The OncoRat provides unique advantages over mouse models for conducting in vivo efficacy evaluation of potential cancer therapies. Better engraftment rates in the OncoRat result in a wider variety of tumor biology. Other advantages include larger tumor, blood and tissue samples for biomarker and downstream analysis as well as a better model for ADME, PK/PD and toxicology.
Hera can consult with your team to select the most appropriate tumor model. Your molecule can be profiled in a variety of tumor models and compared or combined to standards of care for combination studies and IND filing.
If your model of interest is not listed below it can be established in the OncoRat. Model establishment is typically much faster than in mouse, in particular for PDX models due to the larger tumor growth.
|Tumor Model||Rat Engraftment||Ideal for:|
|VCaP Prostate||80-100%||AR resistance, castration resistant studies|
|VCaP MDVR Prostate||90-100%||Anti-androgen drug resistance studies, castration resistant studies|
|LNCaP Prostate||90-100%||AR sensitivity|
|H358 NSCLC||100%||KRAS mutation studies, EGFR - KRAS - BRAF - MEK - ERK signaling|
|MCF-7 Breast||100%||ER+ breast cancer, CDK 4/6 inhibition, early and advanced tumor development, anti-estrogen therapies.|
|HCC1954 Breast||100%||HER2+ studies, ER- studies, AR inhibitors|
|HCT116 colon||75-100%||Tumorigenesis, colorectal cancer metastasis, CDK inhibition, TGFβ +|
|MIA PaCa-2 pancreatic||100%||KRAS, epithelial-to-mesenchymal transition (EMT), circulating tumor markers, radiolabeled nucleotide therapy|
|OCI-AML2 leukemia||100%||NOS and VEGF signaling, angiogenesis inhibitors, DNA methylation studies|
|786-O renal cell carcinoma||100%||VEGF inhibition studies, bone metastasis development, hypoxia and tumor progression|