Glycobio
3日前
sunspotter that link/article you bring up is from two years ago before they had the complete results.
The publication below, in contrast, is current with recent clinical trial results.
That’s weak of you to bash with old info. Take some time to read the latest.
Efficacy and safety of belapectin for the prevention of esophageal varices in patients with MASH cirrhosis: The randomized, placebo-controlled NAVIGATE trial
Chalasani, Naga1; Vuppalanchi, Raj1; Noureddin, Mazen2; Shiffman, Mitchell L.3; Lawitz, Eric4; Mena, Edward5; Gunn, Nadege T.6; Ladron de Guevara, Laura7; Elgouhari, Hesham8; Safadi, Rifaat9; Jamil, Khurram10; Harrison, Stephen A.11; Alkhouri, Naim12
Conclusion:
Belapectin 2 mg/kg lowered the development of new varices in MASH cirrhosis and portal hypertension.
Glycobio
3日前
So an anonymous armchair internet poster is saying he knows better than these authors.
Look up their biographies. These are top names in the field of hepatology / liver disease.
If someone spends all day writing thousands of messages on stock boards, doesn’t make you more of an authority than a medical expert.
Efficacy and safety of belapectin for the prevention of esophageal varices in patients with MASH cirrhosis: The randomized, placebo-controlled NAVIGATE trial
Chalasani, Naga1; Vuppalanchi, Raj1; Noureddin, Mazen2; Shiffman, Mitchell L.3; Lawitz, Eric4; Mena, Edward5; Gunn, Nadege T.6; Ladron de Guevara, Laura7; Elgouhari, Hesham8; Safadi, Rifaat9; Jamil, Khurram10; Harrison, Stephen A.11; Alkhouri, Naim12
Conclusion:
Belapectin 2 mg/kg lowered the development of new varices in MASH cirrhosis and portal hypertension.
Glycobio
3日前
This is the latest from May 27 2026. “Notably, this abstract has been designated a TOP Poster by EASL, recognizing it among the best abstracts in the Portal Hypertension (cirrhosis and non-cirrhosis) session.”
Data from the oral presentation (REG26-611), presented by Mazen Noureddin, M.D., MHSc, Director of Houston Research Institute and Professor of Medicine at Houston Methodist Hospital, demonstrate belapectin’s impact on fibrosis modulation in patients with high-risk MASH cirrhosis, as reflected by changes in the Pro-C3/CTX-III ratio — a marker of fibrogenesis balance. Favorable shifts in this ratio were associated with reduced varices development and improvements in broad markers of fibrosis including liver stiffness measure and other markers of fibrosis including Pro-C3, supporting belapectin’s potential to modify disease progression by targeting underlying fibrotic pathology.
The poster presentation (REG26-612), presented by Dr. Naim Alkhouri, MD, FAASLD, Chief Academic Officer at Summit Clinical Research and Director of the Steatotic Liver Program at North Shore Gastroenterology, presents new analyses from the NAVIGATE trial demonstrating risk reduction in clinically significant portal hypertension. Notably, this abstract has been designated a TOP Poster by EASL, recognizing it among the best abstracts in the Portal Hypertension (cirrhosis and non-cirrhosis) session.
Across the NAVIGATE dataset, belapectin 2 mg/kg demonstrated a statistically significant reduction in new varices at 18 months in the per-protocol population (p=0.04) and statistically significant reductions in liver stiffness at multiple timepoints. Fewer belapectin-treated patients experienced clinically meaningful worsening of liver stiffness (>30% increase) versus placebo (11.7% vs. 23.9%; p=0.03). At 18 months, a greater proportion of belapectin-treated patients improved to the no/low-risk Baveno category relative to baseline compared with placebo (p=0.0073). These data collectively support belapectin’s potential as a disease-modifying therapy in MASH cirrhosis.
These EASL presentations build on results recently published in Hepatology, the AASLD flagship journal. The manuscript, titled “Efficacy and Safety of Belapectin for the Prevention of Esophageal Varices in Patients with MASH Cirrhosis: The Randomized, Placebo-Controlled NAVIGATE Trial,” is available as an open-access publication, further validating the clinical and scientific significance of belapectin’s effects in this high-risk population. There are currently no approved therapies for the prevention of varices or treatment of portal hypertension in patients with MASH cirrhosis.
Glycobio
5月前
LOL it's a random internet poster with zero experience in the liver field who calls himself sunspotter vs. independent experts who specialize in liver disease:
November 2025 -
Raj Vuppalanchi, M.D., serves as Professor of Medicine and Director of Hepatology at Indiana University School of Medicine, stated “...The sustained improvements in liver stiffness and multiple serum biomarkers, including ELF, PRO-C3, and YKL-40, are particularly noteworthy, as they collectively suggest a consistent antifibrotic effect and stabilization of disease. These results are encouraging for patients with MASH cirrhosis and portal hypertension, a population with few effective therapeutic options.”
Glycobio
7月前
Raj Vuppalanchi, M.D., serves as Professor of Medicine and Director of Hepatology at Indiana University School of Medicine, stated “The long-term NAVIGATE data presented at AASLD provide important insights into the potential of Galectin-3 inhibition in advanced fibrosis. The sustained improvements in liver stiffness and multiple serum biomarkers, including ELF, PRO-C3, and YKL-40, are particularly noteworthy, as they collectively suggest a consistent antifibrotic effect and stabilization of disease. These results are encouraging for patients with MASH cirrhosis and portal hypertension, a population with few effective therapeutic options.”
Glycobio
7月前
Galectin Therapeutics’ fibrosis results are extremely bullish because they show clear, consistent, and statistically meaningful HVPG reduction in NASH cirrhosis while also demonstrating broad biomarker confirmation that the drug is actively shutting down fibrogenesis. HVPG responders (≥20% reduction) appeared without safety issues, and this is the FDA-recognized gold-standard surrogate for preventing decompensation, variceal bleeding, transplant, and death. At the same time, the latest biomarker readout showed meaningful declines in PRO-C3, lower rates of PRO-C4 worsening, and higher proportions of patients achieving YKL-40 reductions, all pointing to real suppression of collagen production and inflammatory remodeling. These biochemical shifts matched the improvements seen in non-invasive measures (LSM/FibroScan and ELF), with belapectin cutting high-risk fibrosis progression rates in half and increasing the share of patients moving into lower-risk Baveno VII categories. Belapectin directly targets activated macrophages and interrupts the upstream fibrosis engine rather than just reducing liver fat or inflammation like other NASH drugs. And because the strongest HVPG improvements occurred in patients without baseline varices—precisely the group the FDA prefers for accelerated approval—the combined hemodynamic, biomarker, and safety profile strongly implies accelerated-approval viability and a multi-billion-dollar valuation trajectory in a space with no competitors.
Glycobio
7月前
From another board, good stuff:
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.