On April 16, 2018 Nordic Nanovector ASA (OSE: NANO) reported that a poster reporting the anti-tumour effect of Humalutin (177Lu-conjugated humanized anti-CD37 antibody, 177Lu-NNV003) in preclinical models of non-Hodgkin’s lymphoma (NHL) was presented yesterday at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2018 in Chicago, USA (Press release, Nordic Nanovector, APR 16, 2018, View Source [SID1234553507]). The company previously announced the publication of the poster abstract (abstract 848) on 15 March 2018.

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The poster was entitled "In vitro and in vivo evaluation of the beta-emitting lutetium-177 labeled anti-CD37 antibody radionuclide conjugate 177Lu-NNV003 in DLBCL, CLL and MCL models," and showed that:

In tumour cell lines:

• The unlabelled anti-CD37 antibody (NNV003) kills tumour cells mainly through an immunological process called antibody dependent cellular cytotoxicity

• Humalutin (177Lu-NNV003) was found to inhibit tumour cell growth.

In preclinical lymphoma models:

• Humalutin has shown significant tumour uptake and demonstrated an anti-tumour effect in all three NHL models (mantle cell lymphoma, diffuse large B-cell lymphoma and chronic lymphocytic leukaemia).

On April 16, 2018 Deciphera Pharmaceuticals, Inc. (NASDAQ:DCPH), a clinical-stage biopharmaceutical company focused on addressing key mechanisms of tumor drug resistance, reported the presentation of updated data from its ongoing Phase 1 clinical trial of DCC-2618, the Company’s broad spectrum KIT and PDGFRα inhibitor, in patients with gastrointestinal stromal tumors (GIST) (Press release, Deciphera Pharmaceuticals, APR 16, 2018, View Source [SID1234525340]). Filip Janku, M.D., Ph.D., Assistant Professor, The University of Texas MD Anderson Cancer Center presented the poster titled "Pharmacokinetic (PK), safety, and tolerability profile of DCC-2618 in a phase 1 trial supports 150 mg QD (once daily) selected for a pivotal phase 3 trial in gastrointestinal stromal tumors (GIST)" at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Chicago, IL. The poster includes an assessment of the safety and tolerability profile of DCC-2618 in 100 GIST patients treated at the recommended Phase 2 dose (RP2D) of 150 mg QD, which supports the selection of this dose for the ongoing pivotal, randomized Phase 3 INVICTUS study (NCT03353753).

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"The data presented at AACR (Free AACR Whitepaper) provides a robust assessment of the safety and tolerability profile of DCC-2618 in GIST patients at the 150 mg QD dose selected for the INVICTUS pivotal Phase 3 study in fourth-line and fourth line plus GIST, which we initiated in January 2018," said Michael D. Taylor, Ph.D., President and Chief Executive Officer of Deciphera. "If successful, the INVICTUS study could serve as the basis for a New Drug Application (NDA), providing a much-needed therapeutic option for these patients for whom there are no approved treatment options. We also plan to initiate a second Phase 3 registration study later this year, evaluating DCC-2618 in second-line GIST patients who have progressed, or are intolerant to front-line therapy with imatinib."

The poster presentation includes the following highlights:
Safety and tolerability of DCC-2618 on 100 GIST patients treated at the 150 mg QD dose out of the total of 169 patients treated with DCC-2618, as of the cut-off date of January 18, 2018.
As of March 19, 2018, 81 of 137 GIST patients enrolled at the cut-off date and treated at 100 mg or more per day, remained on study treatment. In addition, 46 patients were treated for more than 6 months, including 10 patients who were treated for more than 12 months.
Employing a population pharmacokinetic (PK) model based on steady state exposure to DCC-2618 and the active metabolite, DP-5439, increasing doses of DCC-2618 resulted in dose proportional increases in the combined exposure.

Preliminary data from the 12 GIST patients dose escalated from 150 mg QD to 150 mg BID following progression by RECIST (Response Evaluation Criteria in Solid Tumors) are immature and do not currently support a conclusion regarding a benefit from intra-patient dose escalation.
Based on the 100 GIST patients treated at the RP2D dose of 150 mg QD, DCC-2618 was well-tolerated, supporting the use of this dose in the pivotal, randomized Phase 3 trial, INVICTUS (NCT03353753).

About DCC-2618
DCC-2618 is a KIT and PDGFRα kinase switch control inhibitor in clinical development for the treatment of KIT and/or PDGFRα-driven cancers, including gastrointestinal stromal tumors, systemic mastocytosis and glioblastoma multiforme. DCC-2618 was specifically designed to improve the treatment of GIST patients by inhibiting a broad spectrum of mutations in KIT and PDGFRα. DCC-2618 is a KIT and PDGFRα inhibitor that blocks initiating KIT mutations in exons 9, 11, 13, 14, 17, and 18, involved in GIST as well as the primary D816V exon 17 mutation involved in SM. DCC-2618 also inhibits primary PDGFRα mutations in exons 12, 14, and 18, including the exon 18 D842V mutation, involved in a subset of GIST.

On April 16, 2018 Personalis, Inc., a provider of advanced genomic sequencing and analytics for immuno-oncology, reported that the company will present four posters at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting being held this year in Chicago, Illinois from April 14-18, 2018 (Press release, Personalis, APR 16, 2018, View Source [SID1234525356]).

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Following is a list of abstracts that will be presented at the meeting.

Session ID / Poster Number

Title & Presenter
Day & Time
Location
PO.BSB01.01
1292
Methods of improving accuracy of neoantigen identification for therapeutic and diagnostic use in immuno-oncology
Presenter: Sean Michael Boyle
April 16
8am-12pm
Poster section
12
PO.BSB01.02
2245
Deconvolution of diverse immune cell populations within tumors using ACE Transcriptome
Presenter: Eric Levy
April 16
1-5pm
Poster section
12
PO.MCB09.08
5385
Supporting neoantigen discovery and monitoring in plasma through analytical validation of a deep Augmented Content Enhanced (ACE) exome
Presenter: Ravi Alla
April 18
8am-12pm
Poster section
17
PO.IM02.04
5710
Molecular profiling of anti-PD-1 treated melanoma patients reveals importance of assessing neoantigen burden and tumor escape mechanisms for clinical treatment
Presenter: Sean Michael Boyle

On April 16, 2018 Galera Therapeutics, Inc., a clinical-stage biotechnology company developing drugs targeting oxygen metabolic pathways with the potential to transform cancer radiotherapy, reported that preclinical data on GC4419, a highly selective and potent small molecule dismutase mimetic, were presented during poster sessions at the 2018 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in Chicago (Press release, Galera Therapeutics, APR 16, 2018, View Source [SID1234525450]).

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/EIN News/ — "New therapies that enhance the efficacy of radiation on cancer cells while actually decreasing toxicity to normal tissue are desperately needed to improve therapeutic outcomes in cancer. We are encouraged that the data presented at AACR (Free AACR Whitepaper) demonstrate our lead candidate, GC4419, has these properties, underscoring its potential to become an important part of cancer radiotherapy," said Mel Sorensen, M.D., President and CEO of Galera. "We look forward to building upon positive results from our Phase 2b clinical trial of GC4419 in head and neck cancer with data like this, and with the Phase 1/2 trial of GC4419 in combination with stereotactic body radiation therapy in patients with locally advanced pancreatic cancer, which is underway at The University of Texas MD Anderson Cancer Center."
The radioprotector GC4419 ameliorates radiation induced lung fibrosis while enhancing the response of non-small cell lung cancer tumors to high dose per fraction radiation exposures

The studies from The University of Texas Southwestern Medical Center covered in this poster highlight that GC4419 can both significantly reduce the normal tissue toxicity of even high-dose radiation and increase tumor response to radiotherapy. Specifically, either pretreatment or mitigation with GC4419 significantly reduced pulmonary fibrosis in focally irradiated (54 Gy single dose) mice, similar to the reduction in severe oral mucositis seen in Galera’s clinical and pre-clinical studies. Separately, mice with H1299, A549, and HCC827 lung tumor xenografts were treated with GC4419 prior to irradiating the tumors with a single 18 Gy dose. Tumor growth in all three tumor types was significantly delayed (p = 0.0022), with the majority of mice apparently tumor-free at study end. Similar enhancements in tumor radiation response were seen with syngeneic lung (LLC) and breast (4T1) tumor models. Subsequent Tumor Cure Dose (TCD50) assays demonstrated that GC4419 enhanced the efficacy of radiation by a factor of 1.67.

GC4419 enhances the response of non-small cell lung carcinoma cell lines to cisplatin and cisplatin plus radiation through a ROS-mediated pathway
These studies from The University of Texas Southwestern Medical Center report that GC4419 synergistically decreased clonogenic survival in H460 and H1299 cells treated with either cisplatin or cisplatin plus radiation. Consistent with the mechanism in combination with radiation alone, GC4419 was found to reduce intracellular superoxide, increase intracellular hydrogen peroxide, and induce early apoptosis. H1299CAT cells were used to demonstrate that this enhancement of cisplatin and cisplatin plus radiation cancer cell killing is also due to elevation of H2O2. The results are particularly intriguing given that the combination of cisplatin and radiotherapy is the primary treatment modality in GC4419’s phase 2b trial in patients with head and neck cancer.

About GC4419
GC4419 is a highly selective and potent small molecule dismutase mimetic that closely mimics the activity of human superoxide dismutase enzymes. GC4419 works to reduce elevated levels of superoxide caused by radiation therapy by rapidly converting superoxide to hydrogen peroxide and oxygen. Left untreated, elevated superoxide can damage noncancerous tissues and lead to debilitating side effects, including oral mucositis (OM), which can limit the anti-tumor efficacy of radiation therapy. Conversion of elevated superoxide to hydrogen peroxide, which is selectively more toxic to cancer cells, can also enhance the effect of radiation on tumors, particularly with stereotactic body radiation therapy (SBRT), which produces high levels of superoxide.
GC4419 has been studied in patients with head and neck cancer, GC4419’s lead indication, for its ability to reduce the duration, incidence and severity of radiation-induced severe oral mucositis (SOM). Results from Galera’s 223-patient, double blind, randomized, placebo-controlled Phase 2b clinical trial demonstrated GC4419’s ability to dramatically reduce the duration of SOM from 19 days to 1.5 days (92 percent), the incidence of SOM through completion of radiation by 34 percent and the severity of patients’ OM by 47 percent, while demonstrating acceptable safety when added to a standard radiotherapy regimen. In addition, in multiple preclinical studies, GC4419 demonstrated an increased tumor response to radiation therapy while preventing toxicity in normal tissue.
The U.S. Food and Drug Administration (FDA) granted Breakthrough Therapy designation to GC4419 for the reduction of the duration, incidence and severity of SOM induced by radiation therapy with or without systemic therapy. The FDA also granted Fast Track designation to GC4419 for the reduction of the severity and incidence of radiation and chemotherapy-induced OM.

On April 16, 2018 Endocyte, Inc. (Nasdaq:ECYT), a biopharmaceutical company developing targeted therapeutics for personalized cancer treatment, reported in a late-breaking poster session the presentation of new research from Endocyte’s chimeric antigen receptor T-cell (CAR T) adaptor molecule (CAM) platform at the AACR (Free AACR Whitepaper) Annual Meeting 2018 in Chicago, IL (Press release, Endocyte, APR 16, 2018, View Source [SID1234525341]).

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"We are pleased to present data that support the utility of our unique CAR T platform, which potentially enables us to control cytokine release syndrome (CRS), manage T-cell exhaustion and address heterogeneity in both solid and liquid tumors through the administration of multiple CAMs," said Chris Leamon, vice president, research and development of Endocyte. "These findings are critical towards identifying the dosing regimen and confirming the anti-tumor activity of EC17/CAR T, our folate-targeted CAM-based therapy, as we look to initiate a phase 1 trial in osteosarcoma later this year."

Endocyte’s CAM-based therapies consist of a single universal autologous CAR T-cell, designed to bind with high affinity to FITC. This universal CAR T-cell can be specifically directed to cancer cells through the administration of a bi-specific adaptor molecule targeted to both FITC and a tumor target, which acts to bridge the universal CAR T-cell with the cancer cells. This allows for control of the antigen target through the administration of the CAM, in contrast to current CAR T-cell therapies, in which the antigen targets are not controlled.

The data presented at AACR (Free AACR Whitepaper) show that EC17 penetrates solid tumors within minutes and is retained due to high affinity for the folate receptor (FR), while unbound EC17 rapidly clears from the blood and receptor-negative tissues. When tested against human xenografts, EC17/CAR T-cell therapy has shown consistent antitumor activity with low or no adverse reactions. For translation into first-in-human testing, clinically relevant dosing regimens were evaluated using tumor-free and tumor-bearing mice to study CAR T-cell proliferation, cytokine production and the onset/mitigation of CRS. Preclinically, EC17/CAR T-cell therapy has demonstrated meaningful efficacy against some of the more aggressive and chemo-resistant FR+ tumors of various histology.

Although CRS could be triggered in this study, it could also be mitigated, or even prevented, using intermittent dosing and/or dose titration of the EC17 CAM. Under extreme conditions where dose cessation failed, intravenous sodium fluorescein (NaFl) could be used as a fast-acting rescue agent to temporarily displace CAR T-cells from their targets and reverse the CRS.

Website Information
Endocyte routinely posts important information for investors on its website, www.endocyte.com, in the "Investors & News" section. Endocyte uses this website as a means of disclosing material information in compliance with its disclosure obligations under Regulation FD. Accordingly, investors should monitor the "Investors & News" section of Endocyte’s website, in addition to following its press releases, SEC filings, public conference calls, presentations and webcasts. The information contained on, or that may be accessed through, Endocyte’s website is not incorporated by reference into, and is not a part of, this document.