Ace Therapeutics offers a comprehensive in vivo animal model development service tailored for overactive bladder (OAB) research and preclinical drug evaluation. Leveraging an extensive suite of validated models across multiple species and induction methods, we support the translation of novel therapeutics from discovery through to proof-of-concept with scientific rigor and efficiency.
Overactive bladder is a complex urological disorder characterized by symptoms such as urinary urgency, frequency, and incontinence, significantly impacting patient quality of life. Animal models are indispensable tools for elucidating the pathophysiology of OAB and for assessing the efficacy and safety of emerging treatments. At Ace Therapeutics, we utilize a broad range of species, including guinea pigs (Cavia porcellus, Dunkin Hartley and Hartley strains), cats (Felis catus), mice (Mus musculus, including Balb/c and C57BL/6 strains), and rats (Rattus norvegicus, Sprague Dawley, Wistar, and Fischer 344 strains). These models are selected for their translational relevance, ability to recapitulate key features of human OAB, and adaptability to diverse experimental paradigms, ensuring robust and clinically meaningful data.
Chemically-induced models involve the administration of agents such as acetic acid, carbachol, oxotremorine methiodide, capsaicin, KCl, or retinol acetate directly into the bladder or systemically to provoke bladder overactivity. This methodology reliably induces OAB-like symptoms by causing neurogenic or inflammatory changes in the bladder wall. Key advantages include rapid induction, reproducibility, and the ability to mimic acute or chronic aspects of OAB. These models are widely used for mechanistic studies, pharmacological screening, and evaluation of anti-inflammatory or neuromodulatory therapies.
Surgically-induced models, such as partial bladder outlet obstruction, urethral ligation, or balloon injury, create mechanical or ischemic stress on the bladder, leading to compensatory changes that mirror the progression of OAB in humans. Procedures may involve ligation, catheterization, or occlusion of the urinary tract. The primary advantages are the ability to study chronic disease development, tissue remodeling, and long-term drug effects. These models are essential for investigating pathophysiological mechanisms, regenerative approaches, and interventions targeting structural or functional bladder changes.
Stress-induced models utilize environmental or physiological stressors, such as cold exposure, water avoidance, fasting, or diuretic administration, to elicit bladder overactivity. These paradigms mimic the impact of psychological and metabolic stress seen in OAB patients. The methodology is non-invasive and suitable for studies focusing on neurogenic and behavioral components of OAB. Advantages include relevance to comorbid conditions and the ability to assess the effects of anxiolytic or lifestyle-modifying interventions.
Genetic models, such as knockout mice (e.g., Hpse2), and those induced by biological agents (e.g., hyaluronidase), enable the study of specific molecular pathways implicated in OAB. These models are created via targeted genetic modifications or the administration of enzymes/proteins affecting bladder function. Their main advantage lies in dissecting gene-environment interactions and validating molecular targets. Applications include target validation, biomarker discovery, and the development of precision therapies.
Dietary and hormonal models involve the use of cholesterol-rich diets, bilateral ovariectomy, or corticosterone administration to induce metabolic or hormonal changes that contribute to OAB. These approaches are valuable for modeling OAB in the context of metabolic syndrome, menopause, or endocrine disorders. They are particularly suited for evaluating interventions targeting metabolic or hormonal pathways.
Ace Therapeutics provides a turnkey solution for in vivo OAB model development, encompassing model selection, induction, dosing, behavioral and physiological assessment, and comprehensive data analysis. Key efficacy endpoints include cystometric evaluation (voiding frequency, bladder capacity, intercontraction interval), urodynamic measurements, histopathological analysis, molecular biomarker quantification, and behavioral assessments. Our analytical capabilities extend to advanced imaging, immunohistochemistry, gene/protein expression profiling, and pharmacokinetic/pharmacodynamic (PK/PD) studies. Rigorous quality control measures are implemented at every stage, including standardized protocols, validation against reference compounds, and adherence to ethical and regulatory standards, ensuring high reproducibility and data integrity.
Partnering with Ace Therapeutics grants you access to an unparalleled breadth of validated OAB animal models, expert scientific guidance, and a commitment to excellence in preclinical research. Our integrated services accelerate the translation of your therapeutic innovations, reduce development risk, and provide robust data packages for regulatory submissions. Contact us today to discuss your overactive bladder research needs and discover how we can help advance your program from concept to clinic.
| Species | Strain | Characteristic (Details) |
|---|---|---|
| Cavia porcellus (guinea pig) | Dunkin Hartley | Diuretic stress-induced; Fasted |
| Cavia porcellus (guinea pig) | Hartley | Distension |
| Cavia porcellus (guinea pig) | Chemical agent-induced (acetic acid) | |
| Felis catus (cat) | Chemical agent-induced (acetic acid) | |
| Felis catus (cat) | Chemical agent-induced (acetic acid); Shock, electrically | |
| Mus musculus (mouse) | Balb/c | Chemical agent-induced (acetic acid) |
| Mus musculus (mouse) | C57BL/6 | Biological agent-induced (hyaluronidase (ovine)); Chemical agent-induced (KCl) |
| Mus musculus (mouse) | C57BL/6 | Chemical agent-induced (661590) |
| Mus musculus (mouse) | C57BL/6J | Chemical agent-induced (trinitrobenzene sulfonic acid) |
| Mus musculus (mouse) | C57BL/6J | Diuretic stress-induced; Fasted |
| Mus musculus (mouse) | Chemical agent-induced (carbachol) | |
| Mus musculus (mouse) | Knockout (Hpse2) | |
| Rattus norvegicus (rat) | Fischer 344 | Chemical agent-induced (oxotremorine methiodide) |
| Rattus norvegicus (rat) | Sprague Dawley | Bilateral iliac artery balloon injury; Cholesterol-rich diet |
| Rattus norvegicus (rat) | Sprague Dawley | Bladder emptying overactivity-induced |
| Rattus norvegicus (rat) | Sprague Dawley | Bladder outlet obstruction |
| Rattus norvegicus (rat) | Sprague Dawley | Bladder outlet occlusion |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (661590) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (L-noradrenaline) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (acetic acid) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (capsaicin) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (oxotremorine methiodide) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (resinferatoxin) |
| Rattus norvegicus (rat) | Sprague Dawley | Chemical agent-induced (sulprostone) |
| Rattus norvegicus (rat) | Sprague Dawley | Cold stress-induced |
| Rattus norvegicus (rat) | Sprague Dawley | Distension |
| Rattus norvegicus (rat) | Sprague Dawley | Fasted |
| Rattus norvegicus (rat) | Sprague Dawley | Middle cerebral artery occlusion |
| Rattus norvegicus (rat) | Sprague Dawley | Partial bladder outlet obstruction |
| Rattus norvegicus (rat) | Sprague Dawley | Partial uretheral obstruction |
| Rattus norvegicus (rat) | Sprague Dawley | Partial urethral ligation |
| Rattus norvegicus (rat) | Sprague Dawley | Partial urethral obstruction |
| Rattus norvegicus (rat) | Sprague Dawley | Spinal cord injured |
| Rattus norvegicus (rat) | Sprague Dawley | Urethral ligation |
| Rattus norvegicus (rat) | Sprague Dawley | Water avoidance stress-induced |
| Rattus norvegicus (rat) | Wistar | Bilateral ovariectomy |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (17-phenyl trinor prostaglandin E2) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (acetic acid) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (acetic acid); Chemical agent-induced (retinol acetate) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (carbachol) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (corticosterone) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (retinol acetate) |
| Rattus norvegicus (rat) | Wistar | Chemical agent-induced (streptozocin) |
| Rattus norvegicus (rat) | Wistar | Partial bladder outlet obstruction |
| Rattus norvegicus (rat) | Wistar | Partial urethral obstruction |
| Rattus norvegicus (rat) | Wistar | Urethral catheterization; Urethral ligation |
| Rattus norvegicus (rat) | Wistar | Urethral ligation |
| Rattus norvegicus (rat) | Cerebral infarction | |
| Rattus norvegicus (rat) | Chemical agent-induced (acetic acid) | |
| Rattus norvegicus (rat) | Chemical agent-induced (carbachol) | |
| Rattus norvegicus (rat) | Ischemia | |
| Rattus norvegicus (rat) | Spinal cord injured | |
| Rattus norvegicus (rat) | Spinal cord transection |
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