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WARNING
ANAPHYLAXIS and INFUSION REACTIONS G6PD DEFICIENCY ASSOCIATED HEMOLYSIS and METHEMOGLOBINEMIA
KRYSTEXXA (pegloticase) is a uric acid specific enzyme which is a PEGylated product that consists of recombinant modified mammalian urate oxidase (uricase) produced by a genetically modified strain of Escherichia coli. Uricase is covalently conjugated to monomethoxypoly (ethylene glycol) [mPEG] (10 kDa molecular weight). The cDNA coding for uricase is based on mammalian sequences. Each uricase subunit has a molecular weight of approximately 34 kDa per subunit. The average molecular weight of pegloticase (tetrameric enzyme conjugated to mPEG) is approximately 540 kDa.
KRYSTEXXA is intended for intravenous infusion.
KRYSTEXXA is a sterile, clear, colorless solution containing 8 mg/mL pegloticase in phosphatebuffered saline.
KRYSTEXXA (pegloticase) concentrations are expressed as concentrations of uricase protein. Each mL of KRYSTEXXA contains 8 mg of uricase protein (conjugated to 24 mg of 10 kDa mPEG), 2.18 mg Disodium Hydrogen Phosphate Dihydrate (Na2HPO4•2H2O), 8.77 mg Sodium Chloride (NaCl), 0.43 mg Sodium Dihydrogen Phosphate Dihydrate (NaH2PO4•2H2O), and Water for Injection to deliver 8 mg of pegloticase (as uricase protein).
The following serious adverse reactions are discussed in greater detail in other sections of the label:
A 52-week, randomized, double-blind trial was conducted in adult subjects with chronic gout refractory to conventional therapy to evaluate administration of KRYSTEXXA 8 mg every 2 weeks co-administered with weekly administration of oral methotrexate 15 mg, compared to KRYSTEXXA alone. In this trial, subjects who were able to tolerate two weeks on methotrexate 15 mg were then randomized to receive four additional weeks on either methotrexate 15 mg or matching placebo prior to initiating KRYSTEXXA therapy. A total of 152 subjects were randomized, and of these, 145 subjects completed the 4-week methotrexate run-in period and received KRYSTEXXA (96 subjects received KRYSTEXXA co-administered with methotrexate and 49 received KRYSTEXXA plus placebo) during the treatment period. All subjects received pre-treatment with an oral antihistamine, intravenous corticosteroid and acetaminophen. These subjects were between the ages of 24 and 83 years (average 55 years); 135 subjects were male and 17 and were female; 105 subjects were White/Caucasian, 22 were Black/African American, 14 were Asian, 5 were Native Hawaiian/Other Pacific Islander and 5 identified as Other; 28 were Hispanic or Latino. Common co-morbid conditions among the enrolled subjects included hypertension (63%), osteoarthritis (25%), hyperlipidemia (24%), gastroesophageal reflux disease (22%), obesity (20%), type 2 diabetes (18%) and depression (16%). Subjects with an eGFR < 40 mL/min/1.73 m2 were excluded from this trial.
The most commonly reported adverse reaction during the methotrexate pre-treatment periods was gout flare. The most commonly reported adverse reactions that occurred in ≥ 5% in either treatment group during the KRYSTEXXA co-administered with methotrexate or KRYSTEXXA alone period are provided in Table 1.
Table 1. Adverse Reactions Occurring in 5% or More of Subjects in Either the KRYSTEXXA Co-administered with Methotrexate or KRYSTEXXA Alone Treatment Period
| Adverse Reaction | KRYSTEXXA with Methotrexate (N = 96) n (%) |
KRYSTEXXA Alone (N = 49) n (%) |
| Gout flare | 64 (67%) | 35 (71%) |
| Arthralgia | 13 (14%) | 5 (10%) |
| COVID-19 | 9 (9%) | 3 (6%) |
| Nausea | 5 (5%) | 6 (12%) |
| Fatigue | 5 (5%) | 2 (4%) |
| Infusion reaction | 4 (4%)a | 15 (31%) |
| Pain in extremity | 1 (1%) | 3 (6%) |
| Hypertension | 1 (1%) | 3 (6%) |
| Vomiting | 0 | 4 (8%) |
|
a Included one case of anaphylaxis. |
||
KRYSTEXXA ALONE
The data described below reflect exposure to KRYSTEXXA in subjects with chronic gout refractory to conventional therapy in two replicate randomized, placebo-controlled, double-blind 24-week clinical trials: 85 subjects were treated with KRYSTEXXA 8 mg every 2 weeks; 84 subjects were treated with KRYSTEXXA 8 mg every 4 weeks; and 43 subjects were treated with placebo. These subjects were between the ages of 23 and 89 years (average 55 years); 173 subjects were male and 39 were female; and 143 patients were White/Caucasian, 27 were Black/African American, 24 were Hispanic/Latino and 18 were all other ethnicities. Common co-morbid conditions among the enrolled subjects included hypertension (72%), dyslipidemia (49%), chronic kidney disease (28%), diabetes (24%), coronary artery disease (18%), arrhythmia (16%), and cardiac failure/left ventricular dysfunction (12%).
During the pre-marketing placebo-controlled clinical trials, the most commonly reported adverse reactions that occurred in greater than or equal to 5% of subjects treated with KRYSTEXXA 8 mg every 2 weeks are provided in Table 2.
Table 2. Adverse Reactions Occurring in 5% or More of Subjects Treated with KRYSTEXXA Compared to Placebo
|
Adverse Reaction |
KRYSTEXXA |
Placebo |
|
Gout flare |
65 (77%) |
35 (81%) |
|
Infusion reaction |
22 (26%) |
2 (5%) |
|
Nausea |
10 (12%) |
1 (2%) |
|
Contusionb or Ecchymosisb |
9 (11%) |
2 (5%) |
|
Adverse Reaction |
KRYSTEXXA |
Placebo |
|
Nasopharyngitis |
6 (7%) |
1 (2%) |
|
Constipation |
5 (6%) |
2 (5%) |
|
Chest Pain |
5 (6%) |
1 (2%) |
|
Anaphylaxis |
4 (5%) |
0 (0%) |
|
Vomiting |
4 (5%) |
1 (2%) |
|
a If the same subject in a given group had more than one occurrence in the same preferred term event category, the subject was counted only once. b Most did not occur on the day of infusion and could be related to other factors (e.g., concomitant medications relevant to contusion or ecchymosis, insulin dependent diabetes mellitus). |
||
The following adverse reactions have been identified during postapproval use of KRYSTEXXA. 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.
General disorders and administration site conditions: asthenia, malaise, peripheral swelling
KRYSTEXXA 8 mg every 2 weeks has been studied in patients with chronic gout refractory to conventional therapy taking concomitant oral methotrexate 15 mg weekly [see Clinical Studies (14)]. Co-administration of methotrexate with KRYSTEXXA may increase pegloticase concentration compared to KRYSTEXXA alone [see Clinical Pharmacology (12.3)].
Because anti-pegloticase antibodies appear to bind to the PEG portion of the drug, there may be potential for binding with other PEGylated products. The impact of anti-PEG antibodies on patients’ responses to other PEG-containing therapeutics is unknown.
Included as part of the PRECAUTIONS section.
In a 52-week controlled trial, which evaluated KRYSTEXXA co-administered with methotrexate compared to KRYSTEXXA alone, subjects were pre-treated with standardized infusion reaction prophylaxis and were discontinued from treatment with KRYSTEXXA if serum uric acid levels increased to above 6 mg/dL at 2 consecutive visits after the initiation of KRYSTEXXA therapy to reduce the risk of anaphylaxis. One subject randomized to the group treated with KRYSTEXXA co-administered with methotrexate (1%) experienced anaphylaxis during the first infusion and no subjects experienced anaphylaxis in the group treated with KRYSTEXXA alone [see Adverse Reactions (6.1), Clinical Studies (14)].
During pre-marketing clinical trials with KRYSTEXXA alone, KRYSTEXXA was not discontinued following 2 consecutive serum uric acid levels above 6 mg/dL. Anaphylaxis was reported with a frequency of 6.5% (8/123) of subjects treated with KRYSTEXXA every 2 weeks and 4.8% (6/126) for the every 4-week dosing regimen. There were no cases of anaphylaxis in subjects receiving placebo. Anaphylaxis generally occurred within 2 hours after treatment.
Diagnostic criteria of anaphylaxis were skin or mucosal tissue involvement, and, either airway compromise, and/or reduced blood pressure with or without associated symptoms, and a temporal relationship to KRYSTEXXA or placebo injection with no other identifiable cause. Manifestations included wheezing, peri-oral or lingual edema, or hemodynamic instability, with or without rash or urticaria, nausea or vomiting. Cases occurred in patients being pre-treated with one or more doses of an oral antihistamine, an intravenous corticosteroid and/or acetaminophen. This pre-treatment may have blunted or obscured symptoms or signs of anaphylaxis and therefore the reported frequency may be an underestimate.
KRYSTEXXA should be administered in a healthcare setting by healthcare providers prepared to manage anaphylaxis. Patients should be pre-treated with antihistamines and corticosteroids. Anaphylaxis may occur with any infusion, including a first infusion, and generally manifests within 2 hours of the infusion. However, delayed type hypersensitivity reactions have also been reported. Patients should be closely monitored for an appropriate period of time for anaphylaxis after administration of KRYSTEXXA. Patients should be informed of the symptoms and signs of anaphylaxis and instructed to seek immediate medical care should anaphylaxis occur after discharge from the healthcare setting.
The risk of anaphylaxis is higher in patients whose uric acid level increases to above 6 mg/dL, particularly when 2 consecutive levels above 6 mg/dL are observed. Monitor serum uric acid levels prior to infusions and discontinue treatment if levels increase to above 6 mg/dL. Because of the possibility that concomitant use of oral urate-lowering therapy and KRYSTEXXA may potentially blunt the rise of serum uric acid levels, it is recommended that before starting KRYSTEXXA patients discontinue oral urate-lowering medications and not institute therapy with oral urate-lowering agents while taking KRYSTEXXA.
In a 52-week, controlled trial which evaluated KRYSTEXXA co-administered with methotrexate compared to KRYSTEXXA alone [see Adverse Reactions (6.1), Clinical Studies (14)], subjects were pre-treated with standardized infusion reaction prophylaxis and were discontinued from treatment with KRYSTEXXA if serum uric acid levels increased to above 6 mg/dL at 2 consecutive visits after the initiation of KRYSTEXXA therapy to reduce the risk of infusion reactions. Infusion reactions were reported in 4% of subjects in the KRYSTEXXA co-administered with methotrexate group compared to 31% of subjects treated with KRYSTEXXA alone experienced infusion reactions [see Adverse Reactions (6.1), Clinical Studies (14)]. In both treatment groups, the majority of infusion reactions occurred at the first or second KRYSTEXXA infusion and during the time of infusion. Manifestations of these infusion reactions were similar to that observed in the pre-marketing trials.
During pre-marketing 24-week controlled clinical trials with KRYSTEXXA alone, KRYSTEXXA was not discontinued following 2 consecutive serum uric acid levels above 6 mg/dL. Infusion reactions were reported in 26% of subjects treated with KRYSTEXXA 8 mg every 2 weeks, and 41% of subjects treated with KRYSTEXXA 8 mg every 4 weeks, compared to 5% of subjects treated with placebo. These infusion reactions occurred in subjects being pre-treated with an oral antihistamine, intravenous corticosteroid and/or acetaminophen. This pre-treatment may have blunted or obscured symptoms or signs of infusion reactions and therefore the reported frequency may be an underestimate.
Manifestations of these reactions included urticaria (frequency of 10.6%), dyspnea (frequency of 7.1%), chest discomfort (frequency of 9.5%), chest pain (frequency of 9.5%), erythema (frequency of 9.5%), and pruritus (frequency of 9.5%). These manifestations overlap with the symptoms of anaphylaxis, but in a given patient did not occur together to satisfy the clinical criteria for diagnosing anaphylaxis. Infusion reactions are thought to result from release of various mediators, such as cytokines. Infusion reactions occurred at any time during a course of treatment with approximately 3% occurring with the first infusion, and approximately 91% occurred during the time of infusion.
KRYSTEXXA should be administered in a healthcare setting by healthcare providers prepared to manage infusion reactions. Patients should be pre-treated with antihistamines and corticosteroids. KRYSTEXXA should be infused slowly over no less than 120 minutes. In the event of an infusion reaction, the infusion should be slowed, or stopped and restarted at a slower rate.
The risk of infusion reaction is higher in patients whose uric acid level increases to above 6 mg/dL, particularly when 2 consecutive levels above 6 mg/dL are observed. Monitor serum uric acid levels prior to infusions and discontinue treatment if levels increase to above 6 mg/dL. Because of the possibility that concomitant use of oral urate-loweringtherapy and KRYSTEXXA may potentially blunt the rise of serum uric acid levels, it is recommended that before starting KRYSTEXXA patients discontinue oral urate-lowering medications and not institute therapy with oral urate-lowering agents while taking KRYSTEXXA.
Life threatening hemolytic reactions and methemoglobinemia have been reported with KRYSTEXXA in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Because of the risk of hemolysis and methemoglobinemia, do not administer KRYSTEXXA to patients with G6PD deficiency [see Contraindications (4)]. Screen patients at risk for G6PD deficiency prior to starting KRYSTEXXA. For example, patients of African, Mediterranean (including Southern European and Middle Eastern), and Southern Asian ancestry are at increased risk for G6PD deficiency.
In a 52-week, randomized, double-blind trial which evaluated KRYSTEXXA co-administered with methotrexate compared to KRYSTEXXA alone, subjects were administered gout flare prophylaxis similar to that in the pre-marketing, placebo-controlled trials. The percentages of subjects with any flare for the first 3 months were 66% and 69% for the group treated with KRYSTEXXA co-administered with methotrexate and the group treated with KRYSTEXXA alone, respectively. In the group treated with KRYSTEXXA co-administered with methotrexate, the percentages of subjects with any flare for the subsequent 3-month increments of treatment were 27% during Month 6, 8% during Month 9 and 9% during Month 12. In the group treated with KRYSTEXXA alone, the percentages of patients with any flare were 14% during Month 6, 9% during Month 9 and 21% during Month 12.
During pre-marketing, 24-week controlled clinical trials with KRYSTEXXA alone, the frequencies of gout flares were high in all treatment groups, but more so with KRYSTEXXA treatment during the first 3 months of treatment, and decreased in the subsequent 3 months of treatment. The percentages of subjects with any flare for the first 3 months were 74%, 81%, and 51%, for KRYSTEXXA 8 mg every 2 weeks, KRYSTEXXA 8 mg every 4 weeks, and placebo, respectively. The percentages of subjects with any flare for the subsequent 3 months were 41%, 57%, and 67%, for KRYSTEXXA 8 mg every 2 weeks, KRYSTEXXA 8 mg every 4 weeks, and placebo, respectively. Subjects received gout flare prophylaxis with colchicine and/or nonsteroidal anti-inflammatory drugs (NSAIDs) starting at least one week before receiving KRYSTEXXA.
Gout flares may occur after initiation of KRYSTEXXA. An increase in gout flares is frequently observed upon initiation of anti-hyperuricemic therapy, due to changing serum uric acid levels resulting in mobilization of urate from tissue deposits. Gout flare prophylaxis with a non-steroidal anti-inflammatory drug (NSAID) or colchicine is recommended starting at least 1 week before initiation of KRYSTEXXA therapy and lasting at least 6 months, unless medically contraindicated or not tolerated. KRYSTEXXA does not need to be discontinued because of a gout flare. The gout flare should be managed concurrently as appropriate for the individual patient [see Dosage and Administration (2)].
KRYSTEXXA has not been formally studied in patients with congestive heart failure, but some subjects in the pre-marketing, 24-week controlled clinical trials experienced exacerbation of congestive heart failure. Two cases of congestive heart failure exacerbation occurred during the trials in subjects receiving treatment with KRYSTEXXA 8 mg every 2 weeks. No cases were reported in placebo-treated subjects. Four subjects had exacerbations of pre-existing congestive heart failure while receiving KRYSTEXXA 8 mg every 2 weeks during the open-label extension study.
Exercise caution when using KRYSTEXXA in patients who have congestive heart failure and monitor patients closely following infusion.
No controlled trial data are available on the safety and efficacy of re-treatment with KRYSTEXXA after stopping treatment for longer than 4 weeks. Due to the immunogenicity of KRYSTEXXA, patients receiving re-treatment may be at increased risk of anaphylaxis and infusion reactions. Therefore, patients receiving re-treatment after a drug-free interval should be monitored carefully [see Adverse Reactions (6.2)].
Long-term animal studies have not been performed to evaluate the carcinogenic potential of pegloticase.
The genotoxic potential of pegloticase has not been evaluated.
There was no evidence of impairment on fertility at pegloticase doses up to 40 mg/kg (approximately 50 times the MRHD on mg/m2 basis) every other day in rats.
Advise patients to read the FDA-approved patient labeling (Medication Guide).
Anaphylaxis and Infusion Reactions
Glucose-6-phosphate dehydrogenase (G6PD) Deficiency
Inform patients not to take KRYSTEXXA if they have a condition known as G6PD deficiency. Explain to patients that G6PD deficiency is more frequently found in individuals of African, Mediterranean, or Southern Asian ancestry and that they may be tested to determine if they have G6PD deficiency, unless already known [see Contraindications (4), Warnings and Precautions (5.3)].
Gout Flares
Explain to patients that gout flares may initially increase when starting treatment with KRYSTEXXA, and that medications to help reduce flares may need to be taken regularly for the first few months after KRYSTEXXA is started [see Warnings and Precautions (5.4), Adverse Reactions (6.1)]. Advise patients that they should not stop KRYSTEXXA therapy if they have a flare.
No reports of overdosage with KRYSTEXXA have been reported. The maximum dose that has been administered as a single intravenous dose is 12 mg as uricase protein.
Patients suspected of receiving an overdose should be monitored, and general supportive measures should be initiated as no specific antidote has been identified.
KRYSTEXXA is contraindicated in:
KRYSTEXXA is a uric acid specific enzyme which is a recombinant uricase and achieves its therapeutic effect by catalyzing the oxidation of uric acid to allantoin, thereby lowering serum uric acid. Allantoin is an inert and water-soluble purine metabolite; it is readily eliminated, primarily by renal excretion.
Approximately 24 hours following the first dose of KRYSTEXXA, mean plasma uric acid levels for subjects in the KRYSTEXXA groups were 0.7 mg/dL for the KRYSTEXXA 8 mg every 2 weeks group. In comparison, the mean plasma uric acid level for the placebo group was 8.2 mg/dL.
In a single-dose, dose-ranging trial, following 1-hour intravenous infusions of 0.5, 1, 2, 4, 8 or 12 mg of pegloticase in 24 patients with symptomatic gout (n = 4 subjects/dose group), plasma uric acid decreased with increasing pegloticase dose or concentrations. The duration of suppression of plasma uric acid appeared to be positively associated with pegloticase dose. Sustained decrease in plasma uric acid below the solubility concentration of 6 mg/dL for more than 300 hours was observed with doses of 8 mg and 12 mg.
Pegloticase levels were determined in serum based on measurements of uricase enzyme activity.
Following single intravenous infusions of 0.5 mg to 12 mg pegloticase in 23 patients with symptomatic gout, maximum serum concentrations of pegloticase increased in proportion to the dose administered.
The population pharmacokinetic analysis showed that age, sex, weight, and creatinine clearance did not influence the pharmacokinetics of pegloticase. Significant covariates impacting pegloticase pharmacokinetics were body surface area and anti-pegloticase antibodies.
Pediatric Patients
The pharmacokinetics of pegloticase has not been studied in children and adolescents.
Patients with Renal or Hepatic Impairment
No formal studies were conducted to examine the effects of either renal or hepatic impairment on pegloticase pharmacokinetics. eGFR was not a significant covariate on pegloticase pharmacokinetics.
Co-administration of methotrexate with KRYSTEXXA decreased anti-pegloticase antibody incidence rate and titers compared to KRYSTEXXA alone, therefore increased pegloticase exposure levels. In patients with chronic gout refractory to conventional therapy receiving KRYSTEXXA 8 mg every 2 weeks co-administered with weekly administration of oral methotrexate 15 mg, higher steady-state peak and trough concentrations (2.65 µg/mL and 1.13 µg/mL, respectively) of pegloticase were observed compared to when KRYSTEXXA is given alone (steady-state peak and trough concentrations at 2.13 µg/mL and 0.59 µg/mL, respectively).
As with all therapeutic proteins, there is a potential for immunogenicity. The observed incidence of antibody positivity in an assay is highly dependent on several factors including assay sensitivity and specificity and assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, the comparison of the incidence of antibodies to pegloticase with the incidence of antibodies to other products may be misleading.
In a 52-week, randomized, double-blind trial which evaluated KRYSTEXXA co-administered with methotrexate compared to KRYSTEXXA alone, approximately 26% of patients had pre-existing antibodies to pegloticase. Patients with an increase in titer from baseline or who were negative at baseline and developed an anti-pegloticase response at one or more post dose time points was 30% and 51%, for the KRYSTEXXA co-administered with methotrexate and KRYSTEXXA alone treatment groups, respectively. Patients with higher antibody titers were more likely to have faster clearance and lower efficacy.
During pre-marketing 24-week controlled clinical trials with KRYSTEXXA alone, anti-pegloticase antibodies developed in 92% of patients treated with KRYSTEXXA every 2 weeks, and 28% for placebo. Anti-PEG antibodies were also detected in 42% of patients treated with KRYSTEXXA. High anti-pegloticase antibody titer was associated with a failure to maintain pegloticase-induced normalization of uric acid. The impact of anti-PEG antibodies on patients’ responses to other PEG-containing therapeutics is unknown.
There was a higher incidence of infusion reactions in patients with high anti-pegloticase antibody titer: 53% (16 of 30) in the KRYSTEXXA every 2 weeks group compared to 6% in patients who had undetectable or low antibody titers.
Medication Guide
KRYSTEXXA® (kris-TEX-a)
(pegloticase)
injection, for intravenous use
Read this Medication Guide before you start receiving KRYSTEXXA and before each treatment. There may be new information. This Medication Guide does not take the place of talking with your doctor about your medical condition or treatment. Talk to your doctor if you have any questions about your treatment with KRYSTEXXA.
What is the most important information I should know about KRYSTEXXA?
Serious allergic reactions may happen in some people who receive KRYSTEXXA. These allergic reactions can be life threatening and usually happen within 2 hours of the infusion.
KRYSTEXXA should be given to you by a doctor or nurse in a healthcare setting where serious allergic reactions can be treated. Your doctor or nurse should watch you for any signs of a serious allergic reaction during and after your treatment with KRYSTEXXA.
Tell your doctor or nurse right away if you have any of these symptoms during or after your treatment with KRYSTEXXA:
What is KRYSTEXXA?
It is not known if KRYSTEXXA is safe and effective in children under 18 years of age.
Who should not receive KRYSTEXXA?
Do not receive KRYSTEXXA if you:
What should I tell my doctor before receiving treatment with KRYSTEXXA?
Before you receive KRYSTEXXA, tell your doctor about all of your medical conditions, including if you:
Tell your doctor about all the medicines you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements. Do not take any other uric acid lowering drug, such as allopurinol, febuxostat (Uloric) or probenecid, while receiving KRYSTEXXA.
Know the medicines you take. Keep a list of your medicines and show them to your doctor and pharmacist when you get a new medicine.
How will I receive KRYSTEXXA?
See “What is the most important information I should know about KRYSTEXXA?”
The most common side effects of KRYSTEXXA when given together with methotrexate include:
The most common side effects of KRYSTEXXA include:
Tell your doctor if you have any side effect that bothers you or that does not go away.
These are not all of the side effects of KRYSTEXXA. For more information, ask your doctor or pharmacist.
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
You may also report side effects to Amgen Inc. at 1-800-77-AMGEN (1-800-772-6436).
General information about the safe and effective use of KRYSTEXXA.
Medicines are sometimes prescribed for purposes other than those listed in a Medication Guide. This Medication Guide summarizes the most important information about KRYSTEXXA. If you would like more information, talk with your doctor. You can ask your pharmacist or doctor for information about KRYSTEXXA that is written for health professionals.
For more information, go to www.KRYSTEXXA.com or call 1-866-479-6742.
What are the ingredients in KRYSTEXXA? Active ingredient: pegloticase Inactive ingredients:
Ready-to-Use KRYSTEXXA 8 mg/50 mL (0.16 mg/mL) single-dose vial: disodium hydrogen phosphate heptahydrate, sodium chloride, sodium dihydrogen phosphate monohydrate, and water for injection.
To-be-Diluted KRYSTEXXA 8 mg/mL single-dose vial: disodium hydrogen phosphate dihydrate, sodium chloride, sodium dihydrogen phosphate dihydrate, and water for injection.
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Manufactured by:
Horizon Therapeutics Ireland DAC
Dublin, Ireland
U.S. License Number 2022
© 2025 Amgen Inc. All rights reserved. V7
This Medication Guide has been approved by the U.S. Food and Drug Administration.
