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Comprehensive Preclinical Package for Anti-Obesity Drug Development
We provide an integrated preclinical platform designed to accelerate drug discovery and support rigorous preclinical drug testing, enabling the development of next-generation anti-obesity therapies through robust disease models and comprehensive assessments of efficacy, safety, and muscle function.
Key Challenges in Anti-Obesity Drug Development

Despite recent advances in incretin-based therapies, anti-obesity drug development remains challenging due to the complex and multifactorial nature of obesity. Effective therapies must achieve sustained body weight reduction while minimizing loss of lean mass, balance metabolic efficacy with gastrointestinal tolerability, and engage central mechanisms that regulate appetite and energy homeostasis. In parallel, early identification of muscle-related safety liabilities has become increasingly critical, as preservation of muscle mass and function is closely linked to long-term metabolic health. To successfully translate preclinical findings into clinically meaningful outcomes, a robust and translational preclinical evaluation strategy is essential to de-risk development and support rational candidate selection.

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We offer in-stock diet-induced obesity (DIO) models in both mice and rats, enabling rapid initiation of efficacy studies without prolonged model induction.

DIO Rat Model
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DIO Mouse Model (C57BL/6J)
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Why Our Integrated Preclinical Platform

Accelerate your metabolic disease research with our end-to-end preclinical solutions, designed to de-risk and expedite your drug discovery pipeline.

Cyagen Mouse Atlas
Multidimensional Efficacy Assessment
Early Safety & Tolerability Screening
Muscle Mass & Function Preservation Evaluation
Translational Decision Support
Relevant Model
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Case 1 - Validation of Therapeutic Efficacy of GLP-1/GIP/GCGR Receptor Agonists in the DIO Mouse Model
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Case2-Validation of Therapeutic Efficacy of GLP-1/GIP/GCGR and Amylin Receptor Agonists in the DIO Rat Model
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Gastrointestinal Side Effect Screening
Gastrointestinal tolerability is a critical determinant of clinical success for anti-obesity drugs. We provide early-stage screening tools in mice and rats to identify potential liabilities:
Assay Description Species
Acute food intake assay Single-dose administration with food intake measured over 24 hours for rapid efficacy screening. Rat/mouse
Conditioned Taste Aversion (CTA) test Early evaluation of drug-induced malaise and gastrointestinal intolerance for early candidate de-selection. Rat/mouse
Gastric emptying assay Blood-based measurements to evaluate gastric motility and support early-stage candidate selection. Rat/mouse
Muscle Preservation & Sarcopenia Assessment
Dexamethasone (Dex)-induced Sarcopenia Mouse Model
Evaluations via grip strength testing, body composition analysis, and histopathology revealed that Dex induction significantly reduced muscle explosive power and whole-body muscle mass, while markedly decreasing the cross-sectional area (CSA) of muscle fibers. These findings indicate significant impairment in both muscle strength and structural integrity. Characterized by stability, controllability, and high reproducibility, this model serves as a robust preclinical tool for evaluating muscle-protective and anti-atrophy agents, making it suitable for both efficacy screening and mechanistic studies.
Figure 1. Schematic illustration of the dexamethasone-induced sarcopenia mouse model.
Figure 2. A significant reduction in grip strength was observed in the Dexa-induced model group after 14 days of treatment. Establishment of the sarcopenia model via chronic dexamethasone (Dexa) administration. Data are presented as Mean±SEM, N=6 mice per group. Statistical analysis was performed using T-test, *p<0.05, **p<0.01 vs. G1-Vehicle, ##p<0.01 vs. G2- Dexa Baseline.
Figure 3. Body composition analysis showing a marked reduction in whole-body muscle mass and muscle proportion after 14 days of Dexatreatment.
Establishment of the sarcopenia model via chronic dexamethasone (Dexa) administration. Data are presented as Mean±SEM, N=6 mice per group. Statistical analysis was performed using T-test, *p<0.05, **p<0.01 vs. G1-Vehicle, ##p<0.01 vs. G2- Dexa Baseline.
Figure 4. Muscle weight analysis demonstrating significant reductions in GAS, TA, and SOL muscle mass after 14 days of Dexa treatment.
Establishment of the sarcopenia model via chronic dexamethasone (Dexa) administration. Data are presented as Mean±SEM, N=6 mice per group. Statistical analysis was performed using T-test, *p<0.05, **p<0.01 vs. G1-Vehicle, ##p<0.01 vs. G2- Dexa Baseline.
Figure 5. The dexamethasone-induced model group showed decreases in muscle fiber cross-sectional area in the gastrocnemius and tibialis anterior muscles.
Establishment of the sarcopenia model via chronic dexamethasone (Dexa) administration. Data are presented as Mean±SEM, N=6 mice per group. Statistical analysis was performed using T-test, *p<0.05, **p<0.01 vs. G1-Vehicle, ##p<0.01 vs. G2- Dexa Baseline.
Figure 6. Dex-induced sarcopenia led to a significant impairment in exercise endurance in mice, as assessed by treadmill testing, with marked reductions in running time and total running distance.
Establishment of the sarcopenia model via chronic dexamethasone (Dexa) administration. Data are presented as Mean±SEM, N=6 mice per group. Statistical analysis was performed using T-test, *p<0.05, **p<0.01 vs. G1-Vehicle, ##p<0.01 vs. G2- Dexa Baseline.
Why Partner with Cyagen?
In-stock validated obesity models
We provide ready-to-use diet-induced obesity (DIO) mouse and rat models to bypass prolonged induction phases and accelerate your research timelines.
Advanced metabolic phenotyping
We offer comprehensive body composition and metabolic monitoring to accurately evaluate fat reduction while assessing muscle mass preservation.
Experienced pharmacology team
Leverage our PhD-level experts to bridge the gap between preclinical data and clinical milestones.
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