Effect of Saroglitazar in MASLD: Latest Indian 2026 Study

Saroglitazar was associated with improvements in liver stiffness, hepatic steatosis, metabolic parameters and non-invasive fibrosis markers in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), according to a recent Indian study.

This study was published in the February 2026 issue of Liver International.

MASLD is a growing global health concern and encompasses a spectrum of liver disorders characterised by excessive hepatic fat accumulation associated with metabolic dysfunction. In India, reported prevalence of MASLD was 68.2% (CAP ≥ 238 dB/m), and 33.7% for fibrosis (LSM ≥ 7 kPa)¹. Its pathogenesis involves hepatic steatosis, lipotoxicity, inflammation and fibrogenesis driven by complex metabolic and endocrine pathways. This has led to the exploration of therapies targeting key regulators such as peroxisomes proliferator-activated receptors (PPARs) that address both liver and metabolic abnormalities.

Saroglitazar is a dual peroxisome proliferator-activated receptor (PPAR)-α/γ agonist. Through PPAR-α activity, it has lipid-modulating effects, while PPAR-γ activity improves insulin sensitivity and glycaemic control, supporting its potential role and evaluation in MASLD.

Study Overview

A prospective, multicentre, single-arm, real-world Phase 4 study² evaluated saroglitazar 4 mg orally once daily for 52 weeks in patients with MASLD. The interim analysis included 500 patients who had completed 24 weeks of treatment. The mean age was 45.7 ± 11.6 years, 69% of patients were male, and the mean BMI was 29.9 ± 4.7 kg/m². Obesity was the most common metabolic comorbidity (42%), followed by dyslipidaemia (20%), type 2 diabetes mellitus (20%) and metabolic syndrome (18%).

The primary endpoint was change in liver stiffness measurement (LSM) from baseline to Week 52, along with the incidence of treatment-emergent and serious adverse events. Secondary assessments included changes in LSM, CAP, UAP, liver enzymes, HbA1c, fasting glucose, weight, BMI and lipid profile at Weeks 24 and 52. However, the published interim analysis reports the findings from the 24-week assessment.

Some of the key results of the study² include:

Effect on Liver Stiffness and Steatosis

• At Week 24, mean LSM decreased by 2.1 kPa (-20.7%), from 10.1 ± 3.17 kPa to 8.0 ± 3.2 kPa (p<0.001), with 32.6% (n=494) of patients achieving ≥30% reduction. CAP decreased by 20.3 dB/m(n=309) and UAP by 22.3 dB/m (n=182) (p<0.001 for both).

Effect on Liver Enzymes and Glycaemic Parameters

• Mean ALT levels decreased by -33.6% from 59.8 ± 39.5 U/L to 39.7 ± 32.9 U/L and AST by -19.6% from 48.9 ± 26.7 U/L to 39.3 ± 21.7 U/L (p<0.001 for both). Among patients with baseline ALT ≥ 40 U/L, 61% achieved ALT normalisation. HbA1c decreased from 6.3% to 6.0%, while fasting glucose decreased from 118.07 ± 44.79 mg/dL to 112.06 ± 46.81 mg/dL.

Effect on Lipid Profile

• Triglycerides decreased from 217±117mg/dL to 163 ± 99mg/dL, representing a -24.8% reduction (p<0.001), while LDL-C decreased by 4.5% (p<0.001). HDL-C increased by 7.3% (p<0.001).

Changes in Non-Invasive Fibrosis Scores

• Significant reductions were observed in FAST, APRI and ALERT scores after 24 weeks (p<0.001 for all). FIB-4 and NFS also showed numerical improvements, although these were not statistically significant. More than 50% of patients achieved at least a one-category improvement in fibrosis risk classification.

Tolerability

• Treatment-emergent adverse events were reported in 68 patients (13.6%), with 85.5% of events being mild and considered unlikely to be related to treatment. No treatment-related serious adverse events or drug-related discontinuations were reported.

Saroglitazar (Lipaglyn) in the Evolving MASLD Landscape

A recently published 2026 review in Frontiers in Gastroenterology³ highlighted saroglitazar (Lipaglyn) as an emerging pharmacotherapeutic option for MASH. As a dual PPAR-α/γ agonist, saroglitazar combines the lipid-lowering effects of PPAR-α activation with the insulin-sensitising effects of PPAR-γ activation. The review highlighted Phase 2 evidence showing reductions in ALT, liver fat, triglycerides and HOMA-IR, along with real-world evidence from a prospective study of 50 patients with MASLD showing improvements in liver stiffness, steatosis and metabolic parameters after six months of treatment. Saroglitazar (Lipaglyn) is approved in India for noncirrhotic MASH, while Phase 2b evaluation is ongoing³.

Overall, the emerging evidence positions saroglitazar as a potential therapeutic option for patients with MASLD, particularly those with coexisting metabolic abnormalities. The 24-week Phase 4 findings add to the growing real-world evidence from India, further supporting interest in its potential clinical utility in the evolving landscape of MASLD management.

Abbreviations: MASLD: metabolic dysfunction-associated steatotic liver disease, MASH: metabolic dysfunction-associated steatohepatitis, PPAR: peroxisome proliferator-activated receptor, PPAR-α: peroxisome proliferator-activated receptor alpha, PPAR-γ: peroxisome proliferator-activated receptor gamma, LSM: liver stiffness measurement, CAP: controlled attenuation parameter, UAP: ultrasound attenuation parameter, ALT: alanine aminotransferase, AST: aspartate aminotransferase, HbA1c: glycated haemoglobin, LDL-C: low-density lipoprotein cholesterol, HDL-C: high-density lipoprotein cholesterol, FAST: FibroScan-AST score, APRI: AST-to-platelet ratio index, ALERT: Agile Liver Fibrosis score, FIB-4: fibrosis-4 index, NFS: NAFLD fibrosis score, TEAE: treatment-emergent adverse event, SAE: serious adverse event, CVD: cardiovascular disease, ASCVD: atherosclerotic cardiovascular disease, AHA: American Heart Association, PREVENT: Predicting Risk of cardiovascular disease EVENTs, HOMA-IR: homeostatic model assessment of insulin resistance, BMI: body mass index, T2DM: type 2 diabetes mellitus.