Amplia Therapeutics Limited (ASX: ATX) has confirmed that researchers at the Garvan Institute have now shown that its AMP945 treatment is able to improve the effectiveness of gemcitabine/Abraxane in a model of human pancreatic cancer.
Previously, Amplia reported that the addition of a pre-treatment with AMP945 to a regimen of the standard chemotherapy drugs gemcitabine/Abraxane resulted in a 27% improvement in survival in the aggressive KPC mouse model of pancreatic cancer .
In the new study, cancer cells derived from a human pancreas cancer were transplanted into the pancreas of laboratory mice (the TKCC-10-LO orthotopic model).
Once pancreatic tumours were established, mice were treated either with gemcitabine/Abraxane or AMP945 in combination with gemcitabine/Abraxane. When intermittent oral doses of Amplia’s AMP945 were added to gemcitabine/Abraxane, survival increased by 33% compared to gemcitabine/Abraxane alone.
We have run this model on several occasions using different FAK inhibitors and now with AMP945. This result clearly shows that AMP945 increases survival in this model and is likely superior to other FAK inhibitors we have tested,” Professor Paul Timpson of the Garvan Institute said.
In this experiment, the median survival time of untreated mice was 68 days, while mice treated with gemcitabine/Abraxane alone exhibited a median survival time of 122 days. Mice treated with a combination of AMP945 and gemcitabine/Abraxane had a median survival time of 163 days, representing a statistically significant 33% increase in median survival (P ≤ 0.05), relative to gemcitabine/Abraxane alone.
“Working with our collaborators at the Garvan, we have shown that AMP945 can improve the current standard of care in a second model of pancreatic cancer and provide further validation of the approach we will use in our Phase 2 clinical trial that is expected to start early in the second quarter,” said John Lambert, CEO of Amplia.
“These data are particularly compelling as AMP945 has been used to treat tumours that have formed from human pancreatic cancer cells. Aside from actually running the clinical trial, this is the most compelling translational evidence we could have to support the approach we are taking.”
