Regression of hepatic fibrosis after pharmacological therapy for nonalcoholic steatohepatitis

Table 1 Pharmacological agents for non-alcoholic steatohepatitis

Drug	Mechanism of action	Side effects	Stage of clinical trials
Vitamin E	Antioxidant, reduces oxidative stress, modulates NF-kB pathway	Nausea, diarrhea, increased bleeding risk, prostate cancer concerns	Approved for use in NAFLD/NASH, widely recommended
GLP-1 RAs (e.g., Semaglutide, Liraglutide)	Increases insulin secretion, suppresses glucagon, reduces steatosis and inflammation	Nausea, diarrhea, risk of pancreatitis	Phase II and III trials ongoing
Pioglitazone	Activates PPAR-γ, improves insulin sensitivity, reduces liver fat	Weight gain, fluid retention, bone loss, risk of heart failure	Phase II and III trials completed
Obeticholic Acid	FXR agonist, reduces hepatic inflammation and fibrosis, promotes bile secretion	Pruritus, dyslipidemia (increased LDL, decreased HDL), fatigue	Phase III trials (REGENERATE study)
Lanifibranor	Pan-PPAR agonist, modulates lipid metabolism, reduces inflammation	Fatigue, nausea, diarrhea	Phase III trials ongoing
Saroglitazar	Dual PPAR-α/γ agonist, reduces liver fat, improves insulin resistance	Gastrointestinal symptoms, rash	Phase II trials ongoing
Cenicriviroc	CCR2/CCR5 antagonist, reduces liver inflammation and fibrosis	Fatigue, diarrhea, headaches	Phase III trials (AURORA study)
Selonsertib	ASK1 inhibitor, reduces fibrosis and inflammation	Nausea, diarrhea, fatigue	Failed in Phase III trials

NAFLD: Nonalcoholic fatty liver disease; NASH: Non-alcoholic steatohepatitis; GLP-1 RAs: Glucagon-like peptide-1 receptor agonists; PPAR: Peroxisome proliferator-activated receptor; FXR: Farnesoid X receptor; LDL: Low-density lipoprotein; HDL: High-density lipoprotein.