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Balb/c-nude nude mouse

Jiangsu Aniphe BioLab, leveraging a high‑standard laboratory animal platform, offers a steady, long‑term supply of Balb/c‑nude nude mice in stock. As the gold‑standard models for tumor xenograft studies (CDX/PDX), cell tumorigenicity assays, and anti‑tumor drug efficacy evaluations, we provide a high‑quality mouse colony characterized by phenotypic stability, profound immunodeficiency, and excellent tumor‑formation rates. With ample inventory and a rapid response system, we enable you to promptly initiate drug screening and mechanistic research, ensuring high reproducibility and rigorous scientific integrity of your data.

Strain Introduction

Balb/c nude mice (Balb/c Foxn1^nu^) are a classic immunodeficient animal model characterized by severe T‑lymphocyte deficiency resulting from thymic developmental defects. Leveraging the Balb/c genetic background, these mice exhibit both high xenograft engraftment efficiency and genetic homogeneity, enabling robust engraftment of human tumor cell lines (CDX) and patient‑derived xenografts (PDX) via multiple routes, including subcutaneous, renal capsule, and orthotopic implantation. Moreover, tumor growth is stable with minimal inter‑individual variability. This strain serves as a foundational model for preclinical anticancer drug evaluation, tumor biology research, and humanized immune reconstitution studies.

Product Advantages

Genetic background is stable.

Homogeneous BALB/c background; excellent reproducibility in tumor transplantation experiments.

Immature T cells

Rejection responses are weak, and the efficiency of human tumor xenografting is high.

Residual innate immunity

Simulating residual immunity in patients for evaluating the efficacy of antibodies and oncolytic viruses;

Hairless for easy observation.

Simplify tumor measurements and reduce interference in in vivo imaging.

Feeding costs are manageable.

Excellent reproductive performance, supporting large-scale, long-term drug administration studies.

Data parameters

Strain Name

Balb/c-nude (Balb/c Foxn1^nu^/Foxn1^nu^)
Targeted gene

Foxn1 (forkhead box N1, also known as Whn or Hfh11)
Mutant site

A spontaneous single‑base deletion in the Foxn1 gene results in a frameshift mutation, leading to a truncated protein that loses its transcriptional activation function and impairs thymic epithelial development.
Types of gene editing

Spontaneous mutation, non‑artificial knockout
Genetic background

Balb/c (homozygous, continuously backcrossed for more than 15 generations)
Microbial Grade

SPF grade

Validate data

Growth curve

The figure shows the body weight growth curve of BALB/c-nude mice from 1 to 12 weeks of age. Both male and female mice exhibit continuous weight gain starting at one week of age; during the early growth phase, the sex‑related weight difference is small, but as age increases, male mice gradually surpass females in body weight, with the gap widening over time. By 12 weeks of age, the mean body weight of males is significantly higher than that of females. This growth curve can serve as a baseline reference for selecting appropriate ages for experimental studies and for converting body weights to dose calculations.

 

 

Validation of lymphocyte subpopulation sorting in BALB/c-nude mice

Flow cytometric analysis of peripheral blood and splenic immune cells revealed that wild-type BALB/c mice of both sexes harbor abundant mature CD3⁺ T lymphocytes, with well‑defined CD4⁺ and CD8⁺ subsets, in both peripheral blood and spleen; in contrast, mature CD3⁺ T cells are virtually absent from the peripheral blood and spleen of male and female BALB/c‑nude mice.

BALB/c-nude mice still harbor innate immune cell subsets, including B lymphocytes, NK cells, dendritic cells (DCs), and macrophages; under the same genetic background, there are no significant differences in the composition of immune cells between male and female mice.

The above results confirm that BALB/c-nude mice exhibit the typical immunological characteristics of nude mice: a profound T-cell deficiency, while retaining a relatively intact innate immune system and B-cell compartment.

 

 

 

 

Peripheral blood and spleen samples were collected from 7-week-old male and female BALB/c and BALB/c-nude mice for flow cytometric analysis, allowing assessment of differences in T cells, B cells, NK cells, dendritic cells, and macrophages. Compared with immunocompetent BALB/c mice, BALB/c-nude mice exhibited nearly complete depletion of T cells, classifying them as T-cell–deficient mice (see Table 1).

 

 

Validate data

Six-week-old male C57BL/6 mice were selected and divided into three groups: a normal chow diet group, a high-fat diet–induced model group, and a high-fat diet plus dulaglutide intervention group. A high-fat diet was administered for 12 weeks to establish the model; subsequently, the intervention group received dulaglutide (1 mg/kg, once every two weeks, for a total of eight doses). Following completion of the treatment regimen, a glucose tolerance test (GTT) was performed.

Body weight indicators (Figures B and C)

During the treatment period, body weight remained stable in the normal‑diet group, whereas it continued to increase in the high‑fat diet model group. Compared with the HFD group, dulaglutide treatment significantly inhibited weight gain in high‑fat–fed mice, resulting in a marked reduction in body weight; the relative weight change curve further confirmed the weight‑loss effect of dulaglutide.

Continuous glucose monitoring (Figure D)

In the high-fat diet–induced model group, blood glucose remained persistently elevated; following treatment with dulaglutide, blood glucose in the high-fat–fed mice decreased significantly and was maintained at a lower range, suggesting that dulaglutide can attenuate hyperglycemia induced by a high-fat diet.

Glucose Tolerance Test (Figures E and F)

Following glucose loading, the HFD group exhibited a higher peak plasma glucose level and a slower clearance rate, with a significantly larger area under the glucose‑time curve (AUC) compared to the normal control group, suggesting that a high‑fat diet induces glucose intolerance.

In the HFD + dulaglutide group, peak blood glucose levels were reduced, and glucose levels returned to baseline more rapidly; the glucose AUC was significantly lower than in the HFD model group, indicating that dulaglutide effectively ameliorates impaired glucose tolerance induced by a high-fat diet.

Dulaglutide treatment effectively suppresses diet‑induced weight gain in mice, lowers fasting blood glucose levels, and improves glucose intolerance in high‑fat–fed mouse models.

 

Application areas

● CDX model construction: suitable for xenografting of various tumor cell lines, used for preliminary screening of small-molecule and ADC drugs, as well as PK/PD analysis.
● PDX model generation: Preserves the original tumor characteristics of the patient, making it suitable for studying individualized drug efficacy and resistance mechanisms.
● Humanized immune models: Support human immune cell engraftment and are used for evaluating bispecific antibodies and immune checkpoint inhibitors.
● Oncolytic biologic agent evaluation: Residual innate immunity better aligns with clinical prediction of the efficacy of oncolytic virus and bacterial therapies;
● Imaging and Radiotherapy Research: The hairless condition facilitates tumor visualization in imaging, making it well-suited for standardized radiotherapy‑related experiments.

Breeding Techniques and Precautions

Strictly control inbreeding systems to mitigate genetic diversity.

Barrier Environment Management and Control

T-cell deficiency predisposes to microbial infections; complete sterilization of all materials and stringent aseptic techniques are employed to prevent fatal infections.

 

Strictly control environmental stimuli to reduce experimental stress.

Temperature, Humidity, and Energy Replenishment

Maintain a constant temperature of 25–28°C and provide timely energy supplementation to sustain the nutritional status of tumor-bearing mice.

Standardize breeding management to improve the survival rate of pups.

Optimize breeding models

Breeding heterozygous female mice with homozygous male mice improves the survival of offspring.

Monitor age-related spontaneous lesions and eliminate experimental confounding.

Ethical Oversight of Tumor-Bearing Experiments

Dynamically monitor the tumor, strictly adhere to ethical guidelines; administer medications with appropriately adjusted dosages and implement analgesia.

Literature support

Scientific papers published by Aniphe customers using this model are eligible for SCI-indexed publication. (Original paper link)
1. Cancer Biol Ther. 2024 Dec 31;25(1):2408042.

Frequently Asked Questions

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Q1: Are Balb/c-nude nude mice and nu/nu BALB/c nude mice the same strain?

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A: Yes, all are homozygous for the Foxn1^nu^ mutation on a BALB/c genetic background, i.e., thymus‑less nude mice. They are sometimes abbreviated as BALB/c nude mice.

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Q2: Why doesn’t it grow fur?

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A: Due to the loss of Foxn1 gene function, the hair shafts lack keratin—whose expression is regulated by Foxn1—and become extremely fragile. As a result, the vast majority of hair shafts fail to penetrate the epidermis properly and instead remain twisted and coiled within the dilated infundibulum of the hair follicle. Compared with normally haired littermates, these mice exhibit no difference in the number or function of their hair follicles; both groups are capable of generating normal hair roots and hair shafts. However, because their hair follicles are functionally impaired, the animals appear hairless.

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Q3: Mutant genes in nude mice

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A: nu (autosomal recessive inheritance). Homozygotes are nu/nu, and heterozygotes are n/+. Heterozygotes are hairy, with males exhibiting 50%–80% of the hairiness seen in normal mice.

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Q4: Characteristics and Applications:

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A: Impaired growth and development, reduced reproductive capacity, and a high susceptibility to severe infections. Thymic aplasia is inherited as an autosomal recessive trait on chromosome 11. Due to the absence of a thymus, only thymic remnants or abnormal epithelium remain, which fail to support normal T‑cell differentiation; consequently, T‑cell immunity is deficient. B cells are normally present but exhibit functional defects, with antibodies predominantly consisting of IgM and only trace amounts of IgG. These mice lack contact hypersensitivity and show no transplant rejection responses, making them highly suitable for research in immunology, oncology, and the mechanisms underlying disease pathogenesis.

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