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Hepatic Fibrosis

Hepatic fibrosis, a condition characterized by the abnormal buildup of extracellular matrix components like collagen in the liver, poses a significant challenge to normal liver function. This accumulation not only alters the structural integrity of the liver but also contributes to scarring and fibrotic changes. Our extensive expertise enables us to offer groundbreaking solutions tailored to the unique requirements of your research aimed at enhancing the deep research of these ailments.

Introduction to Hepatic Fibrosis

Hepatic fibrosis, also known as liver fibrosis, is typically a consequence of prolonged liver injury, which can stem from various factors including chronic viral hepatitis infections, excessive alcohol consumption, or metabolic disorders like non-alcoholic fatty liver disease. As the liver continues to experience damage over time, the formation of scar tissue can gradually replace healthy liver cells, leading to compromised liver function. 

Pathogenesis of Hepatic Fibrosis

Hepatic fibrosis, a progressive condition characterized by the accumulation of scar tissue within the liver. Which can stem from diverse sources, encompassing viral hepatitis infections like hepatitis B and C, prolonged alcohol consumption, autoimmune ailments, and metabolic irregularities. The intricate pathogenesis of hepatic fibrosis unfolds through a series of interconnected events, involving a multitude of signaling cascades, inflammatory reactions, and alterations in the extracellular matrix.

Fig.1 Molecules and mechanisms of hepatic fibrosis.Fig.1 Molecules and mechanisms of hepatic fibrosis. (Zhang, Dan-yan, et al., 2021)

Therapeutics of Hepatic Fibrosis

Small Molecule Drug Therapy

The emergence of small-molecule drugs has offered a ray of hope in slowing down the advancement of hepatic fibrosis. From FXR agonists like tropifexor, cilofexor, and obeticholic acid to anti-inflammatory agents such as pentoxifylline, angiotensin receptor blockers like iosartan, and natural compounds including berberine and silymarin, a repertoire of pharmacological interventions hold promise in mitigating fibrotic progression. These agents target specific pathways implicated in fibrogenesis, offering a targeted approach to curtail the cascade of hepatic fibrosis.

Gene Therapy

The realm of gene therapy presents a realm of novel possibilities for addressing hepatic fibrosis. Innovative modalities such as plasmid DNA delivery, viral vectors, RNA interference, CRISPR/Cas9 gene editing, and nanoparticle-based delivery systems offer a potent arsenal for delivering therapeutic genes to the liver and tackling the underlying molecular mechanisms fueling fibrosis. By leveraging these cutting-edge technologies, researchers aim to intervene at a molecular level, disrupting the fibrotic process and paving the way for more targeted and efficacious therapeutic strategies.

Our Services

Our company has a team of experts with diverse backgrounds in research and development, as well as state-of-the-art technical capabilities that enable us to provide tailored solutions for hepatic fibrosis. Through our extensive experience in the development of animal models and therapeutic platforms, we offer comprehensive support for your preclinical research focused on hepatic fibrosis therapeutics.

Therapy Development Platforms

Animal Models of Hepatic Fibrosis

Animal models is crucial for understanding the underlying mechanisms of hepatic fibrosis and developing effective therapeutics. We can provide chemically induced or genetically engineered animal models to support your research on the pathogenesis of hepatic fibrosis and the development of innovative therapies.

Diet-induced models
The administration of 5-diethoxycarbonyl-1,4-dihydropyridine (DDC) and α-naphthyl isothiocyanate (ANIT) in the feed of experimental animals leads to the development of hepatic fibrosis.
Optional Models
  • DDC model
  • ANIT model
Chemical-induced Models
Carbon tetrachloride (CCl4) and thioacetamide (TAA) are toxic chemicals that are commonly used to induce liver injury in animal models.
Optional Models
  • CCL4 model
  • TAA model
Genetically Engineered Models
Genetic engineering models are caused by transgenic and gene editing technology such as CRISPR/Cas9 to target critical genes of hepatic fibrosis, to study the pathogenesis of hepatic fibrosis, and to test potential therapeutic interventions.
Optional Models
  • α-SMA transgenic model
  • TGFBR2Flox/Flox model
  • TGF-β1 transgenic model
Physical-induced models
In this model, the common bile duct is surgically ligated, leading to cholestasis and liver injury, which can progress to fibrosis.
Optional Models
  • Bile duct ligation (BDL) model
Optional Species Mice, Rats, Others

Our company stands at the forefront of hepatic fibrosis disease research and therapeutic, with our dedicated team and advanced technical capabilities, we can offer you comprehensive service to support your pharmacokinetics analysis and drug safety evaluation.

If you are interested in our services, please feel free to contact us for more details and quotation information of related services.


  • Khanam, Arshi et al. "Pathophysiology and Treatment Options for Hepatic Fibrosis: Can It Be Completely Cured?." Cells 10.5 (2021): 1097.
  • Zhang, Danyan et al. "The Molecular Mechanisms of Liver Fibrosis and Its Potential Therapy in Application." International journal of molecular sciences 23.20 (2022): 12572.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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