 180 mg maintenance regimen and 41% (48/117) of subjects treated with the SKYRIZI 360 mg maintenance regimen, compared to 13% (17/130) of subjects treated with placebo. This endpoint was not statistically significant under the prespecified multiple testing procedure.
In the 12-week induction study (UC-1; NCT03398148), 966 subjects with moderately to severely active ulcerative colitis were randomized and received SKYRIZI 1,200 mg or placebo as an intravenous infusion at Week 0, Week 4, and Week 8. Disease activity was assessed by the modified Mayo score (mMS), a 3-component Mayo score (0-9) which consists of the following subscores (0 to 3 for each subscore): stool frequency (SFS), rectal bleeding (RBS), and findings on centrally read endoscopy score (ES). An ES of 2 was defined by marked erythema, lack of vascular pattern, any friability, and/or erosions; an ES of 3 was defined by spontaneous bleeding and ulceration. Enrolled subjects had a mMS between 5 and 9, with an ES of 2 or 3. Subjects with inadequate response, or intolerance to oral aminosalicylates, corticosteroids, immunomodulators, biologics, Janus Kinase inhibitors (JAKi), and/or sphingosine-1-phosphate receptor modulators (S1PRM) were enrolled.
At baseline in UC-1, the median mMS was 7; 37% had severely active disease (mMS >7); 69% had an ES of 3. In UC-1, 52% (499/966) of subjects had failed (inadequate response or intolerance) treatment with one or more biologics, JAKi or S1PRM. Of these 499 subjects, 484 (97%) failed biologics and 90 (18%) failed JAK inhibitors. Enrolled subjects were permitted to use a stable dose of oral corticosteroids (up to 20 mg/day prednisone or equivalent), immunomodulators, and aminosalicylates. At baseline, 36% of subjects were receiving corticosteroids, 16% of subjects were receiving immunomodulators (including azathioprine, 6- mercaptopurine, methotrexate), and 73% of subjects were receiving aminosalicylates in UC-1.
In UC-1, the primary endpoint was clinical remission defined using the mMS at Week 12 (see Table 13). Key secondary endpoints included clinical response, endoscopic improvement, and histologic endoscopic mucosal improvement (see Table 13).
Table 13: Proportion of Subjects Meeting Efficacy Endpoints at Week 12 — Study UC-1
| Endpoint | Placebo | SKYRIZI 1,200 mg Intravenous Infusiona | Treatment Difference (95% CI)b |
| Clinical Remissionc | |||
| Total Population | N=320 8% | N=646 24% | 16%h (12%, 20%) |
| Prior biologic, JAKi, or S1PRM failured | N=168 6% | N=331 14% | |
| Without prior biologic, JAKi, or S1PRM failure | N=152 9% | N=315 33% | |
| Clinical Responsee | |||
| Total Population | N=320 36% | N=646 65% | 29%h (23%, 35%) |
| Prior biologic, JAKi, or S1PRM failured | N=168 32% | N=331 56% | |
| Without prior biologic, JAKi, or S1PRM failure | N=152 41% | N=315 75% | |
| Endoscopic Improvementf | |||
| Total Population | N=320 12% | N=646 36% | 25%h (20%, 30%) |
| Prior biologic, JAKi, or S1PRM failured | N=168 10% | N=331 26% | |
| Without prior biologic, JAKi, or S1PRM failure | N=152 14% | N=315 47% | |
| Histologic Endoscopic Mucosal Improvement (HEMI)g | |||
| Total Population | N=320 7% | N=646 24% | 17%h (13%, 21%) |
| Prior biologic, JAKi, or S1PRM failured | N=168 7% | N=331 16% | |
| Without prior biologic, JAKi, or S1PRM failure | N=152 8% | N=315 33% | |
| a SKYRIZI 1,200 mg as an intravenous infusion at Week 0, Week 4, and Week 8 b Adjusted treatment difference (95% CI) based on Cochran-Mantel-Haenszel method adjusted for stratification factors c Per mMS: SFS ≤ 1 and not greater than baseline, RBS = 0, and ES ≤ 1 without friability d Prior failure includes inadequate response or intolerance to treatment with one or more of the following: biologic therapies, Janus Kinase inhibitors (JAKi), and/or sphingosine-1-phosphate receptor modulators (S1PRM) e Per mMS: decrease ≥ 2 points and ≥ 30% from baseline, and a decrease in RBS ≥ 1 from baseline or an absolute RBS ≤ 1 f ES ≤ 1 without the evidence of friability g ES ≤ 1 without the evidence of friability and Geboes score ≤ 3.1 (indicating neutrophil infiltration in <5% of crypts, no crypt destruction and no erosions, ulcerations or granulation tissue) h p < 0.001 |
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UC-1 was not designed to evaluate the relationship of histologic endoscopic mucosal improvement at week 12 to disease progression and long-term outcomes.
Rectal Bleeding And Stool Frequency Subscores
Decreases in rectal bleeding and stool frequency subscores in subjects treated with SKYRIZI compared to placebo were observed as early as 4 weeks.
Endoscopic Assessment
Endoscopic remission was defined as ES of 0. At Week 12, a greater proportion of subjects treated with SKYRIZI compared to placebo achieved endoscopic remission (11% vs 3%).
Bowel Urgency
A greater proportion of subjects treated with the SKYRIZI 1,200 mg induction regimen compared to placebo had no bowel urgency (44% vs 27%) at Week 12.
Fatigue
In UC-1, subjects treated with SKYRIZI experienced a clinically meaningful improvement in fatigue, assessed by change from baseline in FACIT-F score, at Week 12, compared to placebotreated subjects. The effect of SKYRIZI to improve fatigue after 12 weeks of induction has not been established.
Other UC Symptoms
The proportion of subjects who had no nocturnal bowel movements was greater in subjects treated with SKYRIZI compared to placebo at Week 12 (67% vs 43%).
The maintenance study (UC-2; NCT03398135) evaluated 547 subjects who received one of three SKYRIZI induction regimens, including the 1,200 mg regimen, for 12 weeks in Studies UC-1 or UC-3 and demonstrated clinical response per mMS after 12 weeks. Subjects were randomized to receive a maintenance regimen of subcutaneous (SC) SKYRIZI 180 mg or SKYRIZI 360 mg or placebo at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks.
In UC-2, 75% (411/547) of subjects had failed (inadequate response or intolerance) treatment with one or more biologics, JAKi, or S1PRM. Of these 411 subjects, 407 (99%) failed biologics and 78 (19%) failed JAK inhibitors.
The primary endpoint in UC-2 was clinical remission using mMS at Week 52 (see Table 14). Key secondary endpoints included corticosteroid-free clinical remission, endoscopic improvement, and histologic endoscopic mucosal improvement (see Table 14).
Table 14: Proportion of Subjects Meeting Efficacy Endpoints at Week 52 — Study UC-2
| Endpoint | Placeboa | SKYRIZI 180 mg SC Injectionb | SKYRIZI 360 mg SC Injectionc |
| Clinical remissiond | |||
| Total Population | N=182 26% | N=179 45% | N=186 41% |
| Treatment Difference vs Placeboe(95% CI) | 20% j | 16%j | |
| [11%, 29%] | [7%, 25%] | ||
| Prior biologic, JAKi, or S1PRM failuref | N=138 | N=134 | N=139 |
| 24% | 41% | 32% | |
| Without prior biologic, JAKi, or S1PRM failure | N=44 | N=45 | N=47 |
| 32% | 58% | 67% | |
| Corticosteroid-free clinical remissiong | |||
| Total Population | N=182 26% | N=179 45% | N=186 40% |
| Treatment Difference vs Placeboe (95% CI) | 20% j | 16% j | |
| [11%, 29%] | [7%, 25%] | ||
| Prior biologic, JAKi, or S1PRM failuref | N=138 | N=134 | N=139 |
| 24% | 40% | 32% | |
| Without prior biologic, JAKi, or S1PRM failure | N=44 | N=45 | N=47 |
| 32% | 58% | 64% | |
| Endoscopic improvementh | |||
| Total Population | N=182 31% | N=179 51% | N=186 48% |
| Treatment Difference vs Placebo e (95% CI) | 20% j | 18% j | |
| [11%, 30%] | [8%, 27%] | ||
| Prior biologic, JAKi, or S1PRM failuref | N=138 | N=134 | N=139 |
| 30% | 48% | 39% | |
| Without prior biologic, JAKi, or S1PRM failure | N=44 | N=45 | N=47 |
| 34% | 60% | 76% | |
| Histologic Endoscopic Mucosal Improvementi | |||
| Total Population | N=182 24% | N=179 43% | N=186 42% |
| Treatment Difference vs Placeboe(95% CI) | 20% j[11%, 29%] | 20% j [11%, 29%] | |
| Prior biologic, JAKi, or S1PRM failuref | N=138 | N=134 | N=139 |
| 22% | 39% | 33% | |
| Without prior biologic, JAKi, or S1PRM failure | N=44 | N=45 | N=47 |
| 30% | 55% | 69% | |
| a The placebo group consisted of subjects who were in response to 12 weeks of SKYRIZI induction and were randomized to receive placebo at the start of maintenance therapy. b SKYRIZI 180 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks c SKYRIZI 360 mg at Week 12 and every 8 weeks thereafter for up to an additional 52 weeks d Per mMS: SFS ≤ 1 and not greater than baseline, RBS = 0, and ES ≤ 1 without friability e Adjusted treatment difference (95% CI) based on Cochran-Mantel-Haenszel method adjusted for stratification factors f Prior failure includes inadequate response or intolerance to treatment with one or more of the following: biologic therapies, Janus Kinase inhibitors (JAKi), and/or sphingosine-1-phosphate receptor modulators (S1PRM) g Clinical remission per mMS at Week 52 and corticosteroid-free for ≥90 days h ES ≤ 1 without the evidence of friability i ES ≤ 1without the evidence of friability and Geboes score ≤ 3.1 (indicating neutrophil infiltration in <5% of crypts, no crypt destruction and no erosions, ulcerations or granulation tissue) j p < 0.001 |
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Endoscopic Assessment
Endoscopic remission was defined as ES of 0. In UC-2, a greater proportion of subjects treated with SKYRIZI 180 mg and SKYRIZI 360 mg compared to placebo achieved endoscopic remission at Week 52 (23% and 24% vs 15%).
Medication Guide
SKYRIZI® (sky-RIZZ-ee)
(risankizumab-rzaa)
injection, for subcutaneous or intravenous use
What is the most important information I should know about SKYRIZI?
SKYRIZI may cause serious side effects, including:
Serious allergic reactions. Stop using SKYRIZI and get emergency medical help right away if you get any of the following symptoms of a serious allergic reaction:
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Infections. SKYRIZI may lower the ability of your immune system to fight infections and may increase your risk of infections. Your healthcare provider should check you for infections and tuberculosis (TB) before starting treatment with SKYRIZI and may treat you for TB before you begin treatment with SKYRIZI if you have a history of TB or have active TB. Your healthcare provider should watch you closely for signs and symptoms of TB during and after treatment with SKYRIZI. Tell your healthcare provider right away if you have an infection or have symptoms of an infection, including:
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See “What are the possible side effects of SKYRIZI?” for more information about side effects.
What is SKYRIZI?
SKYRIZI is a prescription medicine used to treat:
It is not known if SKYRIZI is safe and effective in children.
Who should not use SKYRIZI?
Do not use SKYRIZI if you are allergic to risankizumab-rzaa or any of the ingredients in SKYRIZI.
See the end of this Medication Guide for a complete list of ingredients in SKYRIZI.
Before using SKYRIZI, tell your healthcare provider about all of your medical conditions, including if you:
Tell your healthcare provider about all the medicines you take, including prescription and over-the- counter medicines, vitamins, and herbal supplements.
How should I use SKYRIZI?
See the detailed “Instructions for Use” that comes with SKYRIZI for information on how to prepare and inject a dose of SKYRIZI, and how to properly throw away (dispose of) a used SKYRIZI prefilled pen, prefilled syringe, or prefilled cartridge with on-body injector.
Adults with plaque psoriasis or psoriatic arthritis will receive SKYRIZI as an injection under the skin (subcutaneous injection) using the prefilled pen or prefilled syringe.
Adults with Crohn’s disease or ulcerative colitis will receive their starter doses with SKYRIZI through a vein in the arm (intravenous infusion) in a healthcare facility by a healthcare provider. After completing the starter doses, patients will receive SKYRIZI as 1 or more injections under the skin (subcutaneous injection) using the prefilled cartridge with on-body injector or prefilled syringe.
What are the possible side effects of SKYRIZI?
SKYRIZI may cause serious side effects including:
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The most common side effects of SKYRIZI in people treated for Crohn’s disease and ulcerative colitis include:
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The most common side effects of SKYRIZI in people treated for plaque psoriasis and psoriatic arthritis include:
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These are not all the possible side effects of SKYRIZI.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
How should I store SKYRIZI?
Keep SKYRIZI and all medicines out of the reach of children.
General information about the safe and effective use of SKYRIZI.
Medicines are sometimes prescribed for purposes other than those listed in a Medication Guide. Do not use SKYRIZI for a condition for which it was not prescribed. Do not give SKYRIZI to other people, even if they have the same symptoms that you have. It may harm them. You can ask your pharmacist or healthcare provider for information about SKYRIZI that is written for health professionals.
What are the ingredients in SKYRIZI?
Active ingredient: risankizumab-rzaa.
SKYRIZI 90 mg/mL prefilled syringe inactive ingredients: polysorbate 20, sodium succinate, sorbitol, succinic acid, and Water for Injection, USP.
SKYRIZI 150 mg/mL prefilled pen or prefilled syringe, 180 mg/1.2 mL prefilled syringe or prefilled cartridge, 360 mg/2.4 mL prefilled cartridge, and 600 mg/ 10 mL vial inactive ingredients: glacial acetic acid, polysorbate 20, sodium acetate, trehalose, and Water for Injection, USP.
Manufactured by: AbbVie Inc., North Chicago, IL 60064, U.S.A.
US License Number 1889
SKYRIZI® is a registered trademark of AbbVie Biotechnology Ltd.
© 2019-2025 AbbVie Inc.
For more information, call 1-866-SKYRIZI (1-866-759-7494) or go to www.SKYRIZI.com.
