Care Team Corner | Welcome | Parsabiv® (etelcalcetide)

Indication and Limitations of Use:

  • Parsabiv® (etelcalcetide) is indicated for the treatment of secondary hyperparathyroidism (HPT) in adult patients with chronic kidney disease (CKD) on hemodialysis. Read More
  • Parsabiv® has not been studied in adult patients with parathyroid carcinoma, primary hyperparathyroidism, or with CKD who are not on hemodialysis and is not recommended for use in these populations. Close
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Image of Parsabiv care team nurse
Image of Parsabiv care team nurse

The calcimimetic that
gives me
control over
administration.

Parsabiv® is the first and only IV-administered calcimimetic.

Welcome to the Parsabiv® Care Team Corner

Insights and information on Parsabiv® (etelcalcetide) created especially for members of the dialysis care team

Storing

Prepping

Administering

Celebrating the special
bond between patients
and their care team

A hemodialysis professional shares how his patient inspires him and touches his life every day.

The pathogenesis of sHPT and the complementary effects of treatments1-7

Decreased Kidney Function
Decreased Calcium Absorption
Decreased Activation of CaSR
IncreasedP & Ca release
1,25 D3
Serum Ca
PTH synthesis/secretion
Vitamin D sterols increase Ca/P absorption
Parsabiv® increases activity of CaSRs, lowering PTH
Vitamin D sterols inhibit synthesis of PTH
Phosphate binders and dietary restrictions limit P absorption
Ilustration of the pathogenesis of sHPT and the complementary effects of Parsabiv®, Vitamin D, and Phosphate binders Ilustration of the pathogenesis of sHPT and the complementary effects of Parsabiv®, Vitamin D, and Phosphate binders

Approximately 7 times more patients given Parsabiv® achieved > 30% reduction in mean PTH8

Graph showing 78% of patients on Parsabiv® plus vitamin D and/or phosphate binders* had > 30% iPTH reductions Graph showing 78% of patients on Parsabiv® plus vitamin D and/or phosphate binders* had > 30% iPTH reductions

P < 0.001

Results are combined from two 26-week, randomized, double-blind, placebo-controlled studies comparing Parsabiv® (etelcalcetide) with placebo in patients with chronic kidney disease (CKD) on hemodialysis with intact parathyroid hormone (iPTH) > 400 pg/mL and corrected calcium ≥ 8.3 mg/dL; N = 1023. Patients in both treatment arms could be treated with vitamin D sterols and/or phosphate binders. Mean baseline iPTH in the Parsabiv® group and placebo group were 847 pg/mL and 836 pg/mL, respectively. The primary endpoint of each study was the proportion of patients who achieved a > 30% reduction from baseline in mean iPTH during the EAP (defined as weeks 20 through 27, inclusive).1,9,10

*Vitamin D and/or phosphate binders, if prescribed.10

EAP = efficacy assessment phase.

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Administration, storage, and handling video

Watch this video, geared specifically toward nurses, on how to store and administer Parsabiv®.

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STORING & HANDLING

Learn about dose sizes
and safe storage

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PREPPING PARSABIV®

Vial handling best practices
and withdrawal tips
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RESOURCES

Parsabiv® educational tools that cover all aspects of the only IV calcimimetic

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Important Safety Information for Parsabiv®

Contraindication: Parsabiv® (etelcalcetide) is contraindicated in patients with known hypersensitivity to etelcalcetide or any of its excipients. Hypersensitivity reactions, including face edema and anaphylactic reaction, have occurred.

Hypocalcemia: Parsabiv® lowers serum calcium and can lead to hypocalcemia, sometimes severe. Significant lowering of serum calcium can cause QT interval prolongation and ventricular arrhythmia. Patients with conditions that predispose to QT interval prolongation and ventricular arrhythmia may be at increased risk for QT interval prolongation and ventricular arrhythmias if they develop hypocalcemia due

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Important Safety Information for Parsabiv®

Contraindication: Parsabiv® (etelcalcetide) is contraindicated in patients with known hypersensitivity to etelcalcetide or any of its excipients. Hypersensitivity reactions, including face edema and anaphylactic reaction, have occurred.

Hypocalcemia: Parsabiv® lowers serum calcium and can lead to hypocalcemia, sometimes severe. Significant lowering of serum calcium can cause QT interval prolongation and ventricular arrhythmia. Patients with conditions that predispose to QT interval prolongation and ventricular arrhythmia may be at increased risk for QT interval prolongation and ventricular arrhythmias if they develop hypocalcemia due to Parsabiv®. Closely monitor corrected serum calcium and QT interval in patients at risk on Parsabiv®.

Significant reductions in corrected serum calcium may lower the threshold for seizures. Patients with a history of seizure disorder may be at increased risk for seizures if they develop hypocalcemia due to Parsabiv®. Monitor corrected serum calcium in patients with seizure disorders on Parsabiv®.

Concurrent administration of Parsabiv® with another oral calcimimetic could result in severe, life-threatening hypocalcemia. Patients switching from cinacalcet to Parsabiv® should discontinue cinacalcet for at least 7 days prior to initiating Parsabiv®. Closely monitor corrected serum calcium in patients receiving Parsabiv® and concomitant therapies known to lower serum calcium.

Measure corrected serum calcium prior to initiation of Parsabiv®. Do not initiate in patients if the corrected serum calcium is less than the lower limit of normal. Monitor corrected serum calcium within 1 week after initiation or dose adjustment and every 4 weeks during treatment with Parsabiv®. Measure PTH 4 weeks after initiation or dose adjustment of Parsabiv®. Once the maintenance dose has been established, measure PTH per clinical practice.

Worsening Heart Failure: In Parsabiv® clinical studies, cases of hypotension, congestive heart failure, and decreased myocardial performance have been reported. Closely monitor patients treated with Parsabiv® for worsening signs and symptoms of heart failure.

Upper Gastrointestinal Bleeding: In clinical studies, 2 patients treated with Parsabiv® in 1253 patient years of exposure had upper gastrointestinal (GI) bleeding at the time of death. The exact cause of GI bleeding in these patients is unknown and there were too few cases to determine whether these cases were related to Parsabiv®.

Patients with risk factors for upper GI bleeding, such as known gastritis, esophagitis, ulcers or severe vomiting, may be at increased risk for GI bleeding with Parsabiv®. Monitor patients for worsening of common Parsabiv® GI adverse reactions and for signs and symptoms of GI bleeding and ulcerations during Parsabiv® therapy.

Adynamic Bone: Adynamic bone may develop if PTH levels are chronically suppressed.

Adverse Reactions: In clinical trials of patients with secondary HPT comparing Parsabiv® to placebo, the most common adverse reactions were blood calcium decreased (64% vs. 10%), muscle spasms (12% vs. 7%), diarrhea (11% vs. 9%), nausea (11% vs. 6%), vomiting (9% vs. 5%), headache (8% vs. 6%), hypocalcemia (7% vs. 0.2%), and paresthesia (6% vs. 1%).

Indication

Parsabiv® (etelcalcetide) is indicated for the treatment of secondary hyperparathyroidism (HPT) in adult patients with chronic kidney disease (CKD) on hemodialysis.

Limitations of Use: Parsabiv® has not been studied in adult patients with parathyroid carcinoma, primary hyperparathyroidism, or with CKD who are not on hemodialysis and is not recommended for use in these populations.

Limitations of Use: Parsabiv® has not been studied in adult patients with parathyroid carcinoma, primary hyperparathyroidism, or with CKD who are not on hemodialysis and is not recommended for use in these populations.

Please see Parsabiv® (etelcalcetide) full Prescribing Information.

References: 1. Parsabiv® (etelcalcetide) prescribing information, Amgen. 2. Komaba H, Shiizaki K, Fukagawa M. Pharmacotherapy and interventional treatments for secondary hyperparathyroidism: current therapy and future challenges. Expert Opin Biol Ther. 2010;10:1729-1742. 3. Goodman WG. Calcium and phosphorus metabolism in patients who have chronic kidney disease. Med Clin North Am. 2005;89:631-647. 4. Rodriguez M, et al. The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism. Am J Physiol Renal Physiol. 2005;288:F253-F264. 5. Hruska KA, Mathew S, Lund R, Qiu P, Pratt R. Hyperphosphatemia of chronic kidney disease. Kidney Int. 2008;74:148-157. 6. Wesseling-Perry K, Harkins GC, Wang HJ, et al. The calcemic response to continuous parathyroid hormone (PTH)(1-34) infusion in end-stage kidney disease varies according to bone turnover: a potential role for PTH(7-84). J Clin Endocrinol Metab. 2010;95:2772-2780. 7. Goodman WG, Quarles LD. Vitamin D, calcimimetics, and phosphate-binders. In: Brenner BM, Levine SA, eds. Brenner & Rector’s The Kidney. 8th ed. Philadelphia, PA: Saunders Elsevier; 2008:1904-1927. 8. Data on file, Amgen; [Combined Phase 3 Lab Values Multiple Imputation Approach; 2017]. 9. Data on file, Amgen; [Summary of Clinical Efficacy; 2015]. 10. Block GA, Bushinsky DA, Cunningham J, et al. Effect of etelcalcetide vs placebo on serum parathyroid hormone in patients receiving hemodialysis with secondary hyperparathyroidism: two randomized clinical trials. JAMA. 2017;317:146-155.