American Molecular Laboratories’ provides support beyond traditional service-based laboratories. We offer meaningful scientific strategies that deliver unique solutions in oncology, drug development, and personalized medicine.
Our group has a significant track record of fostering the growth and development of biotechnology and pharmaceutical pipelines. Our strong relationships with pharma customers and proven ability to co-develop diagnostics enhances the success of drug development efforts by companies that createcancer therapeutics.
Previous research from our group has led to a greater understating of a drug’s (and targeted therapy’s) MOA. This resulted in improvements in clinical timelines, indication expansion, and the identification biomarkers of therapeutic response and resistance. Examples of previous MOA studies are shown below:
Resistance to a HER1/HER-2 inhibitor began emerging in HER2-positive breast cancer patients during clinical trials, hindering the likelihood of drug approval.
We designed cellular studies to understand the response and resistance mechanisms associated with the HER1/HER2 inhibitor). The relevance of cell culture-observed resistance mechanisms were then examined in patients.
Results indicated that the Estrogen Receptor (ER) increases when cells and tumors are treated with the HER2 inhibitor. The increase in ER expression allowed the tumor cells to survive in the presence of the HER2 inhibitor. 
Preclinical findings with the HER2 inhibitor led to establishment of a new personalized clinical trial (ER/Aromatase inhibitor combined with HER2 inhibitor) and an accelerated FDA approval.
Researchers designed an internal study to understand the biomarkers of response and resistance to the anti-folate drug in NSCLC.
The study revealed that KRAS mutant NSCLCs are more responsive to antifolate drugs. The study also provided evidence for KRAS mutation status and specific markers of folate pathway activity as possible biomarkers for anti-folate drug that can be further tested in a clinical setting.