Drug Monograph
Cinacalcet (Sensipar)
cinacalcet hydrochloride
Pharmacokinetic Profile
Half-Life
~6 h (initial); 30–40 h (terminal)
Metabolism
CYP3A4, CYP2D6, CYP1A2
Protein Binding
93–97%
Bioavailability
Increased 68% (AUC) with high-fat meal
Volume of Distribution
~1,000 L
Clinical Information
Drug Class
Calcimimetic
Available Doses
30 mg, 60 mg, 90 mg tablets
Route
Oral
Renal Adjustment
No adjustment required
Hepatic Adjustment
Monitor closely; AUC increased 2.4× (moderate) and 4.2× (severe)
Pregnancy
Risk data available; limited human data
Lactation
No human data; excreted in rat milk
Schedule
Prescription only (not controlled)
Generic Available
Yes
Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Secondary hyperparathyroidism in CKD on dialysis | Adults | Monotherapy or adjunctive (with vitamin D sterols and/or phosphate binders) | FDA Approved |
| Hypercalcemia in parathyroid carcinoma | Adults | Monotherapy | FDA Approved |
| Severe hypercalcemia in primary hyperparathyroidism | Adults unable to undergo parathyroidectomy | Monotherapy | FDA Approved |
Cinacalcet is a first-in-class calcimimetic agent that modulates the calcium-sensing receptor on parathyroid chief cells. Its primary role is the management of secondary hyperparathyroidism in adults receiving dialysis for end-stage kidney disease, where it lowers iPTH and calcium-phosphorus product when conventional measures (phosphate binders, vitamin D analogs) are inadequate. Cinacalcet is also approved for controlling hypercalcemia in parathyroid carcinoma and in primary hyperparathyroidism when parathyroidectomy is not feasible. Notably, cinacalcet is not indicated for CKD patients who are not on dialysis due to an increased risk of hypocalcemia in this population (FDA PI).
Off-Label Uses
Calciphylaxis in ESKD/dialysis patients: Cinacalcet has been used off-label as part of multimodal management of calciphylaxis (calcific uremic arteriolopathy). Evidence quality: Low (case series, retrospective data).
Persistent hyperparathyroidism after kidney transplantation: Randomized controlled trial data support efficacy in correcting hypercalcemia and hypophosphatemia post-transplant, though no effect on BMD was demonstrated (KDIGO 2025 Controversies Conference). Evidence quality: Moderate.
Dosing
Adult Dosing by Clinical Scenario
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| Secondary HPT — CKD on dialysis, initial therapy | 30 mg once daily | 30–180 mg once daily | 180 mg/day | Titrate q2–4 wk through 30, 60, 90, 120, 180 mg steps; target iPTH 150–300 pg/mL Median effective dose in phase 3 trials: 90 mg/day |
| Secondary HPT — switching from etelcalcetide (Parsabiv) | 30 mg once daily | Titrate per above | 180 mg/day | Wait ≥4 weeks after stopping etelcalcetide; confirm calcium ≥ LLN before starting Allow full etelcalcetide washout to avoid additive hypocalcemia |
| Parathyroid carcinoma — hypercalcemia management | 30 mg twice daily | 30–90 mg BID or up to 90 mg TID–QID | 90 mg four times daily (360 mg/day) | Titrate q2–4 wk; goal: normalize serum calcium ≤10 mg/dL Median exposure in trials was 229 days |
| Primary HPT — severe hypercalcemia, parathyroidectomy not feasible | 30 mg twice daily | 30–90 mg BID or up to 90 mg TID–QID | 90 mg four times daily (360 mg/day) | Same titration as parathyroid carcinoma; goal: normalize serum calcium Median effective dose in pHPT trial: 60 mg/day |
Clinical Pearl: Administration and Titration
Always take cinacalcet with food or shortly after a meal — a high-fat meal increases systemic exposure by approximately 68% (AUC). Tablets must be swallowed whole; do not crush, chew, or divide. When titrating in secondary HPT, measure iPTH no earlier than 12 hours after the most recent dose to avoid capturing the nadir value, which does not reflect steady-state PTH suppression.
Hepatic Impairment Considerations
| Hepatic Impairment | Dose Adjustment | AUC Change | Half-Life Change | Notes |
|---|---|---|---|---|
| Mild (Child-Pugh A) | No adjustment | Comparable to normal | Comparable to normal | Routine monitoring adequate |
| Moderate (Child-Pugh B) | Monitor closely | Increased 2.4-fold | ~65 hours | Close monitoring of calcium, phosphorus, iPTH required |
| Severe (Child-Pugh C) | Monitor closely | Increased 4.2-fold | ~84 hours | Significantly increased exposure; titrate cautiously |
Pharmacology
Mechanism of Action
Cinacalcet is an allosteric modulator of the calcium-sensing receptor (CaSR) located on the surface of parathyroid chief cells. By binding to the transmembrane domain of CaSR, cinacalcet increases the receptor’s sensitivity to extracellular ionized calcium. This enhanced sensitivity triggers intracellular signaling cascades that suppress parathyroid hormone (PTH) synthesis and secretion, even when ambient calcium concentrations are normal or low. The resulting reduction in PTH leads to a concomitant decrease in serum calcium, phosphorus, and the calcium-phosphorus product. Unlike vitamin D analogs that suppress PTH through VDR-mediated gene transcription, cinacalcet acts directly at the receptor level, providing an independent and complementary mechanism for PTH control. The PTH nadir occurs approximately 2 to 6 hours after oral dosing, coinciding with peak plasma concentrations of cinacalcet.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Tmax 2–6 h; AUC and Cmax increase proportionally over 30–180 mg range; high-fat meal increases Cmax by 82% and AUC by 68% | Must take with food to ensure consistent absorption; dose-proportional kinetics simplify titration |
| Distribution | Vd ~1,000 L; 93–97% protein-bound; blood-to-plasma ratio 0.8 | Extensive tissue distribution; highly protein-bound so hemodialysis is not effective for overdose removal |
| Metabolism | Oxidative N-dealkylation and naphthalene oxidation primarily via CYP3A4, CYP2D6, and CYP1A2; metabolites have minimal calcimimetic activity; strong CYP2D6 inhibitor | CYP3A4 inhibitors significantly increase cinacalcet levels; cinacalcet markedly inhibits CYP2D6 substrates (desipramine AUC +264%) |
| Elimination | Renal excretion of metabolites ~80%; fecal ~15%; terminal t½ 30–40 h; steady state within 7 days; accumulation ratio ~2 (QD), 2–5 (BID) | Dose changes are reflected within about 1 week; no renal dose adjustment needed since parent drug is not renally cleared |
Side Effects
≥10%
Very Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Nausea | 29.1% | Most common adverse effect; dose-related; often improves with continued use; take with food to reduce severity |
| Vomiting | 25.6% | Frequently co-occurs with nausea; severe or prolonged vomiting may lead to dehydration and worsen hypercalcemia |
| Diarrhea | 20.5% | Modest excess over placebo (18.7%); monitor hydration and electrolytes in dialysis patients |
| Dyspnea | 13.4% | May reflect underlying comorbidities in CKD population; modest difference versus placebo (11.5%) |
| Cough | 11.7% | Modest excess over placebo (9.8%); evaluate for alternative causes in dialysis population |
| Hypotension | 11.6% | May be mediated by calcium reduction; caution in patients with impaired cardiac function |
| Headache | 11.5% | Versus 9.6% placebo; usually mild and self-limiting |
| Hypocalcemia | 11.2% | Versus 1.4% placebo; pharmacological effect; 66% of patients had ≥1 calcium <8.4 mg/dL in 26-week studies |
| Muscle spasms | 11.1% | May be a manifestation of subclinical hypocalcemia; check calcium levels if new onset |
| Abdominal pain | 10.9% | Versus 9.6% placebo; evaluate for GI bleeding if persistent or severe |
1–10%
Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Upper abdominal pain | 8.2% | Versus 6.3% placebo; differentiate from GI bleeding symptoms |
| Hyperkalemia | 8.1% | Versus 6.1% placebo; important in dialysis population already at risk |
| Upper respiratory tract infection | 7.6% | Versus 6.3% placebo; common in dialysis population; evaluate for secondary causes |
| Dyspepsia | 7.4% | Versus 4.6% placebo; taking with food may help; consider acid suppression |
| Dizziness | 7.3% | Versus 4.7% placebo; may be related to hypotension or hypocalcemia |
| Decreased appetite | 5.9% | Versus 3.5% placebo; monitor nutritional status in dialysis patients |
| Asthenia | 5.4% | Versus 3.8% placebo; assess for hypocalcemia as contributing factor |
| Constipation | 5.0% | Versus 3.8% placebo; may be compounded by calcium-containing phosphate binders |
| Seizures | 2.5% | Versus 1.6% placebo (long-term); threshold may be lowered by significant hypocalcemia |
| Rash | 2.2% | Versus 1.9% placebo; hypersensitivity reactions including angioedema reported post-marketing |
Serious
Serious (Regardless of Frequency)
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Life-threatening hypocalcemia | Common (~11% symptomatic; 29% Ca <7.5 mg/dL in short-term) | Within weeks of initiation or dose titration; 64% of severe cases in first 6 months | Measure calcium within 1 week of any dose change; supplement calcium, increase phosphate binder, increase vitamin D, or withhold cinacalcet if Ca <7.5 mg/dL |
| QT prolongation / ventricular arrhythmia | Rare (postmarketing reports) | Secondary to hypocalcemia; any time during treatment | ECG monitoring in at-risk patients (congenital long QT, history of QT prolongation); correct hypocalcemia promptly |
| Seizures | Uncommon (1.4–2.5%) | Any time; risk increases with significant hypocalcemia | Monitor calcium in patients with seizure disorders; dose reduce or discontinue if seizure occurs in setting of hypocalcemia |
| Upper GI bleeding | Rare (postmarketing and clinical trials) | Any time during treatment | Monitor patients with risk factors (gastritis, esophagitis, ulcers, severe vomiting); promptly evaluate suspected bleeding |
| Worsening heart failure / arrhythmias | Rare (isolated postmarketing cases) | Variable; may be mediated by calcium reduction | Use with caution in patients with impaired cardiac function; monitor closely |
| Adynamic bone disease | Uncommon (11% had iPTH <100 pg/mL in phase 3 trials) | Gradual; with prolonged over-suppression of iPTH | Reduce dose or discontinue if iPTH falls below 150 pg/mL; consider bone biopsy if clinically suspected |
| Hypersensitivity (including angioedema, urticaria) | Rare (postmarketing) | Any time | Discontinue permanently; provide appropriate treatment including epinephrine for anaphylaxis |
DC
Discontinuation Rates
Secondary HPT (Short-Term, 26-Week Studies)
<1% due to hypocalcemia (each group)
Top reasons: Nausea, vomiting, hypocalcemia. ~30% of cinacalcet patients did not complete studies vs ~20% placebo.
Secondary HPT (Long-Term, Up to 64 Months)
1.1% vs 0.1% placebo (due to hypocalcemia)
Top reasons: Nausea, vomiting, GI intolerance. Overall drug discontinuation rate was 66.7% cinacalcet vs 70.5% placebo over ≤64 months.
| Reason for Discontinuation | Incidence | Context |
|---|---|---|
| Nausea / vomiting (severe) | Most frequent cause | Both parathyroid carcinoma and pHPT single-arm study; 20% (9/46) withdrew due to adverse events, most commonly GI |
| Hypocalcemia | <1% (short-term); 1.1% (long-term) | Fatal case reported in pediatric trial contributing to discontinuation of pediatric development |
| Death (parathyroid carcinoma study) | 24% (7/29 with PC) | Causes: cardiovascular (5), multi-organ failure (1), GI hemorrhage (1), metastatic carcinoma (1); reflects severe underlying disease |
Managing Nausea and Vomiting
Gastrointestinal intolerance is the most frequent reason for treatment discontinuation. Strategies to improve tolerability include: always taking cinacalcet with food, starting at the lowest dose (30 mg), titrating slowly (no more frequently than every 2–4 weeks), and considering short-term antiemetic therapy during dose escalation. Severe or prolonged vomiting warrants electrolyte monitoring because dehydration can exacerbate hypercalcemia in parathyroid carcinoma patients.
Drug Interactions
Cinacalcet is metabolized primarily by CYP3A4, CYP2D6, and CYP1A2, making it susceptible to CYP3A4 inhibitors. Importantly, cinacalcet is itself a strong inhibitor of CYP2D6, substantially increasing exposure to co-administered CYP2D6 substrates. It does not inhibit CYP1A2, CYP2C9, CYP2C19, or CYP3A4, and is not an enzyme inducer.
Major
Ketoconazole / Itraconazole
MechanismStrong CYP3A4 inhibition reduces cinacalcet clearance
EffectKetoconazole increased cinacalcet AUC by 127% and Cmax by 116%
ManagementDose adjustment of cinacalcet may be needed; closely monitor iPTH, calcium, and phosphorus. Consider alternative antifungal if feasible.
FDA PI — In Vivo DDI Study
Major
Flecainide / Thioridazine / Pimozide
MechanismCinacalcet strongly inhibits CYP2D6, increasing levels of narrow TI substrates
EffectRisk of toxicity from elevated concentrations of these agents (arrhythmia, QT prolongation)
ManagementAvoid co-administration when possible; if used, reduce CYP2D6 substrate dose and monitor closely
FDA PI
Major
Desipramine / Tricyclic Antidepressants
MechanismStrong CYP2D6 inhibition by cinacalcet markedly increases TCA exposure
EffectDesipramine AUC increased by 264% and Cmax by 75% with cinacalcet 90 mg daily
ManagementUse lowest effective TCA dose; monitor for TCA toxicity (anticholinergic effects, cardiac conduction). Consider TDM.
FDA PI — In Vivo DDI Study
Moderate
Metoprolol / Carvedilol
MechanismCYP2D6 inhibition by cinacalcet increases beta-blocker exposure
EffectPotential for enhanced beta-blockade: excessive bradycardia, hypotension
ManagementDose reduction of metoprolol/carvedilol may be needed. Monitor heart rate and blood pressure.
FDA PI
Moderate
Amitriptyline
MechanismCYP2D6 inhibition by cinacalcet
EffectAmitriptyline AUC increased 21–22%; nortriptyline (active metabolite) AUC increased 17–23%
ManagementMonitor for TCA adverse effects; dose adjustment may be warranted at higher cinacalcet doses
FDA PI — In Vivo DDI Study
Moderate
Etelcalcetide / Other Calcimimetics
MechanismAdditive calcium-lowering effect via CaSR activation
EffectRisk of severe, potentially life-threatening hypocalcemia
ManagementNever use concurrently; wait ≥4 weeks after stopping etelcalcetide before starting cinacalcet
FDA PI
Minor
Warfarin
MechanismMinimal CYP interaction
EffectNo clinically significant change in R- or S-warfarin AUC (≤1%); no change in prothrombin time
ManagementNo dose adjustment required; routine INR monitoring per standard of care
FDA PI — In Vivo DDI Study
Minor
Midazolam
MechanismCYP3A4 substrate; cinacalcet is not a CYP3A4 inhibitor
EffectNo significant change in midazolam AUC (+5%) or Cmax (-5%)
ManagementNo dose adjustment needed; confirms cinacalcet does not inhibit CYP3A4 in vivo
FDA PI — In Vivo DDI StudyMonitoring
-
Serum Calcium
Within 1 week of initiation or dose change; monthly once stable (secondary HPT); every 2 months (PC/pHPT)
Routine Most critical parameter. If Ca <8.4 mg/dL: increase calcium supplements, phosphate binders, or vitamin D. If Ca <7.5 mg/dL or symptomatic: withhold cinacalcet until Ca ≥8.0 mg/dL, then restart at next lowest dose. -
Serum Phosphorus
Within 1 week of initiation or dose change; monthly once stable
Routine Cinacalcet reduces phosphorus through PTH suppression. Adjust phosphate binders accordingly to maintain target Ca×P product. -
iPTH
1–4 weeks after initiation or dose change; then periodically
Routine Measure no earlier than 12 hours after dosing to avoid capturing the nadir. Target 150–300 pg/mL in secondary HPT (KDIGO). If iPTH <150 pg/mL, reduce cinacalcet dose and/or vitamin D sterol to avoid adynamic bone disease. -
Symptoms of Hypocalcemia
Each visit; patient self-monitoring
Routine Ask about paresthesias, muscle cramps, spasms, seizure-like activity. Educate patients to report these symptoms promptly. -
ECG / QTc Interval
At-risk patients: baseline and during significant dose changes
Trigger-based Indicated in patients with congenital long QT syndrome, history of QT prolongation, family history of sudden cardiac death, or concurrent QT-prolonging medications. -
Hepatic Function
Baseline in patients with known liver disease
Trigger-based Moderate to severe hepatic impairment substantially increases cinacalcet exposure (2.4–4.2-fold). These patients require closer calcium and iPTH monitoring throughout treatment. -
GI Symptoms
Each visit; heightened vigilance in at-risk patients
Trigger-based Monitor for signs of upper GI bleeding in patients with known gastritis, esophagitis, ulcers, or severe vomiting. Evaluate promptly for suspected GI bleeding.
Contraindications & Cautions
Absolute Contraindications
- Serum calcium below the lower limit of the normal range — cinacalcet treatment initiation is contraindicated. The drug’s pharmacological mechanism inherently lowers serum calcium further, risking life-threatening hypocalcemia (FDA PI).
Relative Contraindications (Specialist Input Recommended)
- CKD patients not on dialysis — 80% developed at least one calcium value <8.4 mg/dL (vs 5% placebo) in a phase 3 study. Long-term safety is not established in this population. Use only under specialist guidance with rigorous calcium monitoring.
- Congenital long QT syndrome or history of significant QT prolongation — hypocalcemia from cinacalcet may further prolong the QT interval and increase risk of ventricular arrhythmia.
- Active seizure disorder with poor seizure control — significant hypocalcemia lowers the seizure threshold. Specialist input on risk-benefit is recommended.
- Severe hepatic impairment — cinacalcet AUC increases 4.2-fold, with terminal half-life extending to ~84 hours. Use only when benefits clearly outweigh risks.
Use with Caution
- Moderate hepatic impairment — AUC increased 2.4-fold; close monitoring of calcium and iPTH required throughout treatment.
- Impaired cardiac function — isolated postmarketing reports of hypotension, worsening heart failure, and arrhythmias, possibly mediated by reductions in serum calcium.
- Risk factors for upper GI bleeding — patients with gastritis, esophagitis, peptic ulcer disease, or severe vomiting may be at increased risk.
- Concurrent use of other calcium-lowering agents — risk of severe hypocalcemia when combined with denosumab, bisphosphonates, or other calcimimetics.
- Concurrent strong CYP3A4 inhibitors — may more than double cinacalcet exposure; dose adjustment and intensified monitoring needed.
FDA Safety Warning
Hypocalcemia: Life-Threatening Events and Fatalities
Life-threatening events and fatal outcomes associated with hypocalcemia have been reported in patients treated with cinacalcet, including in pediatric patients. Cinacalcet can lower serum calcium sufficiently to cause paresthesias, myalgias, muscle spasms, tetany, seizures, QT interval prolongation, and ventricular arrhythmia. A fatal outcome was reported in a pediatric clinical trial patient with severe hypocalcemia. The safety and effectiveness of cinacalcet have not been established in pediatric patients.
Serum calcium should be monitored closely, particularly during initiation and dose titration. Corrected serum calcium must be at or above the lower limit of normal before starting therapy.
Patient Counselling
Purpose of Therapy
Cinacalcet helps control elevated parathyroid hormone levels that occur when the kidneys can no longer maintain proper calcium and phosphorus balance. By lowering PTH, cinacalcet protects bones and blood vessels from the damage caused by mineral imbalances. In patients with parathyroid cancer or severe primary hyperparathyroidism, cinacalcet works to bring dangerously high calcium levels back toward normal when surgery is not an option.
How to Take
Take cinacalcet with food or immediately after eating to ensure consistent absorption and to reduce stomach upset. Swallow tablets whole — do not chew, crush, or break them. Take the medication at approximately the same time each day. Do not double up on a missed dose; take the next dose as scheduled.
Low Calcium (Hypocalcemia)
Tell patient
Cinacalcet lowers calcium levels as part of how it works. You may experience tingling around the mouth or in the fingers, muscle cramps, or spasms. These symptoms are usually manageable and your doctor will monitor your calcium with regular blood tests.
Call prescriber
If you develop numbness, severe muscle cramping, twitching, confusion, or seizure-like activity. These may indicate dangerously low calcium and need immediate medical attention.
Nausea & Vomiting
Tell patient
Nausea and vomiting are the most common side effects and occur in roughly 1 in 4 patients. Taking the medication with food helps reduce these symptoms. Many patients find that nausea improves with continued use as the body adjusts.
Call prescriber
If nausea or vomiting is severe, persistent, or if you cannot keep food or fluids down. Prolonged vomiting can cause dehydration and electrolyte problems.
Blood Tests & Follow-Up
Tell patient
Regular blood tests for calcium, phosphorus, and parathyroid hormone levels are essential while taking cinacalcet. These tests are typically needed within a week after starting or changing your dose, and then monthly once your dose is stable.
Call prescriber
If you miss scheduled blood tests, as unmonitored calcium levels can lead to serious complications.
GI Bleeding Risk
Tell patient
There is a small risk of stomach or intestinal bleeding, particularly if you have a history of ulcers or stomach problems. Report any unusual symptoms to your healthcare provider.
Call prescriber
If you notice black, tarry stools, vomit that looks like coffee grounds, or experience unexplained abdominal pain. Seek emergency care for these symptoms.
Heart-Related Cautions
Tell patient
Patients with heart problems should inform their doctor before starting cinacalcet, as it may occasionally worsen heart failure or cause irregular heartbeats due to calcium changes.
Call prescriber
If you experience new or worsening shortness of breath, chest pain, palpitations, fainting, or lightheadedness.
Sources
Regulatory (PI / SmPC)
- Cinacalcet Tablets, USP — Full Prescribing Information. Aurobindo Pharma USA, Inc. Revised 09/2025. DailyMed Primary regulatory source for all dosing, indications, adverse reactions, contraindications, and pharmacokinetic data in this monograph.
- Sensipar (cinacalcet HCl) Tablets — Full Prescribing Information. Amgen Inc. FDA Original brand-name labeling with complete clinical trial data, including phase 3 efficacy results.
- Cinacalcet Tablets — Full Prescribing Information. Ascend Laboratories, LLC. DailyMed Generic label confirming identical indications, dosing, and safety profile.
Key Clinical Trials
- EVOLVE Trial Investigators, Chertow GM, Block GA, Correa-Rotter R, et al. Effect of cinacalcet on cardiovascular disease in patients undergoing dialysis. N Engl J Med. 2012;367(26):2482–2494. doi:10.1056/NEJMoa1205624 Landmark RCT (n=3,883) showing cinacalcet did not significantly reduce cardiovascular events in unadjusted ITT analysis, though adjusted analyses suggested potential benefit.
- Wheeler DC, London GM, Parfrey PS, et al. Effects of cinacalcet on atherosclerotic and nonatherosclerotic cardiovascular events in patients receiving hemodialysis: the EVOLVE trial. J Am Heart Assoc. 2014;3(6):e001363. doi:10.1161/JAHA.114.001363 EVOLVE subanalysis distinguishing atherosclerotic from nonatherosclerotic cardiovascular events; suggests benefits may be on nonatherosclerotic pathways.
- Parfrey PS, Chertow GM, Block GA, et al. Lessons learned from EVOLVE for planning of future randomized trials in patients on dialysis. Clin J Am Soc Nephrol. 2016;11(3):539–546. doi:10.2215/CJN.06580615 Post-hoc analysis and design lessons from EVOLVE, including discussion of crossover rates and nonadherence that limited power.
Guidelines
- 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).
- 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 CKD-MBD update; discusses role of calcimimetics alongside newer agents (etelcalcetide, evocalcet), parathyroidectomy, and post-transplant use.
Mechanistic / Basic Science
- Nemeth EF, Steffey ME, Hammerland LG, et al. Calcimimetics with potent and selective activity on the parathyroid calcium receptor. Proc Natl Acad Sci USA. 1998;95(7):4040–4045. doi:10.1073/pnas.95.7.4040 Foundational paper on the calcimimetic concept and calcium-sensing receptor pharmacology that led to cinacalcet development.
- Junaid SZS, Patel P, Patel JB. Cinacalcet. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; updated February 2024. NCBI Bookshelf Comprehensive review of cinacalcet pharmacology, mechanism of action, indications, and interprofessional management considerations.
Pharmacokinetics / Special Populations
- Padhi D, Harris RZ, Engeman C, et al. Pharmacokinetics and pharmacodynamics of cinacalcet in hepatic impairment: phase I, open-label, parallel-group, single-dose, single-center study. Clin Drug Investig. 2008;28(10):635–643. doi:10.2165/00044011-200828100-00005 Key PK study documenting the 2.4-fold and 4.2-fold AUC increases in moderate and severe hepatic impairment, respectively.
- Sekercioglu N, Busse JW, Sekercioglu MF, et al. Cinacalcet versus standard treatment for chronic kidney disease: a systematic review and meta-analysis. Ren Fail. 2016;38(6):857–874. doi:10.3109/0886022X.2016.1172981 Meta-analysis comparing cinacalcet to standard treatment in CKD, pooling efficacy and safety data from multiple trials.