Method for Treating Primary Sclerosing Cholangitis

Novel therapeutic method patent directed to the treatment of primary sclerosing cholangitis (PSC), a rare hepatobiliary disease with limited approved therapies.

About this asset

PSC is a chronic cholestatic liver disease characterized by progressive inflammation and fibrosis of the bile ducts. This method-of-treatment patent positions Islet Sciences within a high-unmet-need therapeutic area with significant strategic interest from hepatology-focused developers.

Key characteristics

Rare Disease Focus
Targets a recognized area of significant unmet medical need.
Method-of-Use Protection
Establishes a defensible commercial position for downstream development.
Strategic Optionality
Available for licensing, co-development, or asset acquisition.
Hepatology Adjacency
Complements the broader PSC / PBC portfolio held by Islet Sciences.

Potential applications

Primary sclerosing cholangitisHepatobiliary disease franchisesRare-disease pipelines
Disease Pathology · Live Cross-Section

From a healthy duct to obliteration.

PSC progresses through a defined cascade — inflammation, immune infiltration, concentric fibrosis, and eventual bile duct loss. Watch a cross-section evolve.

Normal · stage 1/6
The Biology of PSC

An eight-stage fibro-inflammatory cascade.

Mapped from the patent specification — from immune dysregulation to end-stage liver failure.

  • STAGE 01
    Immune Dysregulation

    Aberrant T-cell and innate-immune activation seeds biliary tropism.

  • STAGE 02
    Inflammatory Bowel Disease

    Concurrent IBD primes gut-derived inflammatory signals.

  • STAGE 03
    Portal Inflammation

    Lymphocytic infiltration in portal tracts surrounding bile ducts.

  • STAGE 04
    Biliary Inflammation

    Cholangiocyte activation, cytokine release, ductular reaction.

  • STAGE 05
    Bile Duct Injury

    Epithelial damage and progressive duct narrowing.

  • STAGE 06
    Fibrosis

    Periductal collagen deposition — the hallmark onion-skin pattern.

  • STAGE 07
    Biliary Cirrhosis

    Architectural distortion, regenerative nodules, portal hypertension.

  • STAGE 08
    Liver Failure

    Decompensation; transplantation may become the only option.

Cellular Mechanism

Immune cell attack on bile duct epithelium.

Activated T-cells, macrophages and innate immune populations target cholangiocytes, driving inflammation, epithelial injury, and periductal fibrosis.

ACTIVATED IMMUNE CELLS · T-CELLS · MACROPHAGESCYTOKINE-MEDIATED ATTACKBile Duct Lumen
EVENT 01
Cholangiocyte activation
Bile duct epithelial cells become immunologically active, presenting antigen and recruiting more immune cells.
EVENT 02
T-cell infiltration
CD4+ and CD8+ populations cluster around portal tracts and target cholangiocytes directly.
EVENT 03
Cytokine storm in microenvironment
TNF-α, IFN-γ, and IL-17 sustain inflammation and signal fibroblast recruitment.
EVENT 04
Periductal fibrosis initiation
Activated stellate cells lay down concentric collagen layers — the onion-skin signature.
Pathology Hallmark

The onion-skin signature of PSC.

Concentric periductal fibrosis is the defining histopathologic feature — visible here as layered collagen rings progressively obliterating the bile duct lumen.

STAGE 1
Healthy
STAGE 2
Early Fibrosis
STAGE 3
Concentric Fibrosis
STAGE 4
Onion-Skin Pattern
STAGE 5
Obliterated Duct
Disease Progression

How PSC progresses over time.

Primary Sclerosing Cholangitis is a progressive fibro-inflammatory disease that damages the bile ducts and liver over many years.

  1. 1

    Healthy Bile Ducts

    Normal bile flow

    Bile flows normally from the liver through healthy bile ducts.

    Cholangiocytes line patent ducts; immune homeostasis is intact and the biliary tree drains freely into the duodenum.
  2. 2

    Chronic Inflammation

    Immune cells appear

    Inflammatory processes begin damaging the bile ducts.

    Activated T-cells and macrophages cluster in portal tracts, releasing cytokines that injure cholangiocytes.
  3. 3

    Fibrosis Formation

    Scar tissue develops

    Repeated injury triggers fibrotic remodeling and scarring.

    Hepatic stellate cells activate and deposit collagen around inflamed ducts — the first scaffold of permanent scarring.
  4. 4

    Onion-Skin Fibrosis

    Concentric scar rings

    The hallmark pathology of PSC begins to develop.

    Concentric layers of collagen wrap around bile ducts in the pathognomonic onion-skin pattern visible on biopsy.
  5. 5

    Bile Duct Narrowing

    Lumen constricts

    Scar tissue progressively obstructs bile flow.

    Fibrotic strictures choke the duct lumen, producing the beaded biliary tree seen on MRCP imaging.
  6. 6

    Cholestasis & Liver Injury

    Bile backs up

    Reduced bile drainage contributes to ongoing liver damage.

    Trapped bile acids become hepatotoxic, driving hepatocyte injury, jaundice, and rising alkaline phosphatase.
  7. 7

    Cirrhosis

    Liver-wide scarring

    Extensive scarring compromises liver function.

    Architectural distortion, regenerative nodules, and portal hypertension mark end-stage fibrotic liver disease.
  8. 8

    Liver Failure / Transplant

    End-stage disease

    Some patients ultimately require liver transplantation.

    Decompensation, MELD progression, and limited medical options drive PSC patients toward orthotopic liver transplant.
Healthy DuctInflammationFibrosisOnion-SkinObstructionLiver DamageCirrhosisTransplant
Gut–Liver Axis

The colon-liver connection in PSC.

Up to 80% of PSC patients have concurrent inflammatory bowel disease. The portal circulation delivers gut-derived inflammatory signals directly to the biliary tree.

ColonIBD-AFFECTEDPORTAL CIRCULATIONLiverBILE DUCT INJURY · PSC
70-80%
of PSC patients have concurrent IBD
Portal
circulation delivers gut signals to liver
Cholangiocyte
is the primary target of injury
Bidirectional
gut-liver axis sustains the disease
Laboratory Signatures

Interactive PSC biomarker dashboard.

Switch between disease stages to watch the cholestatic, hepatocellular, and fibrosis signatures evolve. Hover any panel for reference ranges and clinical interpretation.

ALP
Alkaline Phosphatase
× ULN
Hallmark cholestatic marker3.1×
GGT
Gamma-Glutamyl Transferase
× ULN
Biliary injury indicator3.4×
ALT
Alanine Aminotransferase
× ULN
Hepatocellular damage1.9×
AST
Aspartate Aminotransferase
× ULN
Hepatocellular damage2.0×
TBIL
Total Bilirubin
mg/dL
Prognostic in advanced disease1.8
LSM
Liver Stiffness (FibroScan)
kPa
Non-invasive fibrosis assessment12.8
ELF
Enhanced Liver Fibrosis Score
score
Serum fibrosis panel10.4
Composite signature — Established PSC
Persistently elevated ALP and GGT, rising stiffness and ELF — the trial-enrollment phenotype.
Clinical Burden

A Serious Disease With Limited Treatment Options.

PSC remains a rare but severe disease with significant long-term clinical consequences and a limited approved treatment landscape.

Rare but severe liver disease
A chronic hepatobiliary condition with progressive course.
Progressive bile duct fibrosis
Structural duct damage compounds over time.
Risk of cirrhosis & liver failure
Long-term progression can compromise hepatic function.
Elevated cholangiocarcinoma risk
Associated with increased hepatobiliary malignancy risk.
Potential transplant need
Some patients ultimately require liver transplantation.
Significant unmet need
Limited approved therapies for disease modification.
Patent Concept

Therapeutic Use of SGLT2 Inhibition in PSC.

This patent relates to the use of pharmaceutical compositions involving the SGLT2 inhibitor remogliflozin etabonate for treating Primary Sclerosing Cholangitis.

The patent describes methods and compositions associated with improving or maintaining clinical outcomes related to PSC-associated symptoms and complications.

Important

This patent describes therapeutic-use intellectual property. It does not characterize clinical efficacy, regulatory status, or approved indication.

  1. SGLT2 Inhibition
  2. Metabolic / Inflammatory Pathway Modulation
  3. Potential Liver Disease Application
  4. PSC Therapeutic-Use Opportunity
Patent Science Timeline

From biology to partnership opportunity.

  1. 01
    Disease Biology
  2. 02
    Scientific Hypothesis
  3. 03
    Patent Filing
  4. 04
    Patent Publication
  5. 05
    Development Opportunity
  6. 06
    Strategic Partnership
Strategic Value

Why This Asset May Matter.

Rare Liver Disease

Recognized rare hepatobiliary indication with focused patient populations.

High Unmet Need

Few approved disease-modifying therapeutic options today.

Limited Treatment Landscape

Therapeutic competition remains narrow relative to other liver diseases.

Therapeutic-Use IP

Method-of-use protection focused on a defensible indication.

Potential Repurposing Opportunity

Leverages a clinically validated mechanism of action.

Strategic Partnering Potential

Suitable for hepatology, rare-disease, and specialty pharma partners.

Explore Development or Licensing Opportunities.

Islet Sciences is evaluating strategic partnerships, licensing discussions, and development opportunities for its therapeutic-use intellectual property portfolio.

Contact Business Development Back to portfolio

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