MAIN The introduction of checkpoint inhibitors (pembrolizumab/Keytruda, nivolumab/Optivo), and ipilimumab/Yervoy as novel cancer immunotherapeutic approaches has received regulatory approvals in several cancer types culminating in the 2018 Nobel prize awarded for the discovery of immune checkpoint blockade.1 By the end of 2020, a tsunami of immunotherapies has been evaluated in thousands of clinical trials targeting different malignancies with numerous drugs in pharmaceutical companies’ pipeline. Although great clinical success has been noticed by using therapeutic PD-1/PD-L1 signalling inhibitors, only a subset of patients (10–15%) has responded to monotherapy due to the development of primary and secondary resistance. Ongoing studies that exhibit durable responses and efficacy of treatment depends on the rational design of synergistic combinatorial approaches involving different modalities. Our seminal contribution and hypothesis of B-cell epitope vaccine established over decades of research resulting in the development of a polyclonalinduced B-cell antibody response will be more effective, or as effective with improved safety, compared with current monoclonal antibody (mAb) therapies.2 We have advanced a number of combination strategies of HER-2 with VEGF can significantly enhance anti-tumour effects.3 Additionally, we have demonstrated that combination therapies with HER-2 and IGF-1R or HER-2 and HER-3 and HER-1 and IGF-1R exhibit enhanced anti-tumour responses,4,5 and our HER-2 combination vaccines (B-Vaxx) targeting both trastuzumab and pertuzumab (clinical trials.gov: NCT01376505) showed great effects on patients in a Phase 1 clinical trial6 and is presently in a Phase 2 extension trial at the OSU James Cancer Hospital. We recently introduced a novel PD-1 checkpoint inhibitor vaccine (PD1-Vaxx):7 a chimeric PD-1 B-cell peptide epitope vaccine (amino acid 92–110; PD1-Vaxx) linked to a measles virus fusion “promiscuous” T-cell epitope peptide (MVF) amino acid 288–302 via a four amino acid residue (GPSL). This vaccine when emulsified in Montanide ISA 720VG elicits the production of polyclonal antibodies that block PD-1 signalling and thus trigger anti-cancer effects comparable with the US Food and Drug Administration (FDA)-approved mAb “vivolumab/pembrolizumab” with no evidence of toxicity or autoimmunity. Our results indicated that MVF-PD-1 (92–110) elicited high levels of anti-peptide antibodies that recognised the human recombinant protein PD-1. In a syngeneic BALB/c model, mice were immunised with PD1-Vaxx three times at three weeks’ intervals followed by challenge with CT26 colon carcinoma cells. A mouse surrogate antagonist antibody anti-mPD-1 mAb 29F.1A12 was used to treat mice twice a week as a positive control or PBS as a negative control. We found that mAb and PD1-Vaxx vaccine treatments had a similar and significant reduction in tumour growth. However, in this study, only the MVF-PD-1(92–110) group observed complete tumour regression after day 9 of tumour challenge, which indicated PD1-Vaxx has a better tumour control ability
Check the Website there's plenty of information on PD1-Vaxx
MAIN The introduction of checkpoint inhibitors...
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