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Huachuang Securities Co Ltd female nod scid
Female Nod Scid, supplied by Huachuang Securities Co Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Article Title: Overcoming ADC resistance in advanced colorectal cancer by dual targeting of TROP2 and PERK to suppress Wnt/β-catenin signaling.
Article Snippet: Female NOD/SCID (5–6 weeks old) and male C57BL/6 (8 weeks old) mice were obtained from Jiangsu Huachuang Sino Pharmaceutical Technology Co., Ltd. (Taizhou, China) and housed under specific pathogen-free (SPF) conditions.

Article Title: Overcoming ADC resistance in advanced colorectal cancer by dual targeting of TROP2 and PERK to suppress Wnt/β-catenin signaling
Article Snippet: Female NOD/SCID (5–6 weeks old) and male C57BL/6 (8 weeks old) mice were obtained from Jiangsu Huachuang Sino Pharmaceutical Technology Co., Ltd. (Taizhou, China) and housed under specific pathogen-free (SPF) conditions.



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Inotiv female nod scid mice aged 5
HT29 and HCA46 parental and resistant cells (1:1 mixture with Matrigel) were injected subcutaneously into female <t>NOD-SCID</t> mice <t>(5–9</t> weeks of age). Tumors were measured three times weekly, and once tumors reached 100–150 mm³ mice were randomized in 6 groups ( n = 8 mice per group). Specifically, for the parental models, vehicle and WEE1i, while for the resistant ones: Vehicle, WEE1i, targeted therapy alone (EGFRi for HCA46; BRAFi+EGFRi for HT29), or combination therapy (WEE1i+EGFRi for HCA46; WEE1i+BRAFi+EGFRi for HT29). Treatment dosing and schedule was as follows: For WEE1i-adavosertib (60 mg/kg, twice a day (BID) by oral gavage), EGFRi-cetuximab (10 mg/kg, twice a week (BIW) intraperitoneally), BRAFi-dabrafenib (15 mg/kg, once a day (QD) by oral gavage). Animals were euthanised at ethical endpoint (1200–1500 mm³) or upon >20% body-weight loss. ( A , B ) Tumor growth curves in parental xenografts. ( C , D ) Tumor growth curves in resistant xenografts. ( E , F ) Endpoint tumor volume comparison between parental and resistant tumors. Statistical analysis: Mann–Whitney U test ( A , B , E , F ) or Kruskal–Wallis test with Dunn’s multiple-comparisons correction ( C , D ). Squares indicate removal due to tumor burden; circles indicate removal due to weight loss. Source data are available online for this figure.
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HT29 and HCA46 parental and resistant cells (1:1 mixture with Matrigel) were injected subcutaneously into female NOD-SCID mice (5–9 weeks of age). Tumors were measured three times weekly, and once tumors reached 100–150 mm³ mice were randomized in 6 groups ( n = 8 mice per group). Specifically, for the parental models, vehicle and WEE1i, while for the resistant ones: Vehicle, WEE1i, targeted therapy alone (EGFRi for HCA46; BRAFi+EGFRi for HT29), or combination therapy (WEE1i+EGFRi for HCA46; WEE1i+BRAFi+EGFRi for HT29). Treatment dosing and schedule was as follows: For WEE1i-adavosertib (60 mg/kg, twice a day (BID) by oral gavage), EGFRi-cetuximab (10 mg/kg, twice a week (BIW) intraperitoneally), BRAFi-dabrafenib (15 mg/kg, once a day (QD) by oral gavage). Animals were euthanised at ethical endpoint (1200–1500 mm³) or upon >20% body-weight loss. ( A , B ) Tumor growth curves in parental xenografts. ( C , D ) Tumor growth curves in resistant xenografts. ( E , F ) Endpoint tumor volume comparison between parental and resistant tumors. Statistical analysis: Mann–Whitney U test ( A , B , E , F ) or Kruskal–Wallis test with Dunn’s multiple-comparisons correction ( C , D ). Squares indicate removal due to tumor burden; circles indicate removal due to weight loss. Source data are available online for this figure.

Journal: EMBO Molecular Medicine

Article Title: WEE1 kinase inhibition to overcome acquired resistance to targeted therapies in colorectal cancer

doi: 10.1038/s44321-026-00434-4

Figure Lengend Snippet: HT29 and HCA46 parental and resistant cells (1:1 mixture with Matrigel) were injected subcutaneously into female NOD-SCID mice (5–9 weeks of age). Tumors were measured three times weekly, and once tumors reached 100–150 mm³ mice were randomized in 6 groups ( n = 8 mice per group). Specifically, for the parental models, vehicle and WEE1i, while for the resistant ones: Vehicle, WEE1i, targeted therapy alone (EGFRi for HCA46; BRAFi+EGFRi for HT29), or combination therapy (WEE1i+EGFRi for HCA46; WEE1i+BRAFi+EGFRi for HT29). Treatment dosing and schedule was as follows: For WEE1i-adavosertib (60 mg/kg, twice a day (BID) by oral gavage), EGFRi-cetuximab (10 mg/kg, twice a week (BIW) intraperitoneally), BRAFi-dabrafenib (15 mg/kg, once a day (QD) by oral gavage). Animals were euthanised at ethical endpoint (1200–1500 mm³) or upon >20% body-weight loss. ( A , B ) Tumor growth curves in parental xenografts. ( C , D ) Tumor growth curves in resistant xenografts. ( E , F ) Endpoint tumor volume comparison between parental and resistant tumors. Statistical analysis: Mann–Whitney U test ( A , B , E , F ) or Kruskal–Wallis test with Dunn’s multiple-comparisons correction ( C , D ). Squares indicate removal due to tumor burden; circles indicate removal due to weight loss. Source data are available online for this figure.

Article Snippet: Female NOD SCID mice aged 5–9 weeks were supplied by Envigo.

Techniques: Injection, Comparison, MANN-WHITNEY

Ten millions HT29 and HCA46 parental and resistant cells (1:1 mixture with Matrigel) were injected subcutaneously into female NOD-SCID mice (5–9 weeks old). Tumors were measured three times weekly, and once volume reached 100–150 mm³ mice were randomized and treated ( n = 8 mice per group) twice a week (BIW) intraperitoneally with E: EGFRi-cetuximab (10 mg/kg) and/or twice a day (BID) by oral gavage for W:WEE1i-adavosertib (60 mg/kg) and once a day (QD) by oral gavage for B:BRAFi-dabrafenib (15 mg/kg,). The mean body mass was normalized to the mean value recorded prior to treatment initiation. Circles indicate mice removed from the study due to ≥20% body weight loss. ( A , B ) Body weight monitoring during treatment in HT29_Parental and HT29_Resistant cohorts, respectively. ( C , D ) Body weight monitoring during treatment in HCA46 parental and HCA46_Resistant cohorts, respectively. W: WEE1i; B: BRAFi; E: EGFRi.

Journal: EMBO Molecular Medicine

Article Title: WEE1 kinase inhibition to overcome acquired resistance to targeted therapies in colorectal cancer

doi: 10.1038/s44321-026-00434-4

Figure Lengend Snippet: Ten millions HT29 and HCA46 parental and resistant cells (1:1 mixture with Matrigel) were injected subcutaneously into female NOD-SCID mice (5–9 weeks old). Tumors were measured three times weekly, and once volume reached 100–150 mm³ mice were randomized and treated ( n = 8 mice per group) twice a week (BIW) intraperitoneally with E: EGFRi-cetuximab (10 mg/kg) and/or twice a day (BID) by oral gavage for W:WEE1i-adavosertib (60 mg/kg) and once a day (QD) by oral gavage for B:BRAFi-dabrafenib (15 mg/kg,). The mean body mass was normalized to the mean value recorded prior to treatment initiation. Circles indicate mice removed from the study due to ≥20% body weight loss. ( A , B ) Body weight monitoring during treatment in HT29_Parental and HT29_Resistant cohorts, respectively. ( C , D ) Body weight monitoring during treatment in HCA46 parental and HCA46_Resistant cohorts, respectively. W: WEE1i; B: BRAFi; E: EGFRi.

Article Snippet: Female NOD SCID mice aged 5–9 weeks were supplied by Envigo.

Techniques: Injection