Drug Monograph

Parsabiv (Etelcalcetide)

etelcalcetide injection

Calcimimetic Agent · Intravenous · Calcium-Sensing Receptor Agonist
Pharmacokinetic Profile
Effective Half-Life
3–4 days
Metabolism
Biotransformed by disulfide exchange (not CYP450)
Protein Binding
Covalent binding to albumin; non-covalent fu = 0.53
Bioavailability
100% (IV administration)
Volume of Distribution
~796 L (Vss)
Clinical Information
Drug Class
Calcimimetic (synthetic peptide)
Available Doses
2.5 mg/0.5 mL, 5 mg/1 mL, 10 mg/2 mL vials
Route
IV bolus (end of hemodialysis)
Renal Adjustment
Cleared by hemodialysis; no separate renal adjustment
Hepatic Adjustment
Not studied (not CYP450 metabolized)
Pregnancy
Limited data; animal effects at maternal-toxic doses
Lactation
Not recommended (present in rat milk)
Schedule
Prescription only (not controlled)
Generic Available
No
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
Secondary hyperparathyroidism in CKD on hemodialysisAdultsMonotherapy or adjunctive (with phosphate binders, vitamin D sterols)FDA Approved

Etelcalcetide is a second-generation, intravenous calcimimetic peptide that modulates the calcium-sensing receptor on parathyroid chief cells. Approved by the FDA in February 2017, it is indicated exclusively for the treatment of secondary hyperparathyroidism (sHPT) in adult patients with chronic kidney disease who are receiving hemodialysis. Unlike oral cinacalcet, etelcalcetide is administered as an IV bolus at the end of the hemodialysis session three times weekly, ensuring full adherence under direct observation. This eliminates the pill burden and gastrointestinal first-pass effects associated with oral calcimimetics. Etelcalcetide has not been studied in patients with parathyroid carcinoma, primary hyperparathyroidism, or CKD patients not on hemodialysis, and is not recommended in these populations (FDA PI).

Off-Label Uses

No well-established off-label indications exist at present. Etelcalcetide has been explored in investigator-initiated studies for secondary HPT in peritoneal dialysis patients, but there is insufficient evidence to recommend routine use outside of hemodialysis. Evidence quality: Very low (case reports, pilot data only).

Dose

Dosing

Adult Dosing by Clinical Scenario

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Secondary HPT — new initiation in hemodialysis patient5 mg IV TIW2.5–15 mg IV TIW15 mg TIWAdminister at end of hemodialysis; titrate in 2.5 or 5 mg increments no more frequently than every 4 weeks
Confirm corrected serum calcium ≥ LLN before starting
Secondary HPT — switching from cinacalcet (Sensipar)5 mg IV TIWTitrate per standard protocol15 mg TIWDiscontinue cinacalcet for at least 7 days before starting etelcalcetide
Confirm corrected serum calcium ≥ LLN before initiation
Secondary HPT — re-initiation after dosing interruption >2 weeks5 mg IV TIW (or 2.5 mg if that was last dose)Titrate per standard protocol15 mg TIWResume at starting dose after gaps >2 weeks; for shorter gaps, resume at prescribed dose
Never administer missed doses; resume at next HD session
Secondary HPT — dose reduction for hypocalcemiaRe-initiate 5 mg lower than last doseIndividualized15 mg TIWStop if corrected Ca <7.5 mg/dL or symptomatic; re-initiate only when Ca normalized and symptoms resolved
If last dose was 2.5 or 5 mg, re-initiate at 2.5 mg
Clinical Pearl: Administration Technique

Etelcalcetide is removed by the dialyzer membrane and must be administered after blood is no longer circulating through the dialyzer. Administer by IV bolus into the venous line of the dialysis circuit during rinse-back (followed by at least 150 mL saline) or after rinse-back (followed by at least 10 mL saline flush). Do not mix or dilute prior to administration. If a hemodialysis session is missed, do not administer any missed doses — resume at the next session at the prescribed dose.

PK

Pharmacology

Mechanism of Action

Etelcalcetide is a synthetic D-amino acid peptide that functions as a calcimimetic agent by allosterically modulating the calcium-sensing receptor (CaSR). Unlike cinacalcet, which binds the transmembrane domain of CaSR, etelcalcetide binds to the extracellular domain of the receptor through formation of a covalent disulfide bond with the receptor’s Cys482 residue. This enhances the receptor’s activation by extracellular calcium, triggering downstream signaling that suppresses PTH synthesis and secretion from parathyroid chief cells. Following IV administration, PTH levels begin to decline within 30 minutes, with the magnitude and duration of PTH suppression increasing proportionally with dose. The resulting PTH reduction leads to concomitant decreases in serum calcium, phosphorus, and calcium-phosphorus product.

ADME Profile

ParameterValueClinical Implication
Absorption100% bioavailability (IV route); PTH reduction begins within 30 min of bolus; linear PK over 5–60 mg single doses and 2.5–20 mg repeated dosesPredictable dose-response relationship; ensures full systemic exposure with every administered dose
DistributionVss ~796 L; predominantly bound to plasma albumin via reversible covalent disulfide bonds; non-covalent fraction unbound = 0.53; blood-to-plasma ratio ~0.6Large Vd indicates extensive tissue distribution; covalent albumin binding serves as a circulating reservoir prolonging drug effect
MetabolismNot metabolized by CYP450 enzymes; biotransformed in blood by reversible disulfide exchange with endogenous thiols, predominantly forming conjugates with serum albuminNo CYP450-mediated drug interactions; biotransformation products have ~5-fold higher plasma exposure than parent compound with parallel kinetics
EliminationEffective t½ 3–4 days; hemodialysis clearance 7.66 L/hr; ~60% recovered in dialysate, ~7% in urine/feces (175 days); steady state in 7–8 weeks; accumulation ratio 3–4-foldHemodialysis is the primary elimination pathway in CKD patients; slow accumulation means dose changes take several weeks to reach new steady state
SE

Side Effects

≥10% Very Common
Adverse EffectIncidenceClinical Note
Blood calcium decreased (asymptomatic)64%Vs 10% placebo; defined as asymptomatic reductions below 7.5 mg/dL or clinically significant asymptomatic reductions between 7.5 and <8.3 mg/dL requiring medical management; expected pharmacological effect
Muscle spasms12%Vs 7% placebo; likely secondary to calcium reduction; check serum calcium if new onset
Diarrhea11%Vs 9% placebo; monitor hydration in hemodialysis patients
Nausea11%Vs 6% placebo; less frequent than oral cinacalcet despite IV route; monitor for dehydration
1–10% Common
Adverse EffectIncidenceClinical Note
Vomiting9%Vs 5% placebo; monitor electrolytes and fluid status
Headache8%Vs 6% placebo; usually mild and self-limiting
Hypocalcemia (symptomatic)7%Vs 0.2% placebo; symptomatic reductions in corrected Ca <8.3 mg/dL; requires dose adjustment or discontinuation
Paresthesia (including hypoesthesia)6%Vs 1% placebo; may indicate subclinical hypocalcemia; check calcium levels
Hyperkalemia4%Vs 3% placebo; monitor potassium as part of routine dialysis labs
Myalgia2%Vs 0.2% placebo; may reflect calcium-mediated effects on muscle; assess calcium levels
Heart failure hospitalization2%Vs 1% placebo; causal relationship not established but caution in patients with impaired cardiac function
Hypophosphatemia1%Vs 0.2% placebo; 18% of etelcalcetide patients had at least one phosphorus below 2.2 mg/dL (vs 8.2% placebo)
Serious Serious (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Severe hypocalcemia (Ca <7.0 mg/dL)7.6% (vs 3.1% placebo)Within first weeks of therapy or after dose increaseStop etelcalcetide if Ca <7.5 mg/dL or symptomatic; supplement calcium, increase phosphate binders or vitamin D, increase dialysate calcium; re-initiate at lower dose only when Ca normalized
QTc prolongation / ventricular arrhythmiaQTcF >500 ms: 4.8% vs 1.9% placebo; QTcF increase >60 ms: 1.2% vs 0%Secondary to hypocalcemia; any time during treatmentMonitor QTc in at-risk patients; correct hypocalcemia promptly; consider ECG monitoring during dose titration in patients with cardiac risk factors
Seizures (secondary to hypocalcemia)Rare (postmarketing reports)Variable; risk increases with significant hypocalcemiaMonitor calcium in patients with seizure disorders; dose reduce or discontinue if seizure occurs in setting of hypocalcemia
Worsening heart failure2% vs 1% placebo (HF hospitalization)Variable; may be mediated by calcium reductionClosely monitor for worsening signs and symptoms of HF; consider dose reduction or discontinuation
Upper GI bleedingRare (2 deaths with GI bleeding in 1,253 patient-years vs 0 in 384 patient-years placebo)Any timeMonitor patients with GI risk factors; promptly evaluate any suspected GI bleeding
Anaphylactic reaction / hypersensitivityRare (4.4% any hypersensitivity vs 3.7% placebo; anaphylaxis reported postmarketing)Any time; can occur on first or subsequent exposurePermanently discontinue; treat with standard anaphylaxis protocol including epinephrine
DC Discontinuation Rates
Placebo-Controlled Studies (26 Weeks)
1% vs 0% placebo (due to hypocalcemia)
Context: Mean exposure to etelcalcetide was 23.6 weeks. 79% of patients experienced corrected Ca <8.3 mg/dL at some point, yet formal discontinuation due to low calcium was uncommon.
Open-Label Extension (1 Year)
89.8% experienced ≥1 adverse event
Most common AEs in OLE: Decreased blood Ca (43.3%), diarrhea (10.8%), vomiting (10.4%), nausea (9.6%). Symptomatic hypocalcemia: 3.7%.
Reason for DiscontinuationIncidenceContext
Hypocalcemia (low corrected serum calcium)1% etelcalcetide vs 0% placeboPlacebo-controlled studies; most hypocalcemia was managed with dose adjustment rather than discontinuation
Hypersensitivity reactionsRarePruritic rash, urticaria, face edema reported; anaphylactic reaction reported postmarketing — requires permanent discontinuation
Managing Hypocalcemia: The Dominant Safety Concern

Calcium reduction is the most frequent adverse finding with etelcalcetide. A stepwise approach is recommended: (1) for Ca below LLN but ≥7.5 mg/dL without symptoms, consider dose reduction or concomitant calcium-raising therapy; (2) for Ca <7.5 mg/dL or symptomatic hypocalcemia, stop etelcalcetide, correct calcium, and re-initiate at a dose 5 mg lower once corrected. Proactive adjustment of calcium-based phosphate binders, vitamin D sterols, or dialysate calcium concentration can mitigate hypocalcemia risk during dose titration.

Int

Drug Interactions

Etelcalcetide is a synthetic peptide biotransformed by disulfide exchange in the blood and is not metabolized by CYP450 enzymes. It does not inhibit or induce any CYP isoforms. Consequently, etelcalcetide has no known pharmacokinetic drug-drug interactions. However, pharmacodynamic interactions are clinically important, particularly with agents that lower serum calcium or prolong the QT interval.

Major Cinacalcet (Sensipar)
MechanismBoth agents activate CaSR, causing additive calcium lowering
EffectSevere, life-threatening hypocalcemia
ManagementContraindicated concurrently. Discontinue cinacalcet for at least 7 days before starting etelcalcetide. Confirm corrected Ca ≥ LLN before initiating.
FDA PI
Major Denosumab
MechanismAdditive calcium-lowering via different pathways (CaSR activation + RANKL inhibition)
EffectSevere hypocalcemia; postmarketing reports of concomitant use causing dangerous calcium levels
ManagementUse extreme caution; closely monitor corrected serum calcium; consider dose adjustment of either agent
FDA PI — Postmarketing
Moderate QT-Prolonging Agents (e.g., sotalol, amiodarone, ondansetron)
MechanismEtelcalcetide-induced hypocalcemia may prolong QTc; additive risk with other QT-prolonging drugs
EffectIncreased risk of ventricular arrhythmia; QTcF >500 ms occurred in 4.8% of etelcalcetide patients vs 1.9% placebo
ManagementMonitor QTc interval and corrected serum calcium closely; correct hypocalcemia and electrolyte abnormalities
FDA PI
Moderate Other Calcium-Lowering Therapies (bisphosphonates, loop diuretics)
MechanismAdditive reduction in serum calcium through complementary mechanisms
EffectIncreased risk and severity of hypocalcemia
ManagementMonitor corrected serum calcium more frequently when combined; adjust doses as needed
FDA PI
Minor CYP450 Substrates (warfarin, statins, etc.)
MechanismEtelcalcetide is not metabolized by and does not inhibit or induce CYP450 enzymes
EffectNo pharmacokinetic interactions expected
ManagementNo dose adjustments required; this is a notable advantage over cinacalcet (strong CYP2D6 inhibitor)
FDA PI
Mon

Monitoring

  • Corrected Serum Calcium Prior to initiation; within 1 week after dose initiation or adjustment; every 4 weeks during maintenance
    Routine
    Most critical parameter. Do not initiate if Ca < LLN. If Ca below LLN but ≥7.5 mg/dL without symptoms: consider decreasing dose or using concomitant calcium-raising therapy. If Ca <7.5 mg/dL or symptomatic: stop etelcalcetide, correct calcium, and re-initiate at a dose 5 mg lower.
  • PTH 4 weeks after initiation or dose adjustment; per clinical practice during maintenance
    Routine
    Target: maintain PTH within recommended range. Decrease or discontinue if PTH falls below target to avoid adynamic bone disease.
  • Serum Phosphorus With calcium monitoring schedule
    Routine
    Etelcalcetide reduces phosphorus through PTH suppression. 18% of patients had phosphorus below 2.2 mg/dL. Adjust phosphate binders as needed.
  • Symptoms of Hypocalcemia Each hemodialysis session
    Routine
    Ask about paresthesias, muscle spasms, cramping, or seizure-like activity at each session. Educate patients to report symptoms between sessions.
  • QTc Interval Baseline and during dose titration in at-risk patients
    Trigger-based
    Indicated in patients with congenital long QT syndrome, history of QT prolongation, family history of sudden cardiac death, or concomitant QT-prolonging medications. QTcF >500 ms was observed in 4.8% of etelcalcetide patients.
  • Heart Failure Signs Each visit; heightened vigilance in patients with cardiac history
    Trigger-based
    Heart failure hospitalization occurred in 2% of etelcalcetide patients vs 1% placebo. Monitor for worsening dyspnea, peripheral edema, weight gain.
  • GI Symptoms Each visit; heightened vigilance in at-risk patients
    Trigger-based
    Upper GI bleeding was rare but fatal in clinical studies. Monitor patients with known gastritis, ulcers, or severe vomiting for signs of GI bleeding.
CI

Contraindications & Cautions

Absolute Contraindications

  • Known hypersensitivity to etelcalcetide or any excipient — hypersensitivity reactions including facial edema and anaphylaxis have been reported (FDA PI).

Relative Contraindications (Specialist Input Recommended)

  • Corrected serum calcium below the lower limit of normal — do not initiate, increase dose, or re-initiate until calcium is corrected to ≥ LLN.
  • Concurrent use of cinacalcet or another CaSR agonist — risk of severe, life-threatening hypocalcemia. Cinacalcet must be discontinued for at least 7 days before starting etelcalcetide.
  • Congenital long QT syndrome or significant QT prolongation — hypocalcemia from etelcalcetide may further prolong QTc; 4.8% of etelcalcetide patients had QTcF >500 ms.
  • Active seizure disorder with poor control — hypocalcemia lowers the seizure threshold; postmarketing reports of seizures secondary to etelcalcetide-induced hypocalcemia.

Use with Caution

  • Impaired cardiac function / heart failure — HF hospitalization was 2% vs 1% placebo; causal relationship not excluded; monitor closely.
  • Risk factors for upper GI bleeding — patients with gastritis, esophagitis, peptic ulcer, or severe vomiting may have elevated risk.
  • Concurrent calcium-lowering therapies (denosumab, bisphosphonates) — risk of additive severe hypocalcemia; postmarketing reports confirm this risk.
FDA Safety Warning Hypocalcemia: Potentially Severe and Life-Threatening

Etelcalcetide lowers serum calcium and can lead to hypocalcemia, sometimes severe. Significant lowering of serum calcium can cause paresthesias, myalgias, muscle spasms, seizures, QT interval prolongation, and ventricular arrhythmia. In combined placebo-controlled studies, 7.6% of etelcalcetide patients developed serum calcium below 7.0 mg/dL (vs 3.1% placebo), 27% developed calcium below 7.5 mg/dL (vs 5.5% placebo), and 79% had at least one corrected serum calcium below 8.3 mg/dL (vs 19% placebo). More etelcalcetide patients experienced QTcF >500 ms (4.8% vs 1.9% placebo).

Monitor corrected serum calcium prior to initiation, within 1 week after dose changes, and every 4 weeks during maintenance. Correct hypocalcemia before initiating therapy.

Pt

Patient Counselling

Purpose of Therapy

Etelcalcetide helps control overactive parathyroid glands that develop when the kidneys can no longer maintain mineral balance. By lowering parathyroid hormone levels, it protects bones and blood vessels from damage caused by excess PTH and mineral imbalances. It is given as an injection directly into the dialysis tubing at the end of each hemodialysis session, so patients do not need to take an extra pill at home.

How It Is Given

Your dialysis nurse or technician will administer etelcalcetide through the dialysis line at the end of your hemodialysis treatment, three times per week. You do not need to do anything at home for this medication. Regular blood tests will check your calcium and parathyroid hormone levels to make sure the dose is right for you.

Low Calcium (Hypocalcemia)
Tell patient This medication works by lowering calcium, which is part of how it controls your parathyroid hormone. You may notice tingling around your mouth or fingers, muscle cramps, or spasms. These are common and your care team monitors your calcium regularly. Take any calcium supplements or phosphate binders exactly as prescribed.
Call prescriber If you develop severe muscle cramping, twitching that you cannot control, numbness, confusion, or seizure-like activity. Seek emergency care immediately for these symptoms.
Nausea, Vomiting & Diarrhea
Tell patient Some patients experience nausea, vomiting, or diarrhea during treatment. These symptoms are generally less common than with the oral calcimimetic cinacalcet, but they can still occur. Stay well hydrated between dialysis sessions.
Call prescriber If vomiting or diarrhea is severe, persistent, or if you notice blood in your stool or vomit that looks like coffee grounds.
Heart-Related Cautions
Tell patient Patients with heart problems should make sure their dialysis team is aware. Changes in calcium levels can sometimes affect heart rhythm or worsen heart failure symptoms.
Call prescriber If you experience palpitations, fainting, unusual shortness of breath, or worsening swelling in your legs between dialysis sessions.
Allergic Reactions
Tell patient As with any injectable medication, allergic reactions can occur. Your dialysis staff will monitor you during and after each injection.
Call prescriber If you develop itchy rash, hives, swelling of the face or throat, or difficulty breathing during or after dialysis. These are signs of a serious allergic reaction requiring immediate treatment.
Attending Dialysis Sessions
Tell patient Etelcalcetide is given only during hemodialysis. If you miss a dialysis session, you will not receive that dose. Do not worry about making up missed doses — simply resume at your next scheduled session.
Call prescriber If you have missed more than 2 weeks of dialysis sessions, as your care team may need to adjust your starting dose when you resume.
Ref

Sources

Regulatory (PI / SmPC)
  1. Parsabiv (etelcalcetide) Injection — Full Prescribing Information. Amgen Inc. Revised 01/2025. DailyMed Primary regulatory source for all dosing, indications, adverse reactions, contraindications, pharmacokinetic data, and warnings in this monograph.
  2. Parsabiv (etelcalcetide) Injection — FDA Approval Label. U.S. Food and Drug Administration. 2017. FDA Original brand approval label including complete clinical pharmacology and nonclinical toxicology data.
Key Clinical Trials
  1. 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(2):146–155. doi:10.1001/jama.2016.19456 Two pivotal phase 3 placebo-controlled trials (n=1,023) demonstrating significant PTH reduction with etelcalcetide over 26 weeks; source of primary adverse event data.
  2. Block GA, Bushinsky DA, Chertow GM, et al. Effect of etelcalcetide vs cinacalcet on serum parathyroid hormone in patients receiving hemodialysis with secondary hyperparathyroidism: a randomized clinical trial. JAMA. 2017;317(2):156–164. doi:10.1001/jama.2016.19468 Head-to-head noninferiority/superiority trial (n=683) showing etelcalcetide was noninferior and superior to cinacalcet for PTH reduction over 26 weeks.
  3. Bushinsky DA, Chertow GM, Cheng S, et al. One-year safety and efficacy of intravenous etelcalcetide in patients on hemodialysis with secondary hyperparathyroidism. Nephrol Dial Transplant. 2020;35(10):1769–1778. doi:10.1093/ndt/gfz039 Open-label extension providing 1-year safety data; most common AE was decreased blood calcium (43.3%); no new safety signals.
  4. Block GA, Chertow GM, Bushinsky DA, et al. Etelcalcetide is effective at all levels of severity of secondary hyperparathyroidism in hemodialysis patients. Kidney Int Rep. 2019;4(7):987–994. doi:10.1016/j.ekir.2019.04.010 Post-hoc analysis of the two phase 3 trials showing etelcalcetide effectively lowered PTH across all baseline severity strata.
Guidelines
  1. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD. Kidney Int Suppl. 2017;7(1):1–59. doi:10.1016/j.kisu.2017.04.001 International guideline recommending calcimimetics, calcitriol, or vitamin D analogs for CKD G5D patients requiring PTH-lowering therapy (Rec 4.2.4, 2B).
  2. Ketteler M, et al. Chronic kidney disease–mineral and bone disorder: conclusions from a KDIGO Controversies Conference. Kidney Int. 2025;107(3):405–423. doi:10.1016/j.kint.2024.11.013 Most recent KDIGO update; notes newer calcimimetics (etelcalcetide, evocalcet) have similar or superior PTH-lowering efficacy to cinacalcet but no proven survival benefit.
Mechanistic / Basic Science
  1. Alexander ST, Hunter T, Walter S, et al. Critical cysteine residues in both the calcium-sensing receptor and the allosteric activator AMG 416 underlie the mechanism of action. Mol Pharmacol. 2015;88(5):853–865. doi:10.1124/mol.115.098392 Elucidates the unique mechanism of etelcalcetide binding to CaSR Cys482 via disulfide bond formation, distinguishing it from cinacalcet.
  2. Walter S, Baruch A, Dong J, et al. Pharmacology of AMG 416 (velcalcetide), a novel peptide agonist of the calcium-sensing receptor, for the treatment of secondary hyperparathyroidism in hemodialysis patients. J Pharmacol Exp Ther. 2013;346(2):229–240. doi:10.1124/jpet.113.204834 Preclinical pharmacology of etelcalcetide (originally AMG 416/velcalcetide) demonstrating dose-dependent PTH suppression in animal models.
Pharmacokinetics / Special Populations
  1. Martin KJ, Pickthorn K, Bhatt DL, et al. First-in-human, phase 1 study of AMG 416, a novel peptide for the treatment of secondary hyperparathyroidism in hemodialysis patients. Bone. 2014;68:24–31. doi:10.1016/j.bone.2014.07.035 Phase 1 single- and multiple-dose PK study establishing the dose-response relationship, effective half-life, and hemodialysis clearance parameters.
  2. Middleton JP, Wolf M. Second chances to improve ESRD outcomes with a second-generation calcimimetic. JAMA. 2017;317(2):139–141. doi:10.1001/jama.2016.18631 Editorial contextualizing the etelcalcetide phase 3 program within the evolving landscape of CKD-MBD therapeutics and adherence challenges.