Bio-Path Holdings presents BP1003 data at AACR

Bio-Path Holdings announced that data from pre-clinical studies supporting the potential of BP1003, a liposome-incorporated STAT3 oligodeoxynucleotide inhibitor, for the treatment of pancreatic cancer, non-small cell lung cancer, or NSCLC, and acute myelogenous leukemia, or AML, were presented in a poster at the American Association for Cancer Research, or AACR. The poster highlights four antisense oligo sequences directed against STAT3 mRNA identified by Bio-Path and manufactured using DNAbilize antisense RNAi nanoparticle technology. Cell viability tests and western blots were conducted to determine the inhibitory effects of liposome-incorporated STAT3 antisense oligo on NSCLC and AML cells. An ex vivo live tissue sensitivity assay was performed with a panel of 20 pancreatic ductal adenocarcinoma patient-derived xenografts to study the overall activity of BP1003 alone, and in combination with gemcitabine. Using previously defined criteria, tissue slice viability inhibition greater than 30% and with a less than 0.05 value was considered to be a response. For validation of ex vivo results, tumor bearing mice were administered BP1003 and gemcitabine twice a week for 28 days. Tumor volumes were monitored for up to 49 days. The most potent liposome-incorporated STAT3 antisense sequence in decreasing NSCLC cell viability was selected as the drug candidate BP1003. Further validation in AML cells demonstrated that BP1003 inhibited cell viability and STAT3 protein expression. In the ex vivo LTSA assay, BP1003 at a dose of 10 microM significantly inhibited the tissue slice viability in 9 out of 18 PDAC PDXs by more than 30%. The combination of BP1003 and gemcitabine further enhanced ex vivo efficacy of BP1003 in a subset of PDXs. In the in vivo study, a combination of BP1003 and gemcitabine caused tumor regression during the 28-day drug treatment period. This anti-cancer activity was maintained for another 21 days, even when drug treatment had ceased. Preclinical pancreatic cancer models demonstrated that BP1003 successfully penetrated the stroma into pancreatic tumors. Finally, the results in pancreatic cancer showed that BP1003 inhibited tumor slice viability in nine of 18.

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