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- Funding to advance two of Harpoon's immuno-oncology programmes into clinical trials - LONDON, 25 May, 2017: Arix Bioscience plc (LSE: ARIX) ("Arix Bioscience" or "the Company"), a global healthcare and life science company supporting medical innovation, today announced that Harpoon Therapeutics, a new Arix Group Business, has closed a Series B investment round raising $45 million. Arix Bioscience co-led the financing round with New Leaf Venture Partners, and additional new investor Taiho Ventures. They join founding investor MPM Capital, which also participated. Arix Bioscience's Mark Chin will join Harpoon's Board of Directors. Harpoon created its novel, proprietary trispecific antibody platform (TriTAC(TM)) to harness T cells to kill tumour and other cell types by recruiting T cells and other immune cells. Proceeds from the financing will be used to advance Harpoon's immuno-oncology antibody platform programmes, including moving two lead programmes into clinical trials and expanding the product pipeline through discovery and partnering initiatives. In addition, the company is increasing its commitment to developing research platforms including those that become activated by proteases present in the tumour microenvironment. Harpoon's first clinical candidate, HPN424, is a prostate-specific membrane antigen (PSMA)-targeting TriTAC(TM). HPN424 is in development for the treatment of metastatic prostate cancer and is expected to enter Phase 1 clinical trials in 2018. Harpoon's second clinical candidate has not been publicly disclosed and will move into the clinic within the next year. The company anticipates additional clinical candidates to be identified and progressed. Harpoon was founded in 2015 by a team led by Patrick Baeuerle, PhD, Chief Scientific Officer during the development of bispecific T cell engagers (BiTE) at Micromet, which was acquired by Amgen for $1.2bn in 2012. His pioneering work led to the approval of Amgen's Blincyto® (blinatumomab) in 2014 for patients with refractory acute lymphoblastic leukaemia. Harpoon is based in Brisbane, California. Joe Anderson, Chief Executive Officer of Arix Bioscience plc, commented: "Harpoon's novel T cell engaging platform has great potential in the discovery and development of important new oncology therapeutics. We are very pleased to be joining the company at this exciting stage alongside the impressive founding team and highly experienced co-investors. This is another important deal for Arix, adding to our rapidly growing collection of world-class Group Businesses." For more information, please contact: About Arix Bioscience plc Arix Bioscience plc is a global healthcare and life science company supporting medical innovation. Headquartered in London and with an office in New York, Arix Bioscience sources, finances and builds world class healthcare and life science businesses addressing medical innovation at all stages of development. Operations are supported by privileged access to breakthrough academic science and strategic relationships with leading research accelerators and global pharmaceutical companies. Arix Bioscience plc is listed on the Main Market of the London Stock Exchange. For further information, please visit www.arixbioscience.com About Harpoon Therapeutics Harpoon is a preclinical stage biotechnology company founded by Patrick Baeuerle, Ph.D. and MPM Capital to develop multiple T-cell recruiting platforms leading to therapies for cancer patients and other immunologic disorders. Harpoon created its proprietary TriTAC(TM) biologics platform to harness T cells to kill tumor and other cell types by recruiting T cells and other immune cells. This approach has been optimized to penetrate tissues and extend serum exposure and has the potential to address a broad range of cancers and immunologic diseases. HPN424, a prostate-specific membrane antigen (PSMA)-targeting TriTAC(TM) biologic, is in development for the treatment of prostate cancer and is expected to enter a clinical trial next year. For more information, please visit www.harpoontx.com.


Topp M.S.,University of Würzburg | Kufer P.,Micromet | Gokbuget N.,Goethe University Frankfurt | Goebeler M.,University of Würzburg | And 25 more authors.
Journal of Clinical Oncology | Year: 2011

Purpose: Blinatumomab, a bispecific single-chain antibody targeting the CD19 antigen, is a member of a novel class of antibodies that redirect T cells for selective lysis of tumor cells. In acute lymphoblastic leukemia (ALL), persistence or relapse of minimal residual disease (MRD) after chemotherapy indicates resistance to chemotherapy and results in hematologic relapse. A phase II clinical study was conducted to determine the efficacy of blinatumomab in MRD-positive B-lineage ALL. Patients and Methods: Patients with MRD persistence or relapse after induction and consolidation therapy were included. MRD was assessed by quantitative reverse transcriptase polymerase chain reaction for either rearrangements of immunoglobulin or T-cell receptor genes, or specific genetic aberrations. Blinatumomab was administered as a 4-week continuous intravenous infusion at a dose of 15 μg/m2/24 hours. Results: Twenty-one patients were treated, of whom 16 patients became MRD negative. One patient was not evaluable due to a grade 3 adverse event leading to treatment discontinuation. Among the 16 responders, 12 patients had been molecularly refractory to previous chemotherapy. Probability for relapse-free survival is 78% at a median follow-up of 405 days. The most frequent grade 3 and 4 adverse event was lymphopenia, which was completely reversible like most other adverse events. Conclusion: Blinatumomab is an efficacious and well-tolerated treatment in patients with MRD-positive B-lineage ALL after intensive chemotherapy. T cells engaged by blinatumomab seem capable of eradicating chemotherapy-resistant tumor cells that otherwise cause clinical relapse. © 2011 by American Society of Clinical Oncology.


Lutterbuese R.,Micromet | Raum T.,Micromet | Kischel R.,Micromet | Hoffmann P.,Micromet | And 12 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2010

Epidermal growth factor receptor (EGFR)-specific monoclonal antibodies predominantly inhibit colorectal cancer (CRC) growth by interfering with receptor signaling. Recent analyses have shown that patients with CRC with mutated KRAS and BRAF oncogenes do not profit from treatment with such antibodies. Here we have used the binding domains of cetuximab and pantitumumab for constructing T cell-engaging BiTE antibodies. Both EGFR-specific BiTE antibodies mediated potent redirected lysis of KRAS- and BRAF-mutated CRC lines by human T cells at subpicomolar concentrations. The cetuximab-based BiTE antibody also prevented at very low doses growth of tumors from KRAS- and BRAF-mutated human CRC xenografts, whereas cetuximab was not effective. In nonhuman primates, no significant adverse events were observed during treatment for 3 wk at BiTE serum concentrations inducing, within 1 d, complete lysis of EGFR-overexpressing cancer cells. EGFR-specific BiTE antibodies may have potential to treat CRC that does not respond to conventional antibodies.


PubMed | Micromet
Type: Journal Article | Journal: Proceedings of the National Academy of Sciences of the United States of America | Year: 2010

Epidermal growth factor receptor (EGFR)-specific monoclonal antibodies predominantly inhibit colorectal cancer (CRC) growth by interfering with receptor signaling. Recent analyses have shown that patients with CRC with mutated KRAS and BRAF oncogenes do not profit from treatment with such antibodies. Here we have used the binding domains of cetuximab and pantitumumab for constructing T cell-engaging BiTE antibodies. Both EGFR-specific BiTE antibodies mediated potent redirected lysis of KRAS- and BRAF-mutated CRC lines by human T cells at subpicomolar concentrations. The cetuximab-based BiTE antibody also prevented at very low doses growth of tumors from KRAS- and BRAF-mutated human CRC xenografts, whereas cetuximab was not effective. In nonhuman primates, no significant adverse events were observed during treatment for 3 wk at BiTE serum concentrations inducing, within 1 d, complete lysis of EGFR-overexpressing cancer cells. EGFR-specific BiTE antibodies may have potential to treat CRC that does not respond to conventional antibodies.

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