Endocrine And Thyroid Disruption Assays

For Mechanistic And Regulatory Toxicology

Specialist mechanistic insight to support regulatory confidence

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How can I ensure that my chemical or product meets regulatory expectations for endocrine and thyroid safety?

Regulatory authorities increasingly expect mechanistic clarity to support safe chemical and product development. You need validated, GLP-compliant, in vitro endocrine and thyroid assays designed to support regulatory submissions, clarify mode of action, and generate robust mechanistic evidence for safety assessment. Our scientists understand this and recognize that identifying endocrine and thyroid hazards is only the first step.

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By understanding how and where chemicals interact with hormone systems, we provide actionable insights supporting confident, future-ready regulatory decision-making.

Driving better decisions with endocrine and thyroid testing

Endocrine and thyroid disruption (EDA/TD) presents a complex scientific and regulatory challenge under frameworks including REACH, ECHA, EFSA, FDA and OECD guidance. Increasingly, regulators expect robust mechanistic evidence to demonstrate biological plausibility, clarify mode of action and reduce uncertainty in hazard identification.

Our robust mechanistic toxicology approach is designed to solve these challenges, generating defensible data packages aligned to evolving guidance across EATS (Estrogen, Androgen, Steroidogenesis, Thyroid) modalities.

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By combining scientific depth with regulatory fluency, we help you move from mechanistic signal to confident regulatory conclusion. Our thyroid-focused TPO and DIO inhibition assays are currently under OECD consideration for potential Test Guideline development, reflecting our active role in advancing mechanistic thyroid toxicology.

For a deeper exploration of the scientific and regulatory landscape, read this blog by our Principal Scientist, Dr Ritu S Sharma; Mechanistic Toxicology for Endocrine and Thyroid Disruption - Navigating regulatory expectations with confidence.

Assay portfolio

Endocrine disruptor assays

Access regulator-ready mechanistic data without investing in specialized in-house infrastructure.

Our comprehensive, GLP-compliant suite of EATS assays, using human-relevant systems is designed to align with evolving regulatory expectations and provide regulator-ready mechanistic data to support:

Endocrine disruptor identification.
Mode-of-action (MoA) analysis.
Biological plausibility of adverse outcomes.
Species specificity and human relevance.
Robust weight-of-evidence (WoE) submissions.

What is the aromatase inhibition assay (OCSPP Guideline 890.1200)?

Aromatase catalyzes the conversion of androgens into estrogens and plays a central role in maintaining hormonal balance. Inhibition of aromatase can indirectly disrupt estrogen signaling, even without direct estrogen receptor interaction.

The GLP-compliant aromatase inhibition assay provides mechanistic insight into altered estrogen synthesis, supporting endocrine hazard assessment and mode-of-action interpretation.

Aromatase assay card

What does the estrogen receptor (ER) transactivation assay (OECD TG 455) measure?

The estrogen receptor is a nuclear receptor that regulates gene transcription in response to estrogenic signaling. Chemicals that activate or inhibit ER can disrupt endocrine homeostasis and contribute to reproductive or developmental toxicity.

The OECD TG 455-aligned ER transactivation assay evaluates agonist and antagonist activity under GLP conditions, delivering regulator-ready mechanistic data for estrogenic effects.

ER assay card

What is assessed in the androgen receptor (AR) transactivation assay (OECD TG 458)?

The androgen receptor governs male reproductive development and broader endocrine functions through androgen-responsive gene regulation. Disruption of AR signaling is a key component of endocrine hazard identification.

The GLP-compliant AR transactivation assay assesses both agonist and antagonist activity, providing robust A-modality mechanistic evidence for regulatory evaluation.

AR assay card

What does the steroidogenesis assay (OECD TG 456) evaluate?

Steroidogenesis encompasses the enzymatic pathways responsible for the biosynthesis of steroid hormones. Chemical interference with these pathways can lead to broad endocrine disruption beyond direct receptor effects.

The OECD TG 456-aligned assay evaluates chemical-mediated changes in hormone production, supporting differentiation between direct receptor-mediated and indirect endocrine mechanisms.

Steroidogenesis assay card

Where can I find more information on OECD Testing Guidelines?

OECD Testing Guidelines provide internationally recognized methods for assessing chemical safety, including endocrine disruption endpoints.

Explore OECD Testing Guidelines

Thyroid disruption (T-Modality) assays

Regulatory authorities increasingly expect mechanistic T-modality data to support thyroid hazard identification and weight-of-evidence assessments, particularly where in vivo findings suggest thyroid involvement. Gain future-aligned mechanistic insight that anticipates regulatory expectations and reduces uncertainty in thyroid hazard evaluation with our robust, cost effective, integrated thyroid assay framework.

What is the thyroperoxidase (TPO) inhibition assay?

Thyroperoxidase (TPO) is essential for thyroid hormone synthesis, catalyzing iodination reactions during thyroglobulin processing. Chemical inhibition of TPO can reduce hormone production and disrupt thyroid homeostasis.

The mechanistic TPO inhibition assay uses human and preclinical species microsomes to generate robust data supporting thyroid mode-of-action analysis. This assay is currently progressing toward OECD Test Guideline consideration.

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What does the deiodinase (DIO) inhibition assay measure?

Deiodinases regulate the activation and deactivation of thyroid hormones in peripheral tissues. Inhibition of DIO enzymes (DIO1, DIO2, and DIO3) can alter systemic hormone availability without directly affecting hormone synthesis.

The LC-MS/MS-based DIO inhibition assay evaluates xenobiotic-mediated effects across species, providing mechanistic clarity for indirect thyroid disruption. This assay is currently under OECD consideration for test guideline development.

What is the sodium iodide symporter (NIS) inhibition assay?

The sodium iodide symporter (NIS) mediates iodide uptake into the thyroid gland, a prerequisite for hormone synthesis. Inhibition of iodide transport represents a distinct molecular initiating event in thyroid disruption.

The GLP-aligned NIS inhibition assay supports mechanistic thyroid hazard identification and complements synthesis- and metabolism-focused endpoints.

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What do thyroid hormone receptor (THR) transactivation and inhibition assays evaluate?

Thyroid hormone receptors mediate genomic responses to T3 and T4 through transcriptional regulation. Direct agonism or antagonism at these receptors can disrupt thyroid signaling independently of circulating hormone levels.

The THR transactivation and inhibition assays evaluate receptor-mediated effects, providing mechanistic evidence for T-modality endocrine disruption.

What is the thyroxine-binding prealbumin (TTR) binding assay?

Transthyretin (TTR) transports thyroid hormones in circulation and influences their bioavailability. Chemicals that bind TTR may alter hormone distribution and systemic exposure.

The TTR-binding assay uses a T4-FITC fluorescence-based competitive binding approach to identify compounds that interfere with thyroid hormone transport, supporting interpretation of altered thyroid hormone homeostasis.

How do these assays support an integrated thyroid mechanistic framework?

These assays support a stepwise evaluation of thyroid disruption across key mechanistic events.

Impaired hormone synthesis (TPO, NIS)
Altered activation (DIO)
Disrupted transport (TTR)
Modified receptor signaling (THR)

This integrated approach aligns with current regulatory thinking and strengthens mechanistic interpretation.

Liver-mediated endocrine and thyroid disruption

Hepatic pathways are critical because the liver plays a central role in regulating systemic hormone levels through xenobiotic metabolism. Induction of hepatic enzymes can increase the clearance of endocrine and thyroid hormones, leading to altered circulating levels without direct receptor interaction.

Liver-mediated endocrine and thyroid disruption assays

Understanding liver-mediated mechanisms is essential for interpreting thyroid and endocrine effects. Patnering with us, you can build biologically plausible mode-of-action arguments to confidently support safe product development using hepatocyte-based assays.

What is the in vitro comparative UGT induction assay?

Phase II liver enzyme UDP-glucuronosyltransferases (UGTs) catalyze glucuronidation of thyroid hormones, facilitating their elimination. Induction of UGT enzymes can significantly increase T4 clearance and contribute to systemic thyroid hormone imbalance.

The GLP-compliant comparative UGT induction assay uses primary hepatocytes from rat, human, and dog to assess gene expression and enzymatic activity, linking enzyme induction to functional T4 clearance.

What does the in vitro T4-SULT induction assay measure?

Sulfotransferases (SULTs) contribute to thyroid hormone metabolism via sulfation. Chemical-mediated induction of SULT activity can further accelerate hormone clearance and impact endocrine balance.

This GLP-aligned assay complements UGT induction data and provides additional mechanistic insight into hepatic thyroid disruption pathways.

What is the T4 clearance assay?

The T4 clearance assay, using primary hepatocytes as test system, integrates enzyme induction data into a functional readout of thyroid hormone elimination.

This approach directly links hepatic metabolic activity with systemic endocrine outcomes and is particularly valuable in weight-of-evidence assessments.

What is the role of CYP induction assays?

Cytochrome P450 enzymes are key drivers of xenobiotic metabolism and a central regulatory concern for drug–drug interactions.

GLP-compliant CYP induction assays use primary human hepatocytes in alignment with FDA, EMA, and ICH guidance. Both screening and regulatory-grade formats are available to support early decision-making and formal submissions.

Explore the CYP assay card

How can these studies be integrated into a broader mechanistic strategy?

These assays can be combined with complementary platforms to deliver a comprehensive mechanistic understanding of liver and thyroid biology.

Integrating these capabilities enables a full mechanistic perspective to support regulatory interpretation and decision-making.

The future of thyroid toxicology

Beyond study execution, our scientists actively drive progress in endocrine disruptor assessment, contributing to collaborative initiatives that strengthen the mechanistic understanding regulators rely on. Our thyroid-focused TPO and DIO inhibition assays are currently under OECD consideration for potential Test Guideline development, demonstrating our commitment to regulatory-ready science and forward-looking methodologies.

By advancing thyroid molecular initiating event (MIE) assays, we provide clients with access to future-aligned, mechanistic testing strategies that reduce uncertainty, build confidence in hazard identification, and support the transition toward new approach methodologies (NAMs).

Delivering mechanistic clarity for regulatory confidence

Make regulatory decisions with confidence, backed by transparent, scientific data that strengthens your safety case. By integrating receptor-level, enzymatic, transport, and liver metabolism assays, you can access packages that:

Enable clear hazard identification.
Support robust mode-of-action characterization.
Reduce uncertainty in weight-of-evidence assessments.
Provide GLP-compliant, regulator-ready datasets suitable for regulatory submission.

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