Version July 2025
Primary biliary cholangitis: Oral: 80 mg once daily.
No dosage adjustment necessary.
Hepatic impairment prior to treatment initiation:
Child-Turcotte-Pugh class A: No dosage adjustment necessary.
Child-Turcotte-Pugh class B and C: Avoid use (has not been studied).
Hepatoxicity during treatment: Discontinue use if elafibranor-induced liver injury is suspected or confirmed.
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported incidence may include combination therapy with ursodeoxycholic acid in adults.
>10%:
Endocrine & metabolic: Weight gain (23%)
Gastrointestinal: Abdominal pain (11%), diarrhea (11%), nausea (11%), vomiting (11%)
1% to 10%:
Dermatologic: Skin rash (5%)
Endocrine & metabolic: Weight loss (5%)
Gastrointestinal: Cholelithiasis (3%), constipation (8%), gastroenteritis (<5%), gastroesophageal reflux disease (6%), xerostomia (5%)
Hematologic & oncologic: Anemia (<5%)
Hepatic: Increased serum bilirubin (>3 × ULN: 2%)
Nervous system: Dizziness (<5%)
Neuromuscular & skeletal: Arthralgia (8%), bone fracture (6%), increased creatine phosphokinase in blood specimen (>3 × ULN: 4%), myalgia (4% to 7%)
Renal: Increased serum creatinine (<5%)
<1%: Hepatic: Hepatic injury
Frequency not defined: Neuromuscular & skeletal: Muscle injury (including myopathy, rhabdomyolysis)
There are no contraindications listed in the manufacturer's labeling.
Concerns related to adverse effects:
• Fractures: A higher incidence of fractures occurred in patients taking elafibranor versus placebo.
• Hypersensitivity: Rash and unspecified hypersensitivity reactions requiring treatment or therapy discontinuation have occurred.
• Liver injury: Elafibranor-associated liver injury has been reported in 1 patient at the standard dose and 2 patients at a higher than recommended dose. Liver injury presented as autoimmune hepatitis at a median of 85 days after starting therapy. Elevation in liver biochemistries (ALT/AST >5 times ULN or total bilirubin >3 times ULN) also occurred.
• Muscle-related effects: Rhabdomyolysis, myalgias (with or without CPK elevation), and myopathy have been reported. Risk may increase in patients on concomitant HMG-CoA reductase inhibitor (statin) therapy.
Disease-related concerns:
• Biliary obstruction: Avoid use in patients with known or suspected biliary obstruction.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Iqirvo: 80 mg
No
Tablets (Iqirvo Oral)
80 mg (per each): $458.40
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Oral: Administer with or without food.
This medication is not on the NIOSH (2024) list; however, it may meet the criteria for a hazardous drug. Elafibranor may cause teratogenicity.
Use appropriate precautions for receiving, handling, storage, preparation, dispensing, transporting, administration, and disposal. Follow NIOSH and USP 800 recommendations and institution-specific policies/procedures for appropriate containment strategy (NIOSH 2023; NIOSH 2024; USP-NF 2020).
Note: Facilities may perform risk assessment of some hazardous drugs to determine if appropriate for alternative handling and containment strategies (USP-NF 2020). Refer to institution-specific handling policies/procedures.
Primary biliary cholangitis: Treatment of primary biliary cholangitis, in combination with ursodeoxycholic acid (UDCA), in adults who have had an inadequate response to UDCA, or as monotherapy in patients unable to tolerate UDCA.
Substrate of BCRP, CYP2C8 (Minor), CYP2J2 (Minor), MRP2, UGT1A3, UGT1A4, UGT2B7; Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Bile Acid Sequestrants: May decrease serum concentration of Elafibranor. Management: Separate the administration of elafibranor and bile acid sequestrants by as much time as possible, but at least by 4 hours. Risk D: Consider Therapy Modification
HMG-CoA Reductase Inhibitors (Statins): Elafibranor may increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk of muscle toxicity may be increased. Risk C: Monitor
Hormonal Contraceptives: Elafibranor may decrease serum concentration of Hormonal Contraceptives. Risk X: Avoid
RifAMPin: May decrease serum concentration of Elafibranor. Risk C: Monitor
Verify pregnancy status prior to initiating treatment in patients who could become pregnant.
Patients who could become pregnant should use effective nonhormonal contraception or add a barrier method to hormonal contraceptives during therapy and for 3 weeks after the last dose of elafibranor. Consult drug interactions database for more detailed information related to the use of elafibranor and specific contraceptives.
Based on data from animal studies, in utero exposure to elafibranor may cause fetal harm. Adverse pregnancy outcomes were observed in a pre- and postnatal developmental study of rats with oral doses lower than or approximately equal to exposure at the recommended human dose.
It is not known if elafibranor is present in breast milk.
Due to the potential for serious adverse reactions in the breastfed infant, breastfeeding is not recommended by the manufacturer during therapy and for 3 weeks after the last dose of elafibranor.
Prior to initiating therapy, patients who can become pregnant should have a negative pregnancy test; obtain baseline liver chemistries and bone health assessment. While on therapy, evaluate for new or worsening muscle pain or myopathy, evidence of acute hepatitis (eg, jaundice, right upper quadrant pain or eosinophilia), or bone fractures. Periodically assess liver biochemistries.
Elafibranor and its main metabolite GFT1007 are peroxisome proliferator-activated receptor (PPAR) agonists, which activate PPAR-alpha, gamma, and delta. Elafibranor and GFT1007 are suggested to inhibit bile acid synthesis through activation of PPAR-alpha and delta that subsequently downregulates fibroblast growth factor A21 (FGF21) dependent CYP7A1 activity, a key enzyme in the synthesis of bile acids from cholesterol.
Onset: ALP lowering observed as early as 4 weeks. Steady state achieved at 14 days for elafibranor and 7 days for active metabolite GFT1007.
Distribution: Vd: 4,731 L.
Protein binding: Elafibranor and GFT1007: 99.7%, mainly to albumin.
Metabolism: Extensively metabolized by cytosolic enzyme 15-ketoprostaglandin 13-delta-reductase (PTGR1) to major active metabolite GFT1007, which is further metabolized by CYP2C8 and uridine diphosphate-glucuronosyltransferase (UGT) 1A3 and 2B7; metabolism of elafibranor also occurs by CYP2J2 and UGT1A3, 1A4, and 2B7.
Half-life elimination: Elafibranor: 70.2 hours; GFT1007: 15.4 hours.
Time to peak: Elafibranor and GFT1007: 1.25 hours.
Excretion: Feces (77.1% of dose; 56.7% as elafibranor, 6.08% as GFT1007); urine (19.3%, as metabolites).
