Breakout in progress

GALT is starting a breakout after reporting good news at the AASLD liver conference for the #1 untapped market for big pharma, liver cirrhosis.

There is prior industry precedent that a buyout could send the stock price into the triple digits.

Why GALT’s Fibrosis Data Are Better Than Any Other MASH Company

1. They are showing fibrosis improvement in true compensated cirrhosis (F4) — the population where EVERY OTHER DRUG HAS FAILED.

Almost all other “great” fibrosis results in MASH come from F2–F3 populations (Akero, 89bio, Madrigal).
Fibrosis moves easily there. But in biopsy-confirmed F4 cirrhosis with portal hypertension, fibrosis essentially does not reverse in modern trials.
This is why Gilead, Intercept, NGM, Novartis, Genfit, and Madrigal all failed in this population.

GALT is the first to repeatedly show biomarker improvement AND fewer clinical events in compensated cirrhosis.

No other company has done that.

2. The magnitude of fibrosis-biomarker improvement is unusually large and consistent across ALL major antifibrotic markers.

At 18 months (NAVIGATE):

• Pro-C3 reduction: >50% vs baseline

This is the main “fibrogenesis” marker.
Competitors usually get ~20–30% reduction in easier F2–F3 patients.

• ELF score: clinically meaningful drop

Again, competitors rarely get ELF improvement in cirrhosis.

• FibroScan liver stiffness: improved

Liver stiffness almost always worsens in F4 patients.
Belapectin produced improvement.

• YKL-40 / other collagen markers: improved

Indicates reduced macrophage-driven scarring.

What’s unique:

Other companies may improve one marker (e.g., ALT, MRI-PDFF, or PRO-C3),
but GALT shows simultaneous improvement across the entire fibrosis parameter set in cirrhosis.

That has not been replicated by any other company.

3. Only GALT has shown a link between fibrosis biomarkers → portal pressure improvement → fewer cirrhosis complications.

This is the reason the field is paying attention.

HVPG (portal pressure) improvement

Belapectin produced meaningful drops in HVPG — the FDA’s gold-standard surrogate for preventing variceal bleeding, ascites, transplant, and death.

No other MASH drug has ever shown a consistent HVPG improvement in cirrhosis.

Reduced clinical progression

Belapectin-treated patients developed fewer new esophageal varices, which is the #1 warning sign of impending decompensation.

This matches the HVPG signal.
It matches the biomarkers.

This “full chain” alignment is unmatched:

Fibrosis biomarkers improve

Portal pressure decreases

Varices occur less often

Disease stays compensated

Other companies haven’t shown this chain — not even close.

4. The 36-month follow-up CONFIRMED the benefit keeps going — something almost no MASH drug has ever shown.

At 36 months:

• New varices incidence: 12.4% at 2 mg/kg vs 23.4% placebo

The advantage persisted for 3 years.
This is extremely rare in cirrhosis.

• Biomarker improvements remained stable

PRO-C3, ELF, liver stiffness all stayed improved.

Durability is critical:

Many drugs show an early signal that disappears later.
Belapectin’s signal strengthens with time.

No other MASH drug has shown a 36-month antifibrotic durability signal with matching clinical outcomes.

5. Mechanistically, belapectin is the only drug directly targeting activated macrophage–galectin-3 fibrosis architecture.

Other drugs target:

Fat reduction (Madrigal)

Metabolic pathways (89bio, Akero)

FGF signaling

Lipid metabolism

Inflammation

Those help in F2/F3 — but not in F4.

Belapectin targets the scaffolding of fibrotic architecture itself by inhibiting galectin-3 on activated macrophages.

This mechanism explains why:

• GALT works in cirrhosis but others fail.
• Biomarker improvements line up across every fibrosis marker.
• HVPG drops.
• 36-month clinical progression slows down.

It’s the right mechanism for the right stage of disease.

6. The field desperately needs a drug for compensated cirrhosis — and GALT is alone.

Every other company is fighting over:

F2/F3

Early fibrosis

Resmetirom-like mechanisms

MRI-PDFF reductions

Triglycerides

ALT normalization

Body-weight changes

But none of that matters in F4.

Regulators, hepatologists, and payers want something that:

Slows portal pressure rise

Prevents varices

Delays decompensation

Reduces need for transplant

Only belapectin has shown all of that together.

THE SIMPLE ANSWER

GALT’s fibrosis data are better than any other MASH company because they succeed exactly where every other program has failed: reversing fibrosis biology, lowering portal pressure, and slowing clinical progression in real compensated cirrhosis — with signals that persist out to 36 months and are consistent across all major biomarker categories.

No other company in MASH has shown:

deep PRO-C3 reduction

ELF improvement

liver stiffness improvement

HVPG reduction

fewer varices

36-month durability

in true F4 cirrhosis

with a fibrosis-architecture mechanism

GALT is alone in that category.