How do you distinguish between anxiolysis and sedation?

We always run an OFT or Rotarod alongside anxiety assays. If a drug increases time in the "open arms" of an Elevated Plus Maze (EPM) but decreases total distance traveled, it may be sedating. A true anxiolytic increases open-arm exploration without suppressing overall motor activity.

Can you measure "Panic-like" attacks?

Yes, we use the CO2 Challenge or high-intensity Acoustic Startle Response models to simulate acute panic-like respiratory and motor symptoms.

Do you offer testing in both sexes?

Yes. Given the higher prevalence of anxiety in females, we offer sex-stratified cohorts to identify sex-specific therapeutic windows.

Which anxiety model is most sensitive for testing different neurotransmitter systems?

GABAergic & Serotonergic: The EPM is the gold standard and highly sensitive to benzodiazepines and SSRIs. Neuropeptide & Endocannabinoid: The Light/Dark Box (LDB) is often preferred for these systems as it relies more on spontaneous exploratory conflict.

Can your platform evaluate both acute and chronic drug effects?

Yes. For rapid-onset screening (e.g., benzodiazepine-like), we perform acute administration (single dose). For drugs with a delayed onset of action (e.g., SSRIs), we provide chronic dosing protocols (typically 14-21 days) followed by behavioral batteries to capture steady-state efficacy.

Do you provide physiological markers to support behavioral findings?

Yes. Behavioral data is often paired with HPA-axis profiling. We can measure plasma Corticosterone levels post-test or perform immunohistochemistry (IHC) for c-Fos expression in the amygdala, hippocampus, and prefrontal cortex to map the neural activation patterns associated with your compound.

What controls do you include in a standard anxiety PD study?

Every study includes a Vehicle Control and a Positive Control (Benchmark). Common benchmarks include Diazepam (acute anxiolytic), Buspirone, or Chlordiazepoxide, ensuring the assay's sensitivity is validated for each specific run.

Anxiety Modeling & Pharmacodynamics Services

Introduction

Anxiety disorders represent the most prevalent class of mental health conditions globally, characterized by a 30% lifetime prevalence and a complex pathology involving dysregulation within the amygdala and prefrontal cortex. Creative Biolabs' platform addresses the urgent need for safer, more effective anxiolytics by providing a high-fidelity modeling framework that replicates both state and trait anxiety across various subtypes, including generalized anxiety disorder (GAD), panic disorder (PD), agoraphobia (AG), and specific phobia (SP). By integrating classical ethological assays with high-sensitivity behavioral readouts and neurophysiological assessments, we deliver a rapid, cost-effective, and reproducible environment for early-stage lead optimization. This multidimensional approach provides the quantitative evidence necessary to rigorously de-risk the behavioral and safety profiles of next-generation CNS therapies, accelerating their path from preclinical discovery to clinical application.

Fig.1 Anxiety disorders can be categorized into three groups based on behavior: fear-dominant (SP, AG), mixed (SAD, PD), and anxiety-dominant (GAD). Notably, the anxiety-dominant group is uniquely associated with HPA axis dysregulation. (OA Literature) Fig.1 Brain function related to three anxiety disorder groups: fear-dominant (SP, AG), mixed (SAD, PD), and anxiety-dominant (GAD), based on the intensities of fear, anxiety, and avoidance behaviors. In the anxiety-dominant group, the hypothalamic‒pituitary‒adrenal (HPA) axis has also been implicated.¹

Available Anxiety Models

Our platform provides a standardized suite of anxiety-related behavioral assays to evaluate the anxiolytic or anxiogenic effects of novel compounds. These models rely on the natural conflict between a subject's innate drive to explore new environments and its evolutionary fear of open, brightly lit spaces. Beyond rodent assays, we offer non-human primate (NHP) models that exhibit complex social behaviors and physiological stress profiles, providing a higher-order translational bridge to human psychiatric conditions. By combining these high-throughput screening tools with precision analytics, we offer a rapid, cost-effective framework to de-risk behavioral safety profiles and accelerate the lead optimization of next-generation psychiatric therapies.

Anxiety Models	Modeling Methods	Application Values	Animal Species
Elevated Plus Maze Test	Animals are placed in a cross-shaped maze with two open and two enclosed arms, elevated above the ground.	The gold standard for screening anxiolytic drugs. It measures the ratio of time spent in open vs. closed arms, serving as a highly sensitive readout for GABAergic and serotonergic drug effects.	Mouse, Rat
Light/Dark Box Test	A two-compartment box consisting of a small, dark area and a larger, brightly illuminated area connected by a door.	Measures the spontaneous exploratory behavior and light-aversion. It is particularly valuable for identifying compounds that reduce "state anxiety" without affecting general motor activity.	Mouse, Rat

Evaluation Platform

To provide regulatory-grade evidence for anxiolytic drug discovery, our platform integrates high-resolution behavioral analytics with multidimensional physiological readouts:

Precision Behavioral Tracking: We employ AI-powered computer vision (Any-maze, DeepLabCut) to eliminate observer bias, capturing granular metrics such as zone latency, frequency of visits, and ethological markers like "head dipping" and "stretch-attend" postures.
Integrated Locomotor Controls: All assays are cross-validated via the Open Field Test (OFT) to ensure behavioral shifts are driven by anxiety modulation rather than confounding factors like sedation or motor impairment.
Neuro-Endocrine & Autonomic Profiling: We correlate behavioral phenotypes with objective biomarkers, including plasma Corticosterone (HPA-axis), c-Fos expression (amygdala/PFC), and Heart Rate Variability (HRV) via wireless telemetry.
In Vivo Neurophysiology: Real-time monitoring of Local Field Potentials (LFP) identifies specific Theta and Gamma oscillations within the amygdala-hippocampal circuit, providing a mechanistic link between drug action and circuit-level rescue.
Pharmacological Benchmarking: Every study is validated against clinical standards (e.g., Diazepam, Buspirone) to ensure a robust signal-to-noise ratio and internal study validity.

Applications

Anxiolytic Screening: Validating the efficacy of Gamma-Aminobutyric Acid (GABA) modulators, Selective Serotonin Reuptake Inhibitors (SSRIs), and novel targets like Neuropeptide Y (NPY) or Corticotropin-Releasing Factor (CRF) antagonists.
Post-Traumatic Stress Disorder (PTSD) & Fear Extinction: Testing drugs that facilitate the "unlearning" of traumatic memories.
Safety & Side-Effect Profiling: Evaluating whether anxiolytics induce sedation, ataxia, or cognitive impairment.
Comorbidity Studies: Assessing the link between chronic anxiety and secondary conditions like depression or gut-brain axis dysfunction.

Our Advantages

High Sensitivity to Fast-Acting Modalities: Optimized protocols specifically designed to detect the rapid therapeutic onset of benzodiazepines, GABA-A modulators, and novel neuroactive steroids.
Controlled "Zero-Noise" Environment: Testing is conducted in sound-attenuated, vibration-free suites with standardized lux levels to ensure that "state anxiety" is purely assay-driven, eliminating facility-induced variability.
Integrated PK/PD Correlation: We provide concurrent blood and cerebrospinal fluid (CSF) sampling to establish a direct mathematical correlation between brain/plasma drug concentrations and behavioral anxiolysis.
Stringent Sedation De-risking: Every study includes automated cross-validation with OFT. By analyzing velocity and total distance, we rigorously differentiate true anxiolysis from confounding sedative or motor-impairing effects.
Multidimensional Physiological Corroboration: Behavioral findings are reinforced with objective biomarkers, including plasma Corticosterone (HPA-axis) and heart rate variability (HRV) via real-time wireless telemetry.
Gold-Standard Benchmarking: Access to our extensive longitudinal database of clinical standards (e.g., Diazepam, Buspirone) ensures assay sensitivity and facilitates clear "Best-in-Class" competitive positioning.

Work with Us

Inquiry Stage:

Summarize the project requirements and fill in the information collection form.
Sign a CDA from both parties to further communicate information, such as targets.
Select an animal model, discuss experimental design, and determine assay parameters.
Project costing and project schedule forecasting.

Project Start:

We provide a detailed project plan, including the required sample quantities, methods, and protocols.
Both parties confirm the project details and start the project.
Confirm the timeline of the project.

Project Progress:

We provide periodic results and information on the animal's condition.
We will work together to make project adjustments as necessary.

Project Completion:

We provide a comprehensive project report promptly.
We arrange transportation for the produced samples.
We provide a discussion of the project results and help to arrange the next steps.

After-Sales Support:

Data storage and archiving.

Get in touch!

FAQs

Q: How do you distinguish between anxiolysis and sedation?

A: We always run an OFT or Rotarod alongside anxiety assays. If a drug increases time in the "open arms" of an Elevated Plus Maze (EPM) but decreases total distance traveled, it may be sedating. A true anxiolytic increases open-arm exploration without suppressing overall motor activity.
Q: Can you measure "Panic-like" attacks?

A: Yes, we use the CO₂ Challenge or high-intensity Acoustic Startle Response models to simulate acute panic-like respiratory and motor symptoms.
Q: Do you offer testing in both sexes?

A: Yes. Given the higher prevalence of anxiety in females, we offer sex-stratified cohorts to identify sex-specific therapeutic windows.
Q: Which anxiety model is most sensitive for testing different neurotransmitter systems?

A: GABAergic & Serotonergic: The EPM is the gold standard and highly sensitive to benzodiazepines and SSRIs. Neuropeptide & Endocannabinoid: The Light/Dark Box (LDB) is often preferred for these systems as it relies more on spontaneous exploratory conflict.
Q: Can your platform evaluate both acute and chronic drug effects?

A: Yes. For rapid-onset screening (e.g., benzodiazepine-like), we perform acute administration (single dose). For drugs with a delayed onset of action (e.g., SSRIs), we provide chronic dosing protocols (typically 14-21 days) followed by behavioral batteries to capture steady-state efficacy.
Q: Do you provide physiological markers to support behavioral findings?

A: Yes. Behavioral data is often paired with HPA-axis profiling. We can measure plasma Corticosterone levels post-test or perform immunohistochemistry (IHC) for c-Fos expression in the amygdala, hippocampus, and prefrontal cortex to map the neural activation patterns associated with your compound.
Q: What controls do you include in a standard anxiety PD study?

A: Every study includes a Vehicle Control and a Positive Control (Benchmark). Common benchmarks include Diazepam (acute anxiolytic), Buspirone, or Chlordiazepoxide, ensuring the assay's sensitivity is validated for each specific run.

Published Data

Modulation of the endocannabinoid system (ECS) in mice produces diverse effects on anxiety based on receptor targets and dosage. Anxiolytic activity was uniquely observed with the CB1/CB2 agonist WIN 55,212-2 and the Fatty Acid Amide Hydrolase (FAAH) inhibitor URB 597, whereas other direct modulations of CB1 and CB2 receptors typically induced anxiogenic behavior. These behavioral shifts occurred without confounding effects on motor activity.

Fig.2 Differential Effects of Selective CB1/CB2 Agonists, Antagonists, and FAAH Inhibition on Anxiety Metrics in Mice. (OA Literature) Fig. 2 Effects of Acute Administration of CB1 Agonist Oleamide, AM 251, Mixed CB1/CB2 Agonist WIN 55,212-2, CB2 Agonist JWH 133, AM, and FAAH Inhibitor URB 597 on Anxiety-Related Behaviors in the Mouse Elevated Plus Maze (EPM) Test.²

References

Ohi, Kazutaka et al. "Clinical features and genetic mechanisms of anxiety, fear, and avoidance: A comprehensive review of five anxiety disorders." Molecular Psychiatry vol. 30,10 (2025): 4928-4936. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.1038/s41380-025-03155-1
Kruk-Slomka, Marta et al. "The Effects of Indirect and Direct Modulation of Endocannabinoid System Function on Anxiety-Related Behavior in Mice Assessed in the Elevated Plus Maze Test." Molecules (Basel, Switzerland) vol. 30,4 867. Distributed under Open Access license CC BY 4.0, with modification. https://doi.org/10.3390/molecules30040867