(Sharecast News) - Specialist small molecule drug development company Sareum Holdings announced on Thursday that Sierra Oncology, the licence holder advancing clinical cancer candidate SRA737, had reported that an abstract reporting preclinical data for SRA737 - its Chk1 inhibitor - plus low dose gemcitabine (LDG), in combination with immunotherapy, had been selected for a late-breaking oral presentation at the American Association of Cancer Research annual meeting.The AIM-traded firm said SRA737 - its leading clinical-stage programme - was a "novel" Checkpoint kinase 1 (Chk1) inhibitor, was licensed to NASDAQ-listed Sierra Oncology, and was in Phase 2 clinical trials targeting ovarian and other advanced cancers.It explained that a late-breaking abstract detailed "highly significant and timely" findings in any area of cancer research that was not available at the time of the regular abstract deadline.Only those abstracts that were deemed to be of "high scientific priority" would be accepted for presentation at the meeting."We previously reported that SRA737 activated the innate immune signalling STING pathway and demonstrated significant synergistic anti-tumour activity with immunotherapy in an immunotherapy-refractory small cell lung cancer (SCLC) model," said Dr Lauren Byers, associated professor at the University of Texas MD Anderson Cancer Center in Houston."SRA737 + LDG is a novel drug combination, where gemcitabine acts as a potent inducer of replication stress that potentiates SRA737's activity."Dr Byers said the new studies revealed a "striking" immunomodulatory effect of SRA737 + LDG, that resulted in "some of the most profound" synergistic activity with anti-PD-L1 therapy that they had observed in the model."We are excited by the potential clinical translatability of these findings and their possible broader impact on immune checkpoint blockade strategies."Dr Christian Hassig, chief scientific officer at Sierra Oncology, added that the "dramatic enhancement" of immunotherapy anti-tumour activity in combination with SRA737 + LDG provided a "strong preclinical rationale" for the potential of that replication stress targeting strategy, to broaden the limited clinical efficacy of immunotherapy observed in certain cancers, such as SCLC.