Version July 2025
Primary biliary cholangitis: Oral: 10 mg once daily.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Mild, moderate, or severe impairment: No dosage adjustment necessary.
Hemodialysis: There are no dosage adjustments in the manufacturer’s labeling (has not been studied).
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: Interrupt seladelpar therapy if liver enzymes (eg, AST, ALT, total bilirubin, alkaline phosphatase) increase or signs and symptoms of clinical hepatitis (eg, eosinophilia, jaundice, right upper quadrant pain) occur. Consider discontinuing seladelpar permanently if liver enzymes increase after re-treatment.
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in adults and may include combination therapy with ursodeoxycholic acid (UDCA).
1% to 10%:
Dermatologic: Alopecia (<5%), skin rash (<5%)
Gastrointestinal: Abdominal distention (6%), abdominal pain (7%), dyspepsia (<5%), nausea (6%)
Hematologic & oncologic: Anemia (<5%)
Nervous system: Dizziness (5%), headache (8%)
Neuromuscular & skeletal: Bone fracture (4%)
Renal: Decreased estimated GFR (eGFR) (10%)
Respiratory: Cough (<5%)
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 seladelpar versus placebo.
• Liver test abnormalities: Elevation in liver biochemistries (ALT/AST >3 × ULN) have occurred with higher than recommended doses (eg, 50 mg once daily); levels returned to pretreatment levels upon discontinuation of seladelpar.
Disease-related concerns:
• Biliary obstruction: Avoid use in patients with known or suspected biliary obstruction.
Special populations:
• CYP2C9 poor metabolizers: Systemic exposure of seladelpar is anticipated to be increased in patients who are CYP2C9 poor metabolizers.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral, as lysine:
Livdelzi: 10 mg [contains fd&c blue #2 (indigotine,indigo carmine)]
No
Capsules (Livdelzi Oral)
10 mg (per each): $504.24
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Oral: Administer with or without food.
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.
Limitations of use: Not recommended in patients who have or develop decompensated cirrhosis (eg, ascites, variceal bleeding, hepatic encephalopathy).
Substrate of BCRP, CYP2C8 (Minor), CYP2C9 (Major with inhibitors), CYP2C9 (Minor with inducers), CYP3A4 (Minor), OAT1/3, P-glycoprotein (Minor); 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.
Asciminib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
BCRP/ABCG2 Inhibitors: May increase serum concentration of Seladelpar. Risk C: Monitor
Belumosudil: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid coadministration of belumosudil with these substrates of BCRP for which minimal concentration increases can cause serious adverse effects. If coadministration is required, dose reductions of the BCRP substrate may be required. Risk D: Consider Therapy Modification
Bile Acid Sequestrants: May decrease serum concentration of Seladelpar. Management: Administer seladelpar at least 4 hours before or 4 hours after bile acid sequestrants. Consider a greater dose separation interval when possible. Risk D: Consider Therapy Modification
CarBAMazepine: May decrease serum concentration of Seladelpar. Risk C: Monitor
CYP2C9 Inhibitors (Moderate): May increase serum concentration of Seladelpar. Risk C: Monitor
Danicopan: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Darolutamide: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Elacestrant: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Eltrombopag: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Encorafenib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Fexinidazole: May increase serum concentration of OAT1/3 Substrates (Clinically Relevant). Management: Avoid use of fexinidazole with OAT1/3 substrates when possible. If combined, monitor for increased OAT1/3 substrate toxicities. Risk D: Consider Therapy Modification
Futibatinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Gilteritinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Inhibitors of CYP3A4 and CYP2C9: May increase serum concentration of Seladelpar. Risk C: Monitor
Leniolisib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Lumacaftor and Ivacaftor: May decrease serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may increase serum concentration of CYP2C9 Substrates (High Risk with Inhibitors or Inducers). Risk C: Monitor
OAT1/3 Inhibitors: May increase serum concentration of Seladelpar. Risk X: Avoid
Osimertinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Oteseconazole: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Pretomanid: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Pretomanid: May increase serum concentration of OAT1/3 Substrates (Clinically Relevant). Risk C: Monitor
Regorafenib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
RifAMPin: May decrease serum concentration of Seladelpar. Risk C: Monitor
Rolapitant: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Monitor patients receiving rolapitant for increased exposure to and/or effects of BCRP/ABCG2 substrates. Use the lowest effective rosuvastatin dose when used in combination with rolapitant. Risk C: Monitor
Selpercatinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Sparsentan: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Tafamidis: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Taurursodiol: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Taurursodiol: May increase serum concentration of OAT1/3 Substrates (Clinically Relevant). Risk X: Avoid
Tedizolid: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Vaborbactam: May increase serum concentration of OAT1/3 Substrates (Clinically Relevant). Risk C: Monitor
Vanzacaftor, Tezacaftor, and Deutivacaftor: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Vanzacaftor, Tezacaftor, and Deutivacaftor: May increase serum concentration of CYP2C9 Substrates (High risk with Inhibitors). Risk C: Monitor
Vimseltinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and BCRP substrates when possible. If combined, monitor for increased effects and toxicities of the BCRP substrate and consider dose adjustments. Risk D: Consider Therapy Modification
Adverse events were not observed in animal reproduction studies following oral administration of seladelpar to rats in doses up to 176 times and rabbits in doses up to 49 times the recommended human dose (based on AUC) during the period of organogenesis.
Report patients exposed to seladelpar during pregnancy to Gilead Sciences (1-800-445-3235).
It is not known if seladelpar is present in breast milk.
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother.
LFTs (baseline and as clinically indicated); monitor for signs or symptoms of acute hepatitis (eg, jaundice, right upper quadrant pain), monitor bone health.
Seladelpar is a peroxisome proliferator-activated receptor (PPAR) agonist, which activates PPAR-delta. Seladelpar is suggested to inhibit bile acid synthesis through activation of PPAR-delta that subsequently downregulates fibroblast growth factor 21 (FGF21) dependent CYP7A1 activity, a key enzyme in the synthesis of bile acids from cholesterol.
Distribution: Vd: ~133.2 L.
Protein binding: >99%.
Metabolism: Primarily in vitro by CYP2C9 and to a lesser extent by CYP2C8 and CYP3A4, resulting in the three major pharmacologically inactive metabolites: seladelpar sulfoxide (M1), desethyl-seladelpar (M2), and desethyl-seladelpar sulfoxide (M3).
Half-life elimination: Mean: 6 hours in healthy subjects; range 3.8 to 6.7 hours in primary biliary cholangitis subjects.
Time to peak: 1.5 hours.
Excretion: Urine: ~73.4% (<0.01% as unchanged drug); feces: 19.5% (2.02% as unchanged drug).
Clearance: 12 L/hour.
Hepatic function: In patients with hepatic impairment of various causes, seladelpar AUC increased by 1.1-, 2.5-, and 2.1-fold in patients with mild (Child-Turcotte-Pugh class A), moderate (Child-Turcotte-Pugh class B), and severe (Child-Turcotte-Pugh class C) impairment, respectively; Cmax increased by 1.3-, 5.2-, and 5-fold in patients with mild (Child-Turcotte-Pugh class A), moderate (Child-Turcotte-Pugh class B), and severe (Child-Turcotte-Pugh class C), respectively, after a 10 mg single dose.
Seladelpar Cmax and AUC were 1.7- to1.8-fold higher in primary biliary cholangitis patients with mild impairment with portal hypertension and 1.6- to 1.9-fold higher in primary biliary cholangitis patients with moderate (Child-Turcotte-Pugh class B) impairment after a 10 mg single dose when compared to patients with mild hepatic impairment (Child-Turcotte-Pugh class A) without portal hypertension.
