At Fibrocor Therapeutics, we are not just treating fibrosis; we put patients first in our drug discovery and clinical development process. Our unwavering commitment to research and innovation has led us to discover the most promising and effective drug candidates in fibrosis treatment, setting us apart as industry leaders.

Idiopathic Pulmonary Fibrosis (IPF):

Idiopathic Pulmonary Fibrosis (IPF) is a complex and progressive lung disease affecting approximately 100,000 people in the United States. IPF is characterized by lung scarring, which leads to impaired lung function and challenging symptoms. Unfortunately, a cure for IPF is currently unavailable, and it is often underdiagnosed or misdiagnosed initially, resulting in delayed treatment and poorer outcomes.

While the available treatment options for IPF are limited, Fibrocor’s unique pipeline aims to disrupt the underlying mechanisms of the disease. These advancements offer hope for improved disease management, slowed progression, and enhanced quality of life for individuals living with IPF.

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Alport Syndrome:

Alport Syndrome is a rare genetic disease that affects the kidneys, ears, and eyes. It is caused by a mutation in specific genes responsible for producing essential proteins that maintain the health of these organs.

Currently, there is no cure for Alport syndrome. Treatment primarily focuses on managing symptoms and slowing down the progression of the disease. This approach aims to preserve kidney function and minimize complications. However, these treatments cannot entirely halt the disease’s progression or address the underlying genetic defects. As a result, kidney transplantation becomes necessary for most individuals with Alport syndrome. Transplantation can occur as early as adolescence or teenage years or as late as one’s 40s or 50s for both males and females grappling with this condition.

One of the biggest challenges in treating Alport syndrome is the limited availability of approved therapies designed for this condition. Fibrocor’s innovative therapeutics target the key molecular elements of the fibrotic process at the core of Alport syndrome. These advancements offer hope for the future, as they have the potential to improve outcomes and quality of life for individuals living with this condition.

Fibrosis:

While acute inflammatory reactions typically resolve rapidly, characterized by vascular changes, edema, and neutrophilic inflammation, fibrosis arises from chronic inflammation. Chronic inflammation is an immune response that persists for several months, during which inflammation, tissue remodeling, and repair processes occur concurrently. Despite their distinct causes and clinical presentations, most chronic fibrotic disorders share a common feature: a persistent irritant that triggers the production of growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines. These factors stimulate the deposition of connective tissue elements, which progressively remodel and disrupt the standard architecture of the affected tissue.

Tissue damage can result from various stimuli, including infections, autoimmune reactions, toxins, radiation, and mechanical injuries. The repair process typically unfolds in two distinct phases. First, the regenerative phase involves replacing injured cells with new cells of the same type, leaving no lasting evidence of the damage. Second, the fibroplasia or fibrosis phase ensues, wherein connective tissue replaces normal parenchymal tissue. While the repair process is initially beneficial, it becomes pathogenic when proper control mechanisms fail, leading to excessive extracellular matrix (ECM) components deposition. This results in the replacement of normal tissue with permanent scar tissue. In specific diseases, such as idiopathic pulmonary fibrosis, liver cirrhosis, and kidney fibrosis, extensive tissue remodeling and fibrosis can ultimately lead to organ failure and the need for organ transplantation.

At Fibrocor, our accomplished team has developed a distinctive portfolio of drug candidates that directly address the underlying mechanisms of fibrosis. By targeting critical molecular pathways responsible for fibrosis, our solutions interrupt the pathological progression of scar tissue formation. This approach not only halts the advancement of fibrosis but also facilitates tissue healing and remodeling, paving the way for improved patient outcomes.