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Graves' disease (GD)

Graves' disease (GD) is an immune system disorder that causes the overproduction of thyroid hormones (hyperthyroidism). Although a number of disorders may cause hyperthyroidism, Graves' disease is a common cause. Specialized drug and therapy development services are essential to enhance and expedite Graves' disease research. Our company is well-equipped to address your drug and therapy development requirements in Graves' disease therapy.

Introduction to Graves' disease

  • Graves' disease is an autoimmune condition that primarily affects the thyroid gland.
  • It is the most common cause of hyperthyroidism and can appear at any age, though it is especially common among women during their reproductive years.
  • The prevalence of Graves' disease differs worldwide, with an estimated 0.5% of the global population affected.

Pathogenesis of Graves' disease

In Graves' disease, the overproduction of thyroid hormone is triggered by the activation of thyrotropin receptors through thyroid-stimulating antibodies originating from both within and outside the thyroid gland. Additionally, cytokines like interleukin-1, tumor necrosis factor-α, and interferon-γ, produced by inflammatory cells in the thyroid, prompt the expression of various molecules such as CD54, CD40, and HLA class II. These molecules further stimulate local inflammatory cells. These cytokines also lead thyroid cells to produce more cytokines, which may perpetuate the autoimmune process occurring within the thyroid.

The pathogenesis of Graves’ disease.Fig. 1 Pathogenesis of Graves' disease. (Weetman, A.P., 2000)

Diagnosis Development of Graves' disease

The development of autoantibody detection methods, such as radioimmunoassays and ELISA, has directly identified TSH receptor antibodies, crucial for diagnosing the autoimmune basis of Graves' disease. Advances in genetic and molecular research have begun to reveal the genetic predispositions that contribute to the development of Graves' disease, suggesting future possibilities for personalized medicine. This research holds promise for customizing diagnosis and treatment based on individual genetic makeup, though it is not yet a standard practice in diagnostics.

Therapy Development of Graves' disease

Small Molecule Drugs

Small molecule drugs are typically the frontline treatment options due to their effectiveness in modulating thyroid hormone synthesis. For instance, Methimazole and Propylthiouracil are thionamides that directly inhibit the thyroid peroxidase enzyme, crucial for thyroid hormone production. By reducing the enzyme's activity, these drugs effectively decrease hormone levels, providing relief from hyperthyroid symptoms common in Graves' disease.

Cell Therapies

Cell therapies offer novel approaches to re-establish immune tolerance. An example of such innovative therapy is the use of regulatory T cells (Tregs). These cells help maintain immune balance by suppressing autoreactive T cells that otherwise attack the thyroid. Research into enhancing the function or number of Tregs could potentially lead to therapies that specifically address the autoimmune basis of Graves' disease, reducing the need for generalized immune suppression.

Monoclonal Antibodies

Therapies like Rituximab represent targeted strategies to reduce specific components of the immune system that contribute to the disease. Rituximab targets CD20-positive B cells, which are implicated in the production of thyroid-stimulating immunoglobulins. By depleting these B cells, Rituximab can decrease the levels of harmful antibodies, mitigating the excessive stimulation of the thyroid gland seen in Graves' disease.

Gene Therapies

Gene therapies are on the cutting edge of treating autoimmune conditions like Graves' disease by directly modifying the genetic elements driving the disease. Although still in experimental stages, the use of small interfering RNA (siRNA) to silence genes involved in abnormal thyroid hormone production is a promising direction. This technique could potentially turn down the thyroid gland's overactivity at a genetic level.

Our Services

Our company adopts a partnership-driven approach. We collaborate closely with clients to craft tailored, innovative Graves' disease therapy strategies and ensure robust support throughout the process.

Platforms of Graves' disease Therapy Development

Animal Models of Graves' disease

We have established expertise in developing and utilizing relevant animal models that closely mimic the disease characteristics and response to therapy. These models enable us to evaluate the safety and efficacy of potential therapies.

Non-Genetically Engineering Models
We provide diverse model choices customized to meet specific research needs related to Graves' disease. These models allow researchers to simulate and study the complex biological processes associated with Graves' disease.
Optional Models
  • TSHR Protein Induced Model
  • TSHR Adenovirus-Mediated Gene Delivery Model
  • Co-Administration of Thyroid Antigens with Adjuvants Induced Model
  • Thyroid-Stimulating Immunoglobulins Transferred Model
Genetically Engineered Models
Our expertise in genetic engineering techniques, such as CRISPR/Cas9 technology, allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human Graves' disease.
Optional Models
  • L-TSHR Mice Model
  • Transgenic Mice with Mutated Human TSHR
  • Mice with Site-Specific Mutations in TSHR
  • Foxp3 Knockout Mice Model
  • Conditional Aire Knockout in Thyroid
  • Inducible Knockout Models for PD-1
Optional Species Mice, Rats, Non-human primates, Others

In addition to these models, our comprehensive services encompass other models that target specific signaling pathways and molecular targets.

If our services align with your goals, please contact us for more details.


  • Weetman, A.P., "Graves' disease." N Engl J Med, (2000). 343(17): p. 1236-1248.
  • Ginsberg, J., "Diagnosis and management of Graves' disease." CMAJ, (2003). 168(5): p. 575-585.

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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