PLENAXIS
Clinical safety rating: caution
Comprehensive clinical and safety monograph for PLENAXIS (PLENAXIS).
Selective androgen receptor modulator (SARM); binds to androgen receptors with high affinity, activating anabolic signaling pathways in muscle and bone with reduced androgenic effects on prostate and skin.
| Metabolism | Primarily metabolized by glucuronidation (UGT1A1, UGT1A9) and cytochrome P450 (CYP3A4) oxidation. |
| Excretion | Renal: 70% as unchanged drug; fecal: 10% as metabolites; biliary: 5% as unchanged drug and metabolites. |
| Half-life | Terminal elimination half-life is approximately 24 hours in healthy adults; clinically significant accumulation occurs in renal impairment (CrCl <30 mL/min) with half-life prolonged to 40-60 hours. |
| Protein binding | 99% bound primarily to albumin and alpha-1-acid glycoprotein. |
| Volume of Distribution | Vd is 0.3-0.5 L/kg, indicating distribution mainly in extracellular fluid and plasma; limited tissue penetration. |
| Bioavailability | Oral bioavailability is 70-80% due to moderate first-pass hepatic metabolism; reduced with food intake (by 20%). |
| Onset of Action | Oral: Clinical effect onset occurs within 1-2 hours; peak effect at 4-6 hours. Intravenous: Onset within 5-10 minutes. |
| Duration of Action | Oral: Duration is 12-24 hours based on once-daily dosing for maintenance therapy. IV: Duration approximately 6-12 hours for acute effects. |
Initial: 10 mg orally once daily, titrated to blood pressure and heart rate response; maintenance: 20-80 mg daily in 1-2 divided doses.
| Dosage form | POWDER |
| Renal impairment | No dose adjustment required for GFR ≥30 mL/min; avoid use if GFR <30 mL/min due to limited data. |
| Liver impairment | Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 50%; Child-Pugh C: avoid use. |
| Pediatric use | Not approved for use in pediatric patients; safety and efficacy not established. |
| Geriatric use | Initiate at 5 mg orally once daily; titrate cautiously due to increased sensitivity and risk of hypotension. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for PLENAXIS (PLENAXIS).
| Breastfeeding | Not known if abarelix is excreted in human milk. Due to potential for serious adverse reactions in breastfed infants, breastfeeding is not recommended during treatment and for at least 2 weeks after last dose. M/P ratio: Not established. |
| Teratogenic Risk | Plenaxis (abarelix) is a GnRH antagonist. FDA Pregnancy Category X. Contraindicated in pregnancy due to risk of fetal harm. First trimester: Expected to cause fetal loss or malformations based on mechanism of action (androgen deprivation). Second/third trimester: Potential for oligohydramnios, fetal growth restriction, and developmental abnormalities if exposure occurs. Animal studies showed embryotoxicity and teratogenicity. |
■ FDA Black Box Warning
No FDA boxed warning.
| Serious Effects |
["Known hypersensitivity to enobosarm or any component of the formulation","Pregnancy (potential fetal harm)","Breastfeeding","Severe hepatic impairment (Child-Pugh Class C)","History of myocardial infarction or stroke within past 6 months","Significant cardiovascular disease (e.g., unstable angina, uncontrolled hypertension)"]
| Precautions | ["Hepatotoxicity (monitor liver function tests)","Increased risk of adverse cardiovascular events (e.g., MI, stroke) in patients with established cardiovascular disease","Potential for masculinization in women and virilization in children","May cause fluid retention and exacerbate heart failure","Monitor lipid profile for HDL decreases"] |
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| Fetal Monitoring | Monitoring includes: pregnancy testing before initiation and monthly during therapy; serum testosterone levels; bone mineral density assessment; liver function tests; blood glucose; ECG for QT prolongation. In obstetric use (if inadvertently exposed), monitor fetal growth, amniotic fluid volume, and fetal development via ultrasound. |
| Fertility Effects | Abarelix suppresses pituitary gonadotropins, leading to reduced testicular steroidogenesis and spermatogenesis. Reversible impairment of male fertility is expected. In females, ovulation suppression occurs; fertility returns upon discontinuation. No long-term fertility studies in humans. |