Graves' Disease Research Reagents

Graves' disease is the most common cause of hyperthyroidism, accounting for 60–80% of cases worldwide. The disease is driven by stimulatory autoantibodies (TSI/TRAb) that bind and activate the thyrotropin receptor (TSHR), causing unregulated thyroid hormone production independent of TSH signaling. Genetic susceptibility loci include HLA-DR3, CTLA-4, and TSHR itself. Graves' orbitopathy (GO), the most significant extrathyroidal manifestation, results from autoimmune-mediated inflammation of orbital fibroblasts, involving TSHR/IGF-1R crosstalk and hyaluronan accumulation. Teprotumumab (anti-IGF-1R) represents the first FDA-approved biologic for GO, while treatment of hyperthyroidism includes anti-thyroid drugs, radioactive iodine, and thyroidectomy.

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

Graves' Disease Research Reagents — key pathogenic pathways including TSHR-stimulating autoantibodies, IGF-1R crosstalk in orbital fibroblasts, and TSH suppression

Fig. 1 Key pathogenic pathways and research targets in Graves' disease. TSHR-stimulating autoantibodies drive hyperthyroidism; IGF-1R/TSHR crosstalk mediates orbital fibroblast activation in Graves' orbitopathy; TSH suppression serves as the primary clinical biomarker. Key research targets highlighted in orange.

abinScience provides validated anti-TSHR recombinant antibodies (stimulating and blocking clones), anti-IGF-1R reference antibodies including teprotumumab, ADA ELISA kits, and anti-TSH monoclonal antibodies for thyroid autoimmunity and Graves' orbitopathy research. All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom antibody development.

Key Research Targets

TSHR (TSH Receptor) — TSHR is the central autoantigen in Graves' disease, targeted by three functionally distinct autoantibody classes: stimulating (TSI, driving hyperthyroidism), blocking (causing hypothyroidism, overlapping with Hashimoto's), and neutral/cleavage antibodies. Anti-TSHR recombinant antibodies (M22 stimulating, K1-70 blocking, 3BD10, 1H7) with fluorescent conjugates (FITC, PE, APC, PerCP) support TRAb classification, functional bioassay development, receptor binding studies, and flow cytometric analysis.
→ Browse TSHR antibodies & proteins

IGF-1R (Insulin-like Growth Factor 1 Receptor) — IGF-1R is overexpressed on orbital fibroblasts and B/T lymphocytes in Graves' orbitopathy. The TSHR/IGF-1R signaling complex is critical for orbital tissue remodeling, hyaluronan production, and adipogenesis. Anti-IGF-1R reference antibodies — including teprotumumab (the only FDA-approved biologic for GO), ganitumab, cixutumumab, and figitumumab — as well as a teprotumumab ELISA kit, support mechanism-of-action studies, ADA detection, and biosimilar characterization.
→ Browse IGF-1R antibodies, proteins & ELISA kits

TSH (Thyroid-Stimulating Hormone) — Serum TSH suppression below the lower limit of normal is the hallmark of Graves' hyperthyroidism and the primary biomarker for treatment monitoring. Anti-TSH monoclonal antibodies (matched-pair clones: 1A307, 1A308, 1A309) support sandwich ELISA development and TSH immunoassay calibration for thyroid function testing research.
→ Browse TSH antibodies

TPO (Thyroid Peroxidase) — While anti-TPO autoantibodies are the hallmark of Hashimoto's thyroiditis, they are also present in up to 80% of Graves' disease patients, reflecting the overlap between autoimmune thyroid diseases. Anti-TPO recombinant antibodies (RI-34, RI-33, RI-8) with multiple fluorescent conjugates are available for differential diagnosis research and thyroid autoimmunity profiling.
→ Browse TPO antibodies & proteins

References

1. Smith TJ, et al. Graves' disease. N Engl J Med. 2016;375(16):1552-1565. DOI

2. Douglas RS, et al. Teprotumumab for the treatment of active thyroid eye disease. N Engl J Med. 2020;382(4):341-352. DOI

3. Bahn RS. Graves' ophthalmopathy. N Engl J Med. 2010;362(8):726-738. DOI