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Other pharmacotherapy

TL;DR — Before resmetirom and semaglutide, two off-label agents had the best evidence and both came from PIVENS: vitamin E 800 IU/day improved NASH histology in 43% versus 19% placebo (p=0.001) in non-diabetic adults, while pioglitazone 30 mg missed the prespecified significance threshold (34% vs 19%, p=0.04 against a required p<0.025); neither improved fibrosis (Sanyal 2010, PMID 20427778). Pioglitazone at 45 mg in patients with prediabetes or T2D did far better — 58% met the primary histological endpoint (treatment difference 41 points, 95% CI 23–59) and 51% had NASH resolution, with fibrosis score improving by 0.5 (p=0.039), sustained over 36 months (Cusi 2016, PMID 27322798). Vitamin E has the only observational evidence on hard outcomes: in propensity-matched NASH with bridging fibrosis or cirrhosis, ≥2 years of vitamin E was associated with higher transplant-free survival (78% vs 49%) and lower decompensation (37% vs 62%), adjusted HR 0.30 (0.12–0.74) for death or transplant (Vilar-Gomez 2020, PMID 30506586) — while a 2024 Cochrane review rates the evidence for mortality and serious adverse events as very low certainty (Wen 2024, PMID 39412049). Against this stands a long list of well-conducted failures: selonsertib was flatly negative in two phase 3 trials (Harrison 2020, PMID 32147362), obeticholic acid hit fibrosis but missed NASH resolution and carried 51% pruritus at 25 mg (Younossi 2019, PMID 31813633), aramchol missed its primary endpoint (Ratziu 2021, PMID 34621052), and cenicriviroc missed its primary endpoint while hitting fibrosis (Friedman 2018, PMID 28833331). The emerging classes to watch are FGF21 analogues and pan-PPAR agonists.

The PIVENS-era agents

Agent Trial n Population Primary endpoint result Fibrosis
Vitamin E 800 IU/day PIVENS, 96 weeks (PMID 20427778, NCT00063622) 84 of 247 NASH without diabetes improvement in NASH histology 43% vs 19% placebo, p=0.001 no improvement (p=0.24)
Pioglitazone 30 mg/day PIVENS, same trial 80 of 247 NASH without diabetes 34% vs 19%, p=0.04 — did not meet the prespecified p<0.025 no improvement (p=0.12)
Pioglitazone 45 mg/day Cusi 2016, 18 months double-blind + 18 months open label (PMID 27322798, NCT00994682) 101 NASH with prediabetes or T2D ≥2-point NAS reduction in 2 categories without fibrosis worsening: 58%, treatment difference 41 points (23–59), p<0.001; NASH resolution 51%, difference 32 points (13–51) fibrosis score −0.5 (−0.9 to 0.0), p=0.039
Vitamin E 800 IU or metformin 1000 mg TONIC, 96 weeks, children aged 8–17 (PMID 21521847, NCT00063635) 173 biopsy-confirmed paediatric NAFLD sustained ALT reduction: vitamin E 26% vs placebo 17% (p=0.26), metformin 16% (p=0.83) — primary endpoint not met no significant improvement in other histological features

TONIC nevertheless produced the strongest paediatric histological signal available: ballooning score change −0.5 with vitamin E versus +0.1 placebo (p=0.006) and −0.3 with metformin (p=0.04); NAS change −1.8 versus −0.7 (p=0.02); and among children with NASH, resolution in 58% with vitamin E versus 28% placebo (p=0.006) and 41% with metformin (p=0.23). A trial can miss its primary endpoint and still change practice, which is what happened.

Pioglitazone's side-effect profile constrains it: weight gain 2.5 kg versus placebo in Cusi's trial (PMID 27322798) and greater weight gain than vitamin E or placebo in PIVENS (PMID 20427778). Discontinuation is associated with disease recurrence, so it is a chronic commitment.

Vitamin E and the certainty problem

Two bodies of evidence point in opposite directions on confidence, not on direction.

The outcome cohort. 236 patients with biopsy-proven NASH and bridging fibrosis or cirrhosis at Indiana University, October 2004 – January 2016; 90 took 800 IU/day for ≥2 years, propensity-matched to 90 non-users on fibrosis severity, age, sex, BMI, comorbidities and treatment, LDL, liver biochemistry and follow-up length. Median follow-up 5.62 and 5.6 years (Vilar-Gomez 2020, PMID 30506586):

Outcome Vitamin E Control Adjusted effect
Transplant-free survival 78% 49% HR 0.30 (95% CI 0.12–0.74), p<0.01
Hepatic decompensation 37% 62% sub-HR 0.52 (0.28–0.96), p=0.036
HCC, vascular events, non-hepatic cancers at 10 years — — no difference

Benefits were evident with and without diabetes. This is an observational propensity-matched analysis, not a trial.

The Cochrane review. 16 randomised trials, 1,066 paediatric and adult participants, doses 298–1,000 IU/day, follow-up 2–24 months, 7.9% dropout (Wen 2024, PMID 39412049):

Outcome Effect Certainty
All-cause mortality RR 3.45 (95% CI 0.57–20.86), 3 trials, 351 participants very low
Serious adverse events RR 1.91 (0.30–12.01), 2 trials, 283 participants very low
Liver-related mortality / morbidity no data —
Physical HRQoL MD 0.74 (−0.52 to 2.01) very low
Non-serious adverse events RR 0.86 (0.64–1.17) very low

The two are not in conflict: the trials are short and small and cannot address mortality, while the cohort is long and observational and cannot exclude confounding. The honest position is that vitamin E improves histology in non-diabetic adults with reasonable confidence, and that its effect on death and decompensation is supported by one propensity-matched cohort and by nothing randomised.

The failures, and what each ruled out

Agent (target) Trial Result What it tested
Selonsertib (ASK1 inhibitor) STELLAR-3 (F3) and STELLAR-4 (F4), phase 3, 48 weeks (PMID 32147362, NCT03053050/NCT03053063) Neither met the primary endpoint. STELLAR-3 fibrosis improvement 10% (18 mg), 12% (6 mg), 13% placebo; STELLAR-4 14%, 13%, 13%. Dose-dependent reduction in hepatic phospho-p38 confirmed target engagement, with no effect on biochemistry, non-invasive tests, progression to cirrhosis or adjudicated clinical events Apoptosis-signalling monotherapy in advanced fibrosis. Target engaged, disease unchanged
Obeticholic acid (FXR agonist) REGENERATE phase 3 interim, month 18 (PMID 31813633, NCT02548351) Fibrosis improvement 23% (25 mg, p=0.0002) and 18% (10 mg, p=0.045) vs 12% placebo — met. NASH resolution 12%, 11%, 8% — not met (p=0.13, p=0.18). Pruritus 51% at 25 mg vs 19% placebo FXR agonism. Antifibrotic signal real; tolerability and resolution failure decisive
Aramchol (SCD1 partial inhibitor) ARREST phase 2b, 52 weeks (PMID 34621052, NCT02279524) Primary endpoint (liver triglyceride by MRS at 600 mg) missed: placebo-corrected −3.1 (95% CI −6.4 to 0.2, p=0.066), precluding formal analysis of secondaries. NASH resolution 16.7% vs 5% (OR 4.74, 0.99–22.7); fibrosis improvement 29.5% vs 17.5% (OR 1.88, 0.7–5.0); ALT −29.1 IU/L (−41.6 to −16.5) SCD1 modulation. Suggestive but statistically inconclusive
Cenicriviroc (CCR2/CCR5 antagonist) CENTAUR phase 2b, 1 year (PMID 28833331) Primary (≥2-point NAS improvement without fibrosis worsening) missed: 16% vs 19% (p=0.52); SH resolution 8% vs 6% (p=0.49). Fibrosis endpoint met: 20% vs 10% (p=0.02), with greater benefit at higher baseline activity and fibrosis Chemokine-receptor blockade. Fibrosis signal did not survive to phase 3
Lanifibranor (pan-PPAR agonist) NATIVE phase 2b, 24 weeks (PMID 34670042, NCT03008070) Primary (SAF-A decrease ≥2 without fibrosis worsening) met at 1200 mg: 55% vs 33% (p=0.007); 800 mg 48% (p=0.07). NASH resolution 49% and 39% vs 22%; fibrosis improvement 48% and 34% vs 29%; both 35% and 25% vs 9%. Diarrhoea, nausea, oedema, anaemia and weight gain more frequent Simultaneous PPAR-α/δ/γ agonism. Positive; phase 3 pending

The pattern is instructive. Agents that engage a single inflammatory or fibrogenic node (selonsertib, cenicriviroc) either fail entirely or produce an isolated fibrosis signal that does not replicate, consistent with the network structure of fibrogenesis described in pathogenesis. Agents that act on upstream metabolism (thyromimetics, incretins, PPAR agonists, FASN and SCD1 inhibitors) do better.

Newer metabolic agents

Agent Trial Result
Pegozafermin (glycopegylated FGF21 analogue) ENLIVEN phase 2b, 24 weeks, n=219 with F2–F3 (PMID 37356033, NCT04929483) Fibrosis improvement 7% placebo vs 22% (15 mg), 26% (30 mg, p=0.009), 27% (44 mg q2w, p=0.008). NASH resolution 2% placebo vs 37%, 23%, 26%
Efruxifermin (bivalent FGF21 analogue) HARMONY phase 2b, 96 weeks, n=128 with F2–F3 (PMID 40818852, NCT04767529) ≥1-stage fibrosis improvement without MASH worsening at week 96: 19% placebo, 30% (28 mg, p=0.19), 49% (50 mg, difference 31 points, 95% CI 12–49, p=0.0030). Among 88 with week-96 biopsies: 24%, 46%, 75% (difference 52 points, 31–73, p<0.0001). No drug-induced liver injury or deaths
Efruxifermin in cirrhosis SYMMETRY phase 2b, n=181 compensated MASH cirrhosis (PMID 40341827, NCT05039450) Week 36 negative: 13% placebo, 18% (28 mg, p=0.62), 19% (50 mg, p=0.52). Week 96: 11%, 21%, 29% (50 mg difference 16 points, 95% CI 2–30)
Denifanstat (FASN inhibitor) phase 2b, 52 weeks, n=168 with F2–F3 (PMID 39396529, NCT04906421) ≥2-point NAS improvement without fibrosis worsening: 38% vs 16% (risk difference 21.0%, 95% CI 8.1–33.9, p=0.0035); MASH resolution with ≥2-point NAS improvement 26% vs 11% (13.0%, 0.7–25.3, p=0.0173). Alopecia in 19% vs 4% and dry eye in 9% vs 14%

Pegozafermin ranks first for both endpoints in network meta-analysis (SUCRA 79.92 for fibrosis, 91.75 for resolution) (Souza 2025, PMID 39903735). The HARMONY 96-week completer analysis (75% fibrosis improvement at 50 mg) is the largest single histological effect reported in a randomised MASH trial, and also the analysis most vulnerable to attrition bias — 88 of 128 randomised had week-96 biopsies.

SGLT2 inhibitors: no longer observational

The section below treats SGLT2 inhibitors as an observational signal. That is now out of date for histology. A multicentre, double-blind, placebo-controlled trial that began in 2018 under NASH-era terminology randomised 154 adults with biopsy-defined steatohepatitis, with or without type 2 diabetes, to dapagliflozin 10 mg daily or placebo for 48 weeks across six Chinese tertiary hospitals; the 2025 report describes the population as MASH (Lin 2025, PMID 40467095, NCT03723252):

Endpoint at 48 weeks Dapagliflozin (n=78) Placebo (n=76) Effect
MASH improvement (NAS fall ≥2 or NAS ≤3) without fibrosis worsening — primary 53% (41/78) 30% (23/76) RR 1.73 (1.16–2.58), p=0.006
MASH resolution without fibrosis worsening 23% (18/78) 8% (6/76) RR 2.91 (1.22–6.97), p=0.01
Fibrosis improvement without MASH worsening 45% (35/78) 20% (15/76) RR 2.25 (1.35–3.75), p=0.001
Mean NAS difference — — −1.39 (−1.99 to −0.79), p<0.001
Discontinuation for adverse events 1% (1/78) 3% (2/76) —

The absolute differences were 23 percentage points for the primary endpoint, 15 points for resolution and 25 points for fibrosis improvement. The trial is single-country and modest in size (154), and its placebo fibrosis-improvement rate of 20% sits within the wide range seen across MASH trials, so cross-trial comparison remains unsound (resmetirom and thyromimetics). No SGLT2 inhibitor is licensed for MASH.

The liver-fat evidence that preceded it is consistent and shows a dose of realism about magnitude. In the E-LIFT trial, 50 patients with T2D and NAFLD randomised to empagliflozin 10 mg or standard care for 20 weeks had a between-group MRI-PDFF difference of −4.0% (p<0.0001), with within-group fat falling 16.2% → 11.3% on empagliflozin versus 16.4% → 15.5% on control (Kuchay 2018, PMID 29895557). In non-diabetic MASLD, 97 participants randomised to empagliflozin 10 mg or placebo for 52 weeks showed a median MRI-PDFF change of −2.49% versus −1.43% (p=0.025) — statistically significant but small — with steatosis resolution 44.9% versus 28.6% (p=0.094, ns) and no difference in ALT response, ≥30% PDFF drop, or the composite (Cheung 2024, PMID 38536017); weight fell 2.7 kg versus 0.2 kg. The class therefore has a modest, weight-linked steatosis effect outside diabetes and a larger one within it, which is what a glycosuric mechanism predicts.

Combination therapy: tested, and mostly negative

The argument that a network disease needs combination therapy is made below; it has been tested directly. In the ATLAS phase 2b trial, 392 patients with F3–F4 (56% cirrhotic, 83% with NAS ≥5) were randomised to placebo, selonsertib 18 mg, cilofexor 30 mg or firsocostat 20 mg alone or in two-drug combinations for 48 weeks (Loomba 2021, PMID 33169409):

Arm ≥1-stage fibrosis improvement without worsening NASH
Placebo 11%
Cilofexor + firsocostat 21% (p=0.17)
Cilofexor + selonsertib 19% (p=0.26)
Firsocostat + selonsertib 15% (p=0.62)
Firsocostat 12% (p=0.94)
Cilofexor 12% (p=0.96)

Every arm missed. The secondary picture was more encouraging and is the reason the combination still appears near the top of network meta-analyses (PMID 39903735): cilofexor + firsocostat produced a significant fall in machine-learning NASH CRN fibrosis score (p=0.040) and a shift of biopsy area from F3–F4 to ≤F2 patterns, more ≥2-point NAS reductions, and significant improvements in ALT, AST, bilirubin, bile acids, cytokeratin-18, insulin, eGFR, ELF and transient elastography (all p≤0.05); hepatic collagen by morphometry did not change. Pruritus affected 20–29% on cilofexor versus 15% on placebo. The honest reading is that a combination which fails its ordinal histological primary endpoint while moving a continuous digital measure of the same tissue is exactly the situation the biopsy-reliability data predict (histology and biopsy) — and that this trial cannot distinguish a real modest effect from measurement failure.

Repurposed metabolic drugs: observational evidence

None of these has a randomised histological endpoint trial in MASLD, and all the estimates below are observational.

Drug class Finding Source
Statins In 7,988 MASLD patients with ≥2 VCTE examinations across 16 centres (median follow-up 4.6 years, 40.5% statin users, 17% with cACLD): all-cause mortality adjusted HR 0.233 (95% CI 0.127–0.426); liver-related events HR 0.380 (0.268–0.539); liver-stiffness progression HR 0.542 (0.389–0.755) in cACLD and 0.450 (0.342–0.592) in non-cACLD; no association with stiffness regression (HR 0.914, 0.778–1.074) Zhou 2024, PMID 39089860
SGLT2 inhibitors vs other glucose-lowering drugs In diabetic MASLD (Marketscan, 2013–2021, propensity matched): HCC HR 0.76 (0.62–0.93), cirrhosis 0.80 (0.76–0.84), CVD 0.82 (0.79–0.85), CKD 0.66 (0.62–0.70), non-liver cancer 0.81 (0.76–0.86). Stepwise lower risk with either metformin or SGLT2i (HR 0.76–0.97) and with both (0.58–0.79) Mao 2024, PMID 39122360
Oral antidiabetics, head to head 80,178 Koreans with T2D and NAFLD, 219,941 person-years. NAFLD regression vs sulfonylureas: SGLT2i adjusted sub-HR 1.99 (1.75–2.27), thiazolidinediones 1.70 (1.41–2.05), DPP-4i 1.45 (1.31–1.59); SGLT2i beat thiazolidinediones (1.40, 1.12–1.75) and DPP-4i (1.45, 1.30–1.62). Only SGLT2i lowered adverse liver-related outcomes vs sulfonylureas (sub-HR 0.37, 0.17–0.82) Jang 2024, PMID 38345802

The statin hazard ratio of 0.233 for all-cause mortality is implausibly large for a drug effect and almost certainly reflects healthy-user confounding — patients prescribed statins and retained in a two-elastography cohort differ systematically from those who are not. The internally consistent finding (progression slowed but regression unaffected) is more credible than the magnitude. Statins are nonetheless important here because cardiovascular disease is the leading cause of death in MASLD (cardiovascular and extrahepatic outcomes), and the older concern about statin hepatotoxicity in fatty liver is a barrier to their use — see red flags and safety concerns.

Open questions

  • Should an SGLT2 inhibitor now be considered MASH therapy? Dapagliflozin met all three histological endpoints in a 154-patient randomised trial with effect sizes at or above the approved drugs' (PMID 40467095), and the class already has observational hepatic and cardiovascular benefit (PMIDs: 39122360, 38345802). No regulator has been asked, no confirmatory trial outside China has reported, and no head-to-head against resmetirom or semaglutide exists.
  • Does combination therapy work? ATLAS randomised 392 F3–F4 patients across five active arms and none beat placebo on the histological primary endpoint, while continuous digital fibrosis measures and every biochemical marker improved on cilofexor + firsocostat (PMID 33169409). Whether that dissociation reflects a real modest antifibrotic effect or ordinal-endpoint noise is the single question that determines whether combination programmes are worth continuing, and no adequately powered combination trial has since reported.
  • Should pioglitazone be first-line in MASH with type 2 diabetes? The Cusi trial produced a treatment difference of 41 percentage points on its primary endpoint with fibrosis improvement, sustained to 36 months (PMID 27322798) — arguably a larger effect than resmetirom — in a single-centre trial of 101 patients. It has never been replicated at that scale, and weight gain plus the recurrence-on-discontinuation problem (Bril 2023) limit uptake.
  • Does vitamin E change outcomes? One propensity-matched cohort says yes (PMID 30506586); Cochrane rates randomised evidence on mortality as very low certainty (PMID 39412049). No randomised trial with clinical endpoints has been run, and after two approved drugs it is unlikely one will be.
  • Why did the cenicriviroc and obeticholic acid fibrosis signals not translate? Both hit fibrosis while missing resolution (PMIDs: 28833331, 31813633). Whether this reflects endpoint noise (histology and biopsy), true antifibrotic effect without anti-inflammatory effect, or chance has never been resolved.
  • Is combination therapy the answer? Network meta-analysis ranks two combinations — cilofexor+firsocostat and cilofexor+selonsertib — among the top three for fibrosis regression (PMID 39903735), consistent with the multi-node pathogenesis. Query run 2026-09-02: (NASH OR MASH) AND ("obeticholic acid" OR REGENERATE OR elafibranor OR cenicriviroc OR selonsertib OR lanifibranor OR aramchol OR "simtuzumab") — 1,161 records; no phase 3 combination trial retrieved.
  • Are the SGLT2-inhibitor benefits causal? Two large observational datasets agree on direction and magnitude (PMIDs: 38345802, 39122360), and neither is randomised. No SGLT2-inhibitor trial with histological endpoints in MASH has reported.
  • What should be given to children? TONIC missed its primary endpoint but showed NASH resolution 58% versus 28% with vitamin E (PMID 21521847); no drug is approved for paediatric MASLD, and neither resmetirom nor semaglutide has a paediatric MASH indication.

References

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