Assess Your Small Molecule Drug for Carcinogenicity Faster and at a Lower Cost
New guidelines condense overall carcinogenicity assessment timelines significantly for compounds which receive a two-year rat study waiver. Assess carcinogenic risk in 6 months vs. 2 years.
Faster Testing Means:
- Faster time to market with new drugs
- Lower costs
- Quicker answers on your compounds
- Fewer animals dosed for a shorter period of time
- Significantly lower risk of spontaneous tumors, reducing the incidence of false positives
The gold standard for carcinogenicity testing in vivo
- A rapid, cost-effective, and sensitive carcinogenicity testing model for detection of nongenotoxic and genotoxic carcinogens.
- Accepted by the Food & Drug Administration (FDA), European Medicines Agency (EMA), National Medical Products Administration (NMPA), and other regulatory agencies for use in carcinogenicity testing under the International Conference on Harmonisation (ICH) S1B(R1) Guideline.
- New Weight of Evidence (WoE) criteria enables more drug compounds to forego the 2-year rat study, thereby decreasing testing overall timelines by opting for a 6-month rasH2™ mouse study.
- Substantial phenotypic background data demonstrate that rasH2™ mice have an extremely low incidence of spontaneous tumors at typical testing ages.
- More rapid onset and higher incidence of tumors after treatment with either genotoxic or non-genotoxic compounds.
- Carries a transgenic copy of the human HRAS proto-oncogene in addition to the endogenous murine Ras genes.
- Sold with full research use rights and are readily available in typical study quantities.
- In Japan, contact CLEA Japan, Inc. for purchase of rasH2™ mice.
- Please note that the model nomenclature has been updated. The CIEA designation for the rasH2™ model, CB6F1/Jic-TgrasH2@Tac was used previously.
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Genetic Background:
BALB/cBy x C57BL/6 F1 Hybrid Background Origin:
The rasH2™ mouse was developed in the laboratory of Tatsuji Nomura of the Central Institute for Experimental Animals (CIEA) in Kawaski, Japan. The model was created by microinjecting the human c-Ha-ras gene into C57BL/6 x DBA/2 zygotes. Hybrid transgenes were constructed from two human HRAS (c-Ha-ras) genes isolated from malignant melanoma and bladder carcinoma tumors. The transgene integrated into the murine transgenic genome as 3* copies in tandem array. The resultant mice were backcrossed to C57BL/6J. Taconic received original stock in March 2000 and the line is genetically refreshed at least every five years. Taconic has received original stock for refresh in 2005, 2012, 2016, and 2020. The mice were derived by embryo transfer and are maintained by intercrossing C57BL/6JJic-Tg(HRAS)2Jic hemizygous male mice with BALB/cByJJic female mice, therefore rasH2-Tg and rasH2-Wt are littermates. Genetics:
Carries Nnt mutation Color:
Black Agouti Species:
Mouse Initial Publication:
- Saitoh A, Kimura M, Takahashi R, Yokoyama M, Nomura T, Izawa M, Sekiya T, Nishimura S, Katsuki M. (1990) Most tumors in transgenic mice with human c-Ha-ras gene contained somatically activated transgenes. Oncogene, 5(8):1195-1200.
- *Suemizu H, et al. (2004) Exp. Anim. 53 (5) 463-466.
