10-Q – Quarterly report [Sections 13 or 15(d)]

XBiotech has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission (Filing, 10-Q, XBiotech, 2017, MAY 13, 2016, View Source [SID1234521614]).

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10-Q – Quarterly report [Sections 13 or 15(d)]

vTv Therapeutics has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission (Filing, 10-Q, vTv Therapeutics, 2017, MAY 13, 2016, View Source [SID1234521344]).

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10-Q – Quarterly report [Sections 13 or 15(d)]

CohBar has filed a 10-Q – Quarterly report [Sections 13 or 15(d)] with the U.S. Securities and Exchange Commission (Filing, 10-Q, CohBar, 2017, MAY 13, 2016, View Source [SID1234521269]).

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Enumeral Reports First Quarter Financial Results

On May 13, 2016 Enumeral Biomedical Holdings, Inc. (OTCQB: ENUM) ("Enumeral" or the "Company"), a biotechnology company focused on the discovery and development of novel antibody-based immunotherapies to help the immune system fight cancer and other diseases, reported its financial results for the three months ended March 31, 2016 (Press release, ENUMERAL BIOMEDICALORATION, MAY 13, 2016, View Source;p=irol-newsArticle&ID=2168350 [SID:1234512372]).

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Recent Business Highlights

In April 2016, Enumeral entered into a License and Transfer Agreement with Pieris Pharmaceuticals, Inc. and Pieris Pharmaceuticals GmbH. Pursuant to this agreement, Pieris is licensing from Enumeral specified intellectual property related to Enumeral’s anti-PD-1 antibody program ENUM 388D4 for the potential development and commercialization by Pieris of novel multispecific therapeutic proteins comprising fusion proteins based on Pieris’ Anticalins class of therapeutic proteins and Enumeral antibodies in the field of oncology.
In April 2016, Enumeral presented research findings on the Company’s novel class of anti-PD-1 antibodies in a poster at the AACR (Free AACR Whitepaper) Annual Meeting 2016 in New Orleans, noting that Enumeral’s anti-PD-1 antibody ENUM 244C8 appears to elicit cytokine secretion from cell types associated with innate immunity in ex vivo assays using lung biopsy samples from human patients.
First Quarter 2016 Financial Results

Cash and Cash Equivalents: Cash and cash equivalents as of March 31, 2016 were $1,837,304, as compared to $3,596,262 as of December 31, 2015. As of the date of this press release, Enumeral believes that it only has sufficient liquidity to fund operations through June 2016. If Enumeral is unable to raise additional capital on acceptable terms and on a timely basis, Enumeral may be required to downsize or wind down its operations through liquidation, bankruptcy, or a sale of its assets. The Company is currently exploring a range of potential transactions, which may include public or private equity offerings, debt financings, collaborations and licensing arrangements, and/or other strategic alternatives, including a merger, sale of assets or other similar transactions.
Revenue: Revenue increased by $159,735 to $434,457 for the three months ended March 31, 2016, as compared to $274,722 for the three months ended March 31, 2015. This increase in revenue is attributable to the Company’s collaboration agreement with Merck and its grant from the National Cancer Institute.

Research and Development Expenses: Research and development ("R&D") expenses increased by $239,539 to $1,470,043 for the three months ended March 31, 2016, as compared to $1,230,504 for the three months ended March 31, 2015. This increase is primarily due to increased facility expenses in connection with the Company’s office relocation and an increase in stock-based compensation expense associated with stock option grants issued during the three months ended March 31, 2016.
General and Administrative Expenses: General and administrative ("G&A") expenses decreased by $230,609 to $1,194,334 for the three months ended March 31, 2016, as compared to $1,424,943 for the three months ended March 31, 2015. This decrease is primarily due to a decrease in legal costs and a decrease in exit costs associated with the termination of the Company’s former lease in connection with the Company’s office relocation.

Other Income (Expense): Other income decreased by $3,997,651 to $674,868 for the three months ended March 31, 2016, as compared to $4,672,519 for the three months ended March 31, 2015. This decrease is primarily due to a decrease in non-cash income related to the change in the fair value of derivative liabilities associated with the warrants issued in connection with the Company’s July 2014 private placement transaction. The Company expects that future changes in the fair value of the derivative liabilities will be due primarily to fluctuations in the value of the Company’s common stock and potential exercises of outstanding warrants.

Net Income (Loss): Net income (loss) changed by $3,846,846 to ($1,555,052) for the three months ended March 31, 2016, as compared to $2,291,794 for the three months ended March 31, 2015. This change is primarily due to the decrease in other income described above.

Provectus Biopharmaceuticals Announces Publication of Article in Oncotarget Detailing PV-10’s Immuno-Ablative Mechanism of Action

On May13, 2016 Provectus Biopharmaceuticals, Inc. (NYSE MKT: PVCT, www.pvct.com), a clinical-stage oncology and dermatology biopharmaceutical company ("Provectus" or "the Company"), reported that an article has been published detailing the immuno-ablative mechanism of action of PV-10, the Company’s novel investigational drug for cancer (Press release, Provectus Pharmaceuticals, MAY 13, 2016, https://www.pvct.com/pressrelease.html?article=20160513.1 [SID:1234512371]).

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The article, titled, "Intralesional Rose Bengal in Melanoma Elicits Tumor Immunity Via Activation of Dendritic Cells by the Release of High Mobility Group Box 1," appears as an advance publication in Oncotarget, an Open-Access journal, and can be accessed by visiting:

View Source

The article documents results of a multi-year, multidisciplinary translational medicine program led jointly by Shari Pilon-Thomas and Amod A. Sarnaik of Moffitt Cancer Center in Tampa, Florida. The authors report detailed data on the mode in which intralesional injection of PV-10 (rose bengal) selectively kills tumor cells and the immunologic signaling that results from tumor ablation, starting with release of High Mobility Group Box 1 (HMGB1, a Damage-Associated Molecular Pattern molecule released by dying cancer cells that can serve as an immunological adjuvant to promote phagocytosis, antigen-presentation, and dendritic cell activation). The authors then follow this signaling through antigen uptake and dendritic cell activation, T cell priming and activation in peripheral blood, and culminating in a tumor-specific immune response marked by T cell infiltration and regression of uninjected tumors.

Eric Wachter, CTO of Provectus, observed, "The Moffitt researchers have systematically documented each of the key steps in the immuno-oncology cycle described by Chen and Mellman in their landmark review article (Oncology Meets Immunology: the Cancer-Immunity Cycle. Immunity 2013; 39: 1-10). In an exemplary demonstration of translational medicine, this team identified important immunologic markers in model systems and verified key facets of these in clinical trial participants, and similarly identified other markers in clinical trial participants and substantiated these in mouse models. While a number of their main observations were previously reported at scientific meetings, these are presented here in detailed, integrated fashion for the first time."

Shari Pilon-Thomas of Moffitt, stated, "Concordance of tumor-specific T cells in peripheral blood of clinical trial participants and mice led us to look for triggers of T cell activation. Working back from these observations, we found that HMGB1 release was common in mouse and man after tumor ablation with PV-10. These results support PV-10 ablation and the resulting tumor necrosis as the upstream trigger for systemic anti-tumor response."

Wachter noted, "This paper is a watershed event in the development of PV-10, walking the reader through all the steps of immune activation after PV-10 injection, from immunogenic cell death and signaling via release of HMGB1, dendritic cell recruitment and infiltration into draining lymph nodes, activation of tumor-specific T cells, and killing of uninjected tumors upon infiltration by these T cells."

Wachter added, "This mechanism of action informed the design of the two active PV-10 clinical trials: NCT02288897 in patients with locally advanced cutaneous melanoma (melanoma limited to the skin) to test the hypothesis that PV-10 alone can produce a systemic immune response that translates to longer progression free survival (PFS); and NCT02557321 in patients with later stage melanoma to test whether combination of PV-10 with the recently approved systemic immunotherapy, pembrolizumab, can ‘induce and boost’ an immune response against melanoma."